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GABAergics FAQ: Pharmacology & Withdrawal (focus on Benzos)
GABAergics: How they work and how to withdraw With an emphasis on BenzodiazepineWithdrawal
A general introduction to (Z)-Benzos, GABAergics, their action and stopping them.
Sources: a lot of this comes from the DF and http://www.benzo.org.uk/manual/bzsched.htm Other sources: The DF, especially specific subsections on respective topics and the methampethamine and opioid w/d stickies. Thanks guys, sorry i didn't ask every single one for permission. I assume it, as this article will help many. Also Wikipedia, Google.. etc.
Copy it! As far as I am concerned, feel free to use all my writing wherever you want to! Free the world!
Several Picture are uploaded for my convenience regarding posting them on Imageshack but all are also attachted to this article.
Help me: I have worked at least 30 hours on this post already. So things may be wrong or missing. Please consider that when you criticism and find mistakes, be constructive and suggestive and help make this FAQ better.
Before reading anything else or considering the information provided, please make sure to read the medical disclaimer at the end of the post or click here.
For more links on equivalence tables look further down
[h2]List of Benzodiazepines, Brandnames, Therapeutic use, half-life, chemical structure, etc.[/h2]
Ok, this list is not necessarily "complete", as some Research Benzos or unknown ones may not be included. But hopefully all of the common ones are: **This information is unverified and from Wikipedia. The Equivalence tables as well as other Pharmcological information in this list may or may not be accurate. Always verify by research and don't rely on this list. This list is only intended to display a list of common Benzos*** I think most of it is pretty accurate though. (For better and more equivalence tables see below)
Atypical benzodiazepine receptor ligands:
Another List of Benzodiazepines by Chemical Subgroup
Bentazepam • Devazepide • Ketazolam • Razobazam • Tifluadom Sketch of Structural Relation of Benzos
Click on the picture to enlarge it!
You can use this link to download and view the picture as well by clicking here (uploaded to the DF database).
[h2]Potency & Elimination (incl. Drug tests)[/h2]
A large number of benzodiazepines are available (Table 1). There are major differences in potency between different benzodiazepines, so that equivalent doses vary as much as 20-fold. For example, 0.5 milligrams (mg) of alprazolam (Xanax) is approximately equivalent to 10mg of diazepam (Valium). Thus a person on 6mg of alprazolam daily, a dose not uncommonly prescribed in the US, is taking the equivalent of about 120mg of diazepam, a very high dose. These differences in strength have not always been fully appreciated by doctors, and some would not agree with the equivalents given here. Nevertheless, people on potent benzodiazepines such as alprazolam, lorazepam (Ativan) or clonazepam (Klonopin) tend to be using relatively large doses. This difference in potency is important when switching from one benzodiazepine to another, for example changing to diazepam during the withdrawal, as described in the next chapter.
Speed of elimination
Benzodiazepines also differ markedly in the speed at which they are metabolised (in the liver) and eliminated from the body (in the urine) (Table 1). For example, the "half-life" (time taken for the blood concentration to fall to half its initial value after a single dose) for triazolam (Halcion) is only 2-5 hours, while the half-life of diazepam is 20-100 hours, and that of an active metabolite of diazepam (desmethyldiazepam) is 36-200 hours. This means that half the active products of diazepam are still in the bloodstream up to 200 hours after a single dose. Clearly, with repeated daily dosing accumulation occurs and high concentrations can build up in the body (mainly in fatty tissues). As Table 1 shows, there is a considerable variation between individuals in the rate at which they metabolise benzodiazepines.
Table 1. BENZODIAZEPINES AND SIMILAR DRUGS
Also check these links for more infos about equivalences, as they may differ slightly.
1. Half-life: time taken for blood concentration to fall to half its peak value after a single dose. Half-life of active metabolite shown in square brackets. This time may vary considerably between individuals.
2. Market aim: although all benzodiazepines have similar actions, they are usually marketed as anxiolytics (a), hypnotics (h) or anticonvulsants (e).
3. These equivalents do not agree with those used by some authors. They are firmly based on clinical experience but may vary between individuals.
4. These drugs are chemically different from benzodiazepines but have the same effects on the body and act by the same mechanisms.
5. All these drugs are recommended for short-term use only (2-4 weeks maximum).
[h2]Duration of effects[/h2]
The speed of elimination of a benzodiazepine is obviously important in determining the duration of its effects. However, the duration of apparent action is usually considerably less than the half-life. With most benzodiazepines, noticeable effects usually wear off within a few hours. Nevertheless the drugs, as long as they are present, continue to exert subtle effects within the body. These effects may become apparent during continued use or may appear as withdrawal symptoms when dosage is reduced or the drug is stopped.
Therapeutic actions of benzodiazepines. Regardless of their potency, speed of elimination or duration of effects, the actions in the body are virtually the same for all benzodiazepines. This is true whether they are marketed as anxiolytics, hypnotics or anti-convulsants (Table 1). All benzodiazepines exert five major effects which are used therapeutically: anxiolytic, hypnotic, muscle relaxant, anticonvulsant and amnesic (impairment of memory) (Table 2).
[h2]Therapeutic use of Benzos[/h2]
Other clinical uses, utilising combined effects: Alcohol detoxification
Acute psychosis with hyperexcitability and aggressiveness
These actions, exerted by different benzodiazepines in slightly varying degrees, confer on the drugs some useful medicinal properties. Few drugs can compete with them in efficacy, rapid onset of action and low acute toxicity. In short-term use, benzodiazepines can be valuable, sometimes even life-saving, across a wide range of clinical conditions as shown in Table 2. Nearly all the disadvantages of benzodiazepines result from long-term use (regular use for more than a few weeks). The UK Committee on Safety of Medicines in 1988 recommended that benzodiazepines should in general be reserved for short-term use (2-4 weeks only).
[h2]Mechanisms of GABAergics/Benzos[/h2]
Anyone struggling to get off their benzodiazepines will be aware that the drugs have profound effects on the mind and body apart from the therapeutic actions. Directly or indirectly, benzodiazepines in fact influence almost every aspect of brain function. For those interested to know how and why, a short explanation follows of the mechanisms through which benzodiazepines are able to exert such widespread effects.
All benzodiazepines act by enhancing the actions of a natural brain chemical, GABA (gamma-aminobutyric acid). GABA is a neurotransmitter, an agent which transmits messages from one brain cell (neuron) to another. The message that GABA transmits is an inhibitory one: it tells the neurons that it contacts to slow down or stop firing. Since about 40% of the millions of neurons all over the brain respond to GABA, this means that GABA has a general quietening influence on the brain: it is in some ways the body's natural hypnotic and tranquilliser. This natural action of GABA is augmented by benzodiazepines which thus exert an extra (often excessive) inhibitory influence on neurons (Fig. 1).
Fig. 1. Diagram of mechanism of action of the natural neurotransmitter GABA (gamma-aminobutyric acid) and benzodiazepines on nerve cells (neurons) in the brain
(1,2) Nerve impulse causes release of GABA from storage sites on neuron 1 (3) GABA released into space between neurons (4) GABA reacts with receptors on neuron 2; the reaction allows chloride ions (Cl-) to enter the neuron (5) This effect inhibits further progress of the nerve impulse (6,7) Benzodiazepines react with booster site on GABA receptors (8) This action enhances the inhibitory effects of GABA; the ongoing nerve impulse may be completely blocked
The way in which GABA sends its inhibitory message is by a clever electronic device. Its reaction with special sites (GABA-receptors) on the outside of the receiving neuron opens a channel, allowing negatively charged particles (chloride ions) to pass to the inside of the neuron. These negative ions "supercharge" the neuron making it less responsive to other neurotransmitters which would normally excite it. Benzodiazepines also react at their own special sites (benzodiazepine receptors), situated actually on the GABA-receptor. Combination of a benzodiazepine at this site acts as a booster to the actions of GABA, allowing more chloride ions to enter the neuron, making it even more resistant to excitation. Various subtypes of benzodiazepine receptors have slightly different actions. One subtype (alpha 1) is responsible for sedative effects, another (alpha 2) for anti-anxiety effects, and both alpha 1 and alpha 2, as well as alpha 5, for anticonvulsant effects. All benzodiazepines combine, to a greater or lesser extent, with all these subtypes and all enhance GABA activity in the brain.
As a consequence of the enhancement of GABA's inhibitory activity caused by benzodiazepines, the brain's output of excitatory neurotransmitters, including norepinephrine (noradrenaline), serotonin, acetyl choline and dopamine, is reduced. Such excitatory neurotransmitters are necessary for normal alertness, memory, muscle tone and co-ordination, emotional responses, endocrine gland secretions, heart rate and blood pressure control and a host of other functions, all of which may be impaired by benzodiazepines. Other benzodiazepine receptors, not linked to GABA, are present in the kidney, colon, blood cells and adrenal cortex and these may also be affected by some benzodiazepines. These direct and indirect actions are responsible for the well-known adverse effects of dosage with benzodiazepines.
This is mainly copied from Wikipedia, but is interesting to further understand the working of the Receptors that Benzos affect.
The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid (GABA), the chief inhibitory neurotransmitter in the vertebrate central nervous system. There are two classes of GABA receptors: GABAA and GABAB.
GABAA receptors are ligand-gated ion channels (also known as ionotropic receptors), whereas GABAB receptors are G protein-coupled receptors (also known as metabotropic receptors).
Thus, GABAA receptors are ligand-gated ion channels, whereas GABAB receptors are G protein-coupled receptors.
This has a parallel to several other receptors in the body, in which a single molecule binds to receptors which function in completely different ways:
* acetylcholine binds to nicotinic and muscarinic acetylcholine receptors
* serotonin binds to 5-HT3 and metabotropic receptors
* glutamate binds to ionotropic and metabotropic receptors
* purines bind to ionotropic nucleotide-gated P2X and G protein-coupled P2Y receptors
γ-Aminobutyric acid (GABA) (IPA: [ˈgćmə əˈmiːnoʊbjuːˈtɪrɨk ˈćsɨd]) is the chief inhibitory neurotransmitter in the mammalian central nervous system. It plays a role in regulating neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone. In insect species GABA acts only on excitatory nerve receptors.
Although chemically it is an amino acid, GABA is rarely referred to as such in the scientific or medical communities, because the term "amino acid," used without a qualifier, refers to the alpha amino acids, which GABA is not, nor is it incorporated into proteins.
In spastic diplegia in humans, GABA absorption by some nerves becomes impaired, which leads to hypertonia of the muscles signaled by those nerves.
In vertebrates, GABA acts at inhibitory synapses in the brain by binding to specific transmembrane receptors in the plasma membrane of both pre- and postsynaptic neuronal processes. This binding causes the opening of ion channels to allow the flow of either negatively charged chloride ions into the cell or positively charged potassium ions out of the cell. This action results in a negative change in the transmembrane potential, usually causing hyperpolarization. Two general classes of GABA receptor are known: GABAA in which the receptor is part of a ligand-gated ion channel complex, and GABAB metabotropic receptors, which are G protein-coupled receptors that open or close ion channels via intermediaries (G proteins).
Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the adult vertebrate. Medium Spiny Cells are a typical example of inhibitory CNS GABAergic cells. In contrast, GABA exhibits excitatory actions in insects, mediating muscle activation at synapses between nerves and muscle cells, and also the stimulation of certain glands. In mammals, some GABAergic neurons, such as chandelier cells, are also able to excite their glutamatergic counterparts.
GABAA receptors are chloride channels, that is, when activated by GABA, they allow the flow of chloride ions across the membrane of the cell. Whether this chloride flow is excitatory/depolarizing (makes the voltage across the cell's membrane less negative), shunting (has no effect on the cell's membrane) or inhibitory/hyperpolarizing (makes the cell's membrane more negative) depends on the direction of the flow of chloride. When net chloride flows out of the cell, GABA is excitatory or depolarizing; when the net chloride flows into the cell, GABA is inhibitory or hyperpolarizing. When the net flow of chloride is close to zero, the action of GABA is shunting. Shunting inhibition has no direct effect on the membrane potential of the cell, however it minimises the effect of any coincident synaptic input essentially by reducing the electrical resistance of the cell's membrane (essentially equivalent to Ohm's law). A developmental switch in the molecular machinery controlling concentration of chloride inside the cell and hence the direction of this ion flow, is responsible for the changes in the functional role of GABA between the neonatal and adult stages. That is to say, GABA's role changes from excitatory to inhibitory as the brain develops into adulthood.
In hippocampus and neocortex of the mammalian brain, GABA has primarily excitatory effects early in development, and is in fact the major excitatory neurotransmitter in many regions of the brain before the maturation of glutamate synapses - See developing cortex.
In the developmental stages preceding the formation of synaptic contacts, GABA is synthesized by neurons and acts both as an autocrine (acting on the same cell) and paracrine (acting on nearby cells) signalling mediator.
GABA regulates the proliferation of neural progenitor cells the migration and differentiation the elongation of neurites and the formation of synapses.
GABA also regulates the growth of embryonic and neural stem cells. GABA can inﬂuence the development of neural progenitor cells via brain-derived neurotrophic factor (BDNF) expression. GABA activates the GABAA receptor, causing cell cycle arrest in the S-phase, limiting growth.
Beyond the nervous system
GABAergic mechanisms have been demonstrated in various peripheral tissues and organs including, but not restricted to the intestine, stomach, pancreas, Fallopian tube, uterus, ovary, testis, kidney, urinary bladder, lung and liver.
In 2007, an excitatory GABAergic system was described in the airway epithelium. The system activates following exposure to allergens and may participate in the mechanisms of asthma. GABAergic systems have also been found in the testis and in the eye lens.
Structure and conformation
GABA is found mostly as a zwitterion, that is, with the carboxyl group deprotonated and the amino group protonated. Its conformation depends on its environment. In the gas phase, a highly folded conformation is strongly favored because of the electrostatic attraction between the two functional groups. The stabilization is about 50 kcal/mol, according to quantum chemistry calculations. In the solid state, a more extended conformation is found, with a trans conformation at the amino end and a gauche conformation at the carboxyl end. This is due to the packing interactions with the neighboring molecules. In solution, five different conformations, some folded and some extended are found as a result of solvation effects. The conformational flexibility of GABA is important for its biological function, as it has been found to bind to different receptors with different conformations. Many GABA analogues with pharmaceutical applications have more rigid structures in order to control the binding better.
[h3]GABAergic Drugs explained and listed[/h3]
Drugs that act as agonists of GABA receptors (known as GABA analogues or GABAergic drugs) or increase the available amount of GABA typically have relaxing, anti-anxiety and anti-convulsive effects. Many of the substances below are known to cause anterograde amnesia and retrograde amnesia.
It has been suggested that orally administered GABA increases the amount of Human Growth Hormone, but this is questionable since it is unknown whether GABA can pass the blood-brain barrier.
There are two things to keep in mind here: First, any of these (and other drugs working on this system) should be avoided during and after withdrawal for the chemicals in the brain to get into a natural balance again. Anything from "outside" the brain may intterup this balance and also cause a relapse. However, during withdrawal some people like to use certain types of these drugs to alleviate withdrawal symptoms and help them get over the worst parts of withdrawal. I would not recommend this, and if doing so thorough research is necessary. Also check for experiences in the approporiate forum in the DF.
There are more to the following list, but i think these are the most common.
As said again, a very few of these are as well in the Supplements for Recovery Aid list, as this list include both substances the enhance the GABA system as well as substances that suppress it (agonsts, antagonists) and precursor and such and many work on a lot of different systems in the body as well. Some weak ones of certain groups can help with withdrawals, most however should be avoided.
This list is intended just for general curiosity or in case SWIY takes one of those in addition to a Benzo he wants to stop taking. For each of these research and a doctors opinion ins necessary.
GABA Positive allosteric modulators
Theses are drugs that generally interfere wih the GABA system.
A positive allosteric modulator (PAM) is a drug which increases the activity of a receptor indirectly via activation of an allosteric site on the protein. PAMs are similar to agonists in that they contribute to overall receptor activation, but they are different due to the fact that they do so in a functionally distinctive way.
Again, these should be avoid during or after cessation of a Benzo or similar, as the may cause a substituted addiction or prolong withdrawal and prolong the recovery of the natural brain chemistry. However, in some people and some situations temporary use may help avoid the very bad phases during withdrawal.
Benzodiazepine overdose describes the ingestion of one of the drugs in the benzodiazepine class in quantities greater than are recommended or generally practiced. Death as a result of benzodiazepines is uncommon but does occasionally happen. Deaths after hospital admission are considered to be low. However, combinations of high doses of benzodiazepines with alcohol, barbiturates, opioids or tricyclic antidepressants are particularly dangerous, and may lead to severe complications such as coma or death. The most common symptoms of overdose include central nervous system (CNS) depression and intoxication with impaired balance, ataxia, and slurred speech. Severe symptoms include coma and respiratory depression. Supportive care is the mainstay of treatment of benzodiazepine overdose. There is an antidote, flumazenil, but its use is controversial. Worldwide benzodiazepines are commonly involved in overdoses.
Benzodiazepines were implicated in 39% of suicides by drug poisoning in Sweden, with nitrazepam and flunitrazepam accounting for 90% of benzodiazepine implicated suicides, in the elderly over a period of 2 decades. In cases where benzodiazepines contributed to death but were not the sole cause drowning, typically in the bath was a common method used. Benzodiazepines were the predominant drug class in suicides in this review of Swedish death certificates. In 72% of the cases benzodiazepines were the only drug consumed. Thus many of deaths associated with benzodiazepine overdoses may not be a direct result of the toxic effects but due to being combined with either other drugs or used as a tool to complete suicide using a different method, e.g. drowning.
In Short: Many people who try to commit suicide with Benzos either end up waking up again after several hours or days, even if extremely high dosage are consumed or they get injured/die because of accidents while being intoxicated. As far as dying of Benzo overdose is concerned, Benzos are generally considered to be quite safe as long as they are not mixed with other drugs.
[h3]Toxicity & Signs/Symptoms[/h3]
Benzodiazepines have a wide therapeutic index and taken alone in overdose rarely cause severe complications or fatalities. They are, however, not devoid of serious toxicity and cases of severe coma or fatality have been reported. Taken in overdose in combination with alcohol, barbiturates, opioids, tricyclic antidepressants, or sedating antipsychotics, anticonvulsants, or antihistamines are particularly dangerous. In the case of alcohol and barbiturates not only do they have an additive effect, they also increase the binding affinity of benzodiazepines to the benzodiazepine binding site which results in a very significant potentiation of the CNS and respiratory depressant effects. Additionally, the elderly and those with chronic illnesses are much more vulnerable to lethal overdose with benzodiazepines. Fatal overdoses can occur at relatively low doses in these individuals. DO NOT MIX BENZOS WITH OTHER DRUGS LIKE ALCOHOL OR OPIOIDS ETC, as fatal overdoses can occur in relatively low doses even for healthy individuals as the effects potentiate each other.
Signs and symptoms
Following an acute overdose of a benzodiazepine the onset of symptoms is typically rapid with most developing symptoms within 4 hours. Patients initially present with mild to moderate impairment of central nervous system function. Initial signs and symptoms include intoxication, somnolence, diplopia, impaired balance, impaired motor function, anterograde amnesia, ataxia, and slurred speech. Most patients with pure benzodiazepine overdose will usually only exhibit these mild CNS symptoms. Paradoxical reactions such as anxiety, delirium, combativeness, hallucinations, and aggression can also occur following benzodiazepine overdose. Gastrointestinal symptoms such as nausea and vomiting have also been occasionally reported.
Cases of severe overdose have been reported and symptoms displayed may include prolonged deep coma or deep cyclic coma, apnea, respiratory depression, hypoxemia, hypothermia, hypotension, bradycardia, cardiac arrest, and pulmonary aspiration, with the possibility of death. Severe consequences are rare following overdose of benzodiazepines alone but the severity of overdose is increased significantly if benzodiazepines are taken in overdose in combination with other medications. Significant toxicity may result following recreation drug misuse in conjunction with other CNS depressants such as opioids or ethanol. The duration of symptoms following overdose is usually between 12 and 36 hours in the majority of cases. The majority of drug-related deaths involve misuse of heroin or other opiods in combination with benzodiazepines or other CNS depressant drugs. In most cases of fatal overdose it is likely that lack of opiod tolerance combined with the depressant effects of benzodiazepines is the cause of death.
The symptoms of an overdose such as sleepiness, agitation and ataxia occur much more frequently and severely in children. Hypotonia may also occur in severe cases. In overdose situations this pharmacological effect is extended leading to a more severe CNS depression and potentially coma.
[h3]Treatment of an Overdose[/h3]
Medical observation and supportive care are the mainstay of treatment of benzodiazepine overdose. Although benzodiazepines are adsorbed by activated charcoal, gastric decontamination with activated charcoal is not beneficial in pure benzodiazepine overdose as the risk of adverse effects would outweigh any potential benefit from the procedure. It is only recommended if benzodiazepines have been taken in combination with other drugs that may benefit from decontamination. Gastric lavage (stomach pumping) or whole bowel irrigation are similarly not recommended. Enhancing elimination of the drug with hemodialysis, hemoperfusion, or forced diuresis is unlikely to be beneficial as these procedures have little effect on the clearance of benzodiazepines due to their large volume of distribution and lipid solubility.
Supportive measures include observation of vital signs, especially Glasgow Coma Scale and airway patency. IV access with fluid administration and maintenance of the airway with intubation and artificial ventilation may be required if respiratory depression or pulmonary aspiration occurs. Supportive measures should be put in place prior to administration of any benzodiazepine antagonist in order to protect the patient from both the withdrawal effects and possible complications arising from the benzodiazepine. A determination of possible deliberate overdose should be considered with appropriate scrutiny, and precautions taken to prevent any attempt by the patient to commit further bodily harm. Hypotension is corrected with fluid replacement, although catecholamines such as norepinephrine or dopamine may be required to increase blood pressure. Bradycardia is treated with atropine or an infusion of norepinephrine to increase coronary blood flow and heart rate.
[h3]Flumazenil - The Antidote to Benzos[/h3]
Flumazenil (also known as flumazepil, code name Ro 15-1788, trade names Anexate, Lanexat, Mazicon, Romazicon) is a benzodiazepine antagonist. It has been used as an antidote in the treatment of benzodiazepine overdoses. It reverses the effects of benzodiazepines by competitive inhibition at the benzodiazepine binding site on the GABAA receptor. There are many complications that must be taken into consideration when used in the acute care setting.
It has been found to be effective in overdoses of non-benzodiazepine sleep enhancers, namely zolpidem and zaleplon.
Flumazenil is of benefit in patients who become excessively drowsy after benzodiazepines are used for either diagnostic or therapeutic procedures.
The onset of action is rapid and usually effects are seen within one to two minutes. The peak effect is seen at six to ten minutes. The recommended dose for adults is 200 μg every 1–2 minutes until the effect is seen, to a maximum of 3 mg per hour. It is available as a clear, colourless solution for intravenous injection, containing 500 μg in 5 mL.
Many benzodiazepines (including midazolam) have longer half-lives than flumazenil. Therefore, repeat doses of flumazenil may be required to prevent recurrent symptoms of overdosage once the initial dose of flumazenil wears off. It is hepatically metabolised to inactive compounds which are excreted in the urine. Subjects who are physically dependent on benzodiazepines may suffer benzodiazepine withdrawal symptoms, including seizure, upon administration of flumazenil.
Treatment with Flumazenil
Flumazenil (Anexate) is a competitive benzodiazepine receptor antagonist that can be used as an antidote for benzodiazepine overdose. Its use, however, is controversial as it has numerous contraindications. It is contraindicated in patients who are on long-term benzodiazepines, those who have ingested a substance that lowers the seizure threshold, or in patients who have tachycardia, widened QRS complex on ECG, anticholinergic signs, or a history of seizures. Due to these contraindications and the possibility of it causing severe adverse effects including seizures, adverse cardiac effects, and death, in the majority of cases there is no indication for the use of flumazenil in the management of benzodiazepine overdose as the risks generally outweigh any potential benefit of administration. It also has no role in the management of an unknown overdoses. Additionally, if full airway protection has been achieved, a good outcome is expected and therefore flumazenil administration is unlikely to be required.
Flumazenil is very effective at reversing the CNS depression associated with benzodiazepines but is less effective at reversing respiratory depression. One study found that only 10% of the patient population presenting with a benzodiazepine overdose are suitable candidates for flumazenil. In this select population who are naive to and overdose solely on a benzodiazepine it can be considered. Due to its short half life the duration of action of flumazenil is usually less than 1 hour and multiple doses may be needed. When flumazenil is indicated the risks can be reduced or avoided by slow dose titration of flumazenil. Due to risks and its many contraindications, flumazenil should only be administered after discussion with a medical toxicologist.
This is something that only people with extensive knowledge and experience in that field should do. Otherwise it is only for informational purposes, knowing that in case of an overdose going to the ER or calling an ambulance may actually help a good deal.
Oversedation is a dose-related extension of the sedative/hypnotic effects of benzodiazepines. Symptoms include drowsiness, poor concentration, incoordination, muscle weakness, dizziness and mental confusion. When benzodiazepines are taken at night as sleeping pills, sedation may persist the next day as "hangover" effects, particularly with slowly eliminated preparations (Table 1). However, tolerance to the sedative effects usually develops over a week or two and anxious patients taking benzodiazepines during the day rarely complain of sleepiness although fine judgement and some memory functions may still be impaired.
Oversedation persists longer and is more marked in the elderly and may contribute to falls and fractures. Acute confusional states have occurred in the elderly even after small doses of benzodiazepines. Oversedation from benzodiazepines contributes to accidents at home and at work and studies from many countries have shown a significant association between the use of benzodiazepines and the risk of serious traffic accidents. People taking benzodiazepines should be warned of the risks of driving and of operating machinery.
Benzodiazepines have additive effects with other drugs with sedative actions including other hypnotics, some antidepressants (e.g. amitriptyline [Elavil], doxepin [Adapin, Sinequan]), major tranquillisers or neuroleptics (e.g. prochlorperazine [Compazine], trifluoperazine [Stelazine]), anticonvulsants (e.g. phenobarbital, phenytoin [Dilantin], carbamazepine [Atretol, Tegretol]), sedative antihistamines (e.g. diphenhydramine [Benadryl], promethazine [Phenergan]), opiates (heroin, morphine, meperidine), and, importantly, alcohol. Patients taking benzodiazepines should be warned of these interactions. If sedative drugs are taken in overdose, benzodiazepines may add to the risk of fatality.
Benzodiazepines have long been known to cause amnesia, an effect which is utilised when the drugs are used as premedication before major surgery or for minor surgical procedures. Loss of memory for unpleasant events is a welcome effect in these circumstances. For this purpose, fairly large single doses are employed and a short-acting benzodiazepine (e.g. midazolam) may be given intravenously.
Oral doses of benzodiazepines in the dosage range used for insomnia or anxiety can also cause memory impairment. Acquisition of new information is deficient, partly because of lack of concentration and attention. In addition, the drugs cause a specific deficit in "episodic" memory, the remembering of recent events, the circumstances in which they occurred, and their sequence in time. By contrast, other memory functions (memory for words, ability to remember a telephone number for a few seconds, and recall of long-term memories) are not impaired. Impairment of episodic memory may occasionally lead to memory lapses or "blackouts". It is claimed that in some instances such memory lapses may be responsible for uncharacteristic behaviours such as shop-lifting.
Benzodiazepines are often prescribed for acute stress-related reactions. At the time they may afford relief from the distress of catastrophic disasters, but if used for more than a few days they may prevent the normal psychological adjustment to such trauma. In the case of loss or bereavement they may inhibit the grieving process which may remain unresolved for many years. In other anxiety states, including panic disorder and agoraphobia, benzodiazepines may inhibit the learning of alternative stress-coping strategies, including cognitive behavioural treatment.
[h2]Paradoxical stimulant effects[/h2]
Benzodiazepines occasionally cause paradoxical excitement with increased anxiety, insomnia, nightmares, hallucinations at the onset of sleep, irritability, hyperactive or aggressive behaviour, and exacerbation of seizures in epileptics. Attacks of rage and violent behaviour, including assault (and even homicide), have been reported, particularly after intravenous administration but also after oral administration. Less dramatic increases in irritability and argumentativeness are much more common and are frequently remarked upon by patients or by their families. Such reactions are similar to those sometimes provoked by alcohol. They are most frequent in anxious and aggressive individuals, children, and the elderly. They may be due to release or inhibition of behavioural tendencies normally suppressed by social restraints. Cases of "baby-battering", wife-beating and "grandma-bashing" have been attributed to benzodiazepines.
[h2]Depression, emotional blunting[/h2]
Long-term benzodiazepine users, like alcoholics and barbiturate-dependent patients, are often depressed, and the depression may first appear during prolonged benzodiazepine use. Benzodiazepines may both cause and aggravate depression, possibly by reducing the brain's output of neurotransmitters such as serotonin and norepinephrine (noradrenaline). However, anxiety and depression often co-exist and benzodiazepines are frequently prescribed for mixed anxiety and depression. Sometimes the drugs seem to precipitate suicidal tendencies in such patients. Of the first 50 of the patients attending my withdrawal clinic (reported in 1987), ten had taken drug overdoses requiring hospital admission while on chronic benzodiazepine medication; only two of these had a history of depressive illness before they were prescribed benzodiazepines. The depression lifted in these patients after benzodiazepine withdrawal and none took further overdoses during the 10 months to 3.5 years follow-up period after withdrawal. In 1988 the Committee on Safety of Medicines in the UK recommended that "benzodiazepines should not be used alone to treat depression or anxiety associated with depression. Suicide may be precipitated in such patients".
"Emotional anaesthesia", the inability to feel pleasure or pain, is a common complaint of long-term benzodiazepine users. Such emotional blunting is probably related to the inhibitory effect of benzodiazepines on activity in emotional centres in the brain. Former long-term benzodiazepine users often bitterly regret their lack of emotional responses to family members - children and spouses or partners - during the period when they were taking the drugs. Chronic benzodiazepine use can be a cause of domestic disharmony and even marriage break-up.
[h2]Adverse effects in the elderly[/h2]
Older people are more sensitive than younger people to the central nervous system depressant effects of benzodiazepines. Benzodiazepines can cause confusion, night wandering, amnesia, ataxia (loss of balance), hangover effects and "pseudodementia" (sometimes wrongly attributed to Alzheimer’s disease) in the elderly and should be avoided wherever possible. Increased sensitivity to benzodiazepines in older people is partly because they metabolise drugs less efficiently than younger people, so that drug effects last longer and drug accumulation readily occurs with regular use. However, even at the same blood concentration, the depressant effects of benzodiazepines are greater in the elderly, possibly because they have fewer brain cells and less reserve brain capacity than younger people.
For these reasons, it is generally advised that, if benzodiazepines are used in the elderly, dosage should be half that recommended for adults, and use (as for adults) should be short-term (2 weeks) only. In addition, benzodiazepines without active metabolites (e.g. oxazepam [Serax], temazepam [Restoril]) are tolerated better than those with slowly eliminated metabolites (e.g. chlordiazepoxide [Librium], nitrazepam [Mogadon]). Equivalent potencies of different benzodiazepines are approximately the same in older as in younger people (Table 1).
[h2]Adverse effects in pregnancy[/h2]
Benzodiazepines cross the placenta, and if taken regularly by the mother in late pregnancy, even in therapeutic doses, can cause neonatal complications. The foetus and neonate metabolise benzodiazepines very slowly, and appreciable concentrations may persist in the infant up to two weeks after birth, resulting in the "floppy infant syndrome" of lax muscles, oversedation, and failure to suckle. Withdrawal symptoms may develop after about two weeks with hyperexcitability, high-pitched crying and feeding difficulties.
Benzodiazepines in therapeutic doses appear to carry little risk of causing major congenital malformations. However, chronic maternal use may impair foetal intrauterine growth and retard brain development. There is increasing concern that such children in later life may be prone to attention deficit disorder, hyperactivity, learning difficulties, and a spectrum of autistic disorders.
Tolerance to many of the effects of benzodiazepines develops with regular use: the original dose of the drug has progressively less effect and a higher dose is required to obtain the original effect. This has often led doctors to increase the dosage in their prescriptions or to add another benzodiazepine so that some patients have ended up taking two benzodiazepines at once.
However, tolerance to the various actions of benzodiazepines develops at variable rates and to different degrees. Tolerance to the hypnotic effects develops rapidly and sleep recordings have shown that sleep patterns, including deep sleep (slow wave sleep) and dreaming (which are initially suppressed by benzodiazepines), return to pre-treatment levels after a few weeks of regular benzodiazepine use. Similarly, daytime users of the drugs for anxiety no longer feel sleepy after a few days.
Tolerance to the anxiolytic effects develops more slowly but there is little evidence that benzodiazepines retain their effectiveness after a few months. In fact long-term benzodiazepine use may even aggravate anxiety disorders. Many patients find that anxiety symptoms gradually increase over the years despite continuous benzodiazepine use, and panic attacks and agoraphobia may appear for the first time after years of chronic use. Such worsening of symptoms during long-term benzodiazepine use is probably due to the development of tolerance to the anxiolytic effects, so that "withdrawal" symptoms emerge even in the continued presence of the drugs. However, tolerance may not be complete and chronic users sometimes report continued efficacy, which may be partly due to suppression of withdrawal effects. Nevertheless, in most cases such symptoms gradually disappear after successful tapering and withdrawal of benzodiazepines. Among the first 50 patients attending my clinic, 10 patients became agoraphobic for the first time while taking benzodiazepines. Agoraphobic symptoms abated dramatically within a year of withdrawal, even in patients who had been housebound, and none were incapacitated by agoraphobia at the time of follow-up (10 months to 3.5 years after withdrawal).
Tolerance to the anticonvulsant effects of benzodiazepines makes them generally unsuitable for long-term control of epilepsy. Tolerance to the motor effects of benzodiazepines can develop to a remarkable degree so that people on very large doses may be able to ride a bicycle and play ball games. However, complete tolerance to the effects on memory and cognition does not seem to occur. Many studies show that these functions remain impaired in chronic users, recovering slowly, though sometimes incompletely, after withdrawal.
Tolerance is a phenomenon that develops with many chronically used drugs (including alcohol, heroin and morphine and cannabis). The body responds to the continued presence of the drug with a series of adjustments that tend to overcome the drug effects. In the case of benzodiazepines, compensatory changes occur in the GABA and benzodiazepine receptors which become less responsive, so that the inhibitory actions of GABA and benzodiazepines are decreased. At the same time there are changes in the secondary systems controlled by GABA so that the activity of excitatory neurotransmitters tends to be restored. Tolerance to different effects of benzodiazepines may vary between individuals - probably as a result of differences in intrinsic neurological and chemical make-up which are reflected in personality characteristics and susceptibility to stress. The development of tolerance is one of the reasons people become dependent on benzodiazepines, and also sets the scene for the withdrawal syndrome, described in the next chapter.
Benzodiazepines are potentially addictive drugs: psychological and physical dependence can develop within a few weeks or months of regular or repeated use. There are several overlapping types of benzodiazepine dependence.
[h3]Therapeutic dose dependence[/h3]
People who have become dependent on therapeutic doses of benzodiazepines usually have several of the following characteristics.
1. They have taken benzodiazepines in prescribed "therapeutic" (usually low) doses for months or years.
2. They have gradually become to "need" benzodiazepines to carry out normal, day-to-day activities.
3. They have continued to take benzodiazepines although the original indication for prescription has disappeared.
4. They have difficulty in stopping the drug, or reducing dosage, because of withdrawal symptoms.
5. If on short-acting benzodiazepines (Table 1) they develop anxiety symptoms between doses, or get craving for the next dose.
6. They contact their doctor regularly to obtain repeat prescriptions.
7. They become anxious if the next prescription is not readily available; they may carry their tablets around with them and may take an extra dose before an anticipated stressful event or a night in a strange bed.
8. They may have increased the dosage since the original prescription.
9. They may have anxiety symptoms, panics, agoraphobia, insomnia, depression and increasing physical symptoms despite continuing to take benzodiazepines.
The number of people world-wide who are taking prescribed benzodiazepines is enormous. For example, in the US nearly 11 per cent of a large population surveyed in 1990 reported some benzodiazepine use the previous year. About 2 per cent of the adult population of the US (around 4 million people) appear to have used prescribed benzodiazepine hypnotics or tranquillisers regularly for 5 to 10 years or more. Similar figures apply in the UK, over most of Europe and in some Asian countries. A high proportion of these long-term users must be, at least to some degree, dependent. Exactly how many are dependent is not clear; it depends to some extent on how dependence is defined. However, many studies have shown that 50-100 per cent of long-term users have difficulty in stopping benzodiazepines because of withdrawal symptoms, which are described later.
[h3]Prescribed high dose dependence[/h3]
A minority of patients who start on prescribed benzodiazepines begin to "require" larger and larger doses. At first they may persuade their doctors to escalate the size of prescriptions, but on reaching the prescriber's limits, may contact several doctors or hospital departments to obtain further supplies which they self-prescribe. Sometimes this group combines benzodiazepine misuse with excessive alcohol consumption. Patients in this group tend to be highly anxious, depressed and may have personality difficulties. They may have a history of other sedative or alcohol misuse. They do not typically use illicit drugs but may obtain "street" benzodiazepines if other sources fail.
[h3]Recreational benzodiazepine abuse[/h3]
Recreational use of benzodiazepines is a growing problem. A large proportion (30-90 per cent) of polydrug abusers world-wide also use benzodiazepines. Benzodiazepines are used in this context to increase the "kick" obtained from illicit drugs, particularly opiates, and to alleviate the withdrawal symptoms of other drugs of abuse (opiates, barbiturates, cocaine, amphetamines and alcohol). People who have been given benzodiazepines during alcohol detoxification sometimes become dependent on benzodiazepines and may abuse illicitly obtained benzodiazepines as well as relapsing into alcohol use. Occasionally high doses of benzodiazepines are used alone to obtain a "high".
Recreational use of diazepam, alprazolam, lorazepam, temazepam, triazolam, flunitrazepam and others has been reported in various countries. Usually the drugs are taken orally, often in doses much greater than those used therapeutically (e.g.100mg diazepam or equivalent daily) but some users inject benzodiazepines intravenously. These high dose users develop a high degree of tolerance to benzodiazepines and, although they may use the drugs intermittently, some become dependent. Detoxification of these patients may present difficulties since withdrawal reactions can be severe and include convulsions.
The present population of recreational users may be relatively small, perhaps one tenth of that of long-term prescribed therapeutic dose users, but probably amounts to some hundreds of thousands in the US and Western Europe, and appears to be increasing. It is a chastening thought that medical overprescription of benzodiazepines, resulting in their presence in many households, made them easily available and undoubtedly aided their entry into the illicit drug scene. Present sources for illicit users are forged prescriptions, theft from drug stores, or illegal imports.
Socioeconomic costs of long-term benzodiazepine use. The socio-economic costs of the present high level of long-term benzodiazepine use are considerable, although difficult to quantify. Most of these have been mentioned above and are summarised in Table 3. These consequences could be minimised if prescriptions for long-term benzodiazepines were decreased. Yet many doctors continue to prescribe benzodiazepines and patients wishing to withdraw receive little advice or support on how to go about it. The following chapter gives practical information on withdrawal which, it is hoped, will be of use both to long-term benzodiazepine users and to their physicians.
[h1]How to prepare yourself to quit (+"Why come off at all?!")[/h1]
As described in before, long-term use of benzodiazepines can give rise to many unwanted effects, including poor memory and cognition, emotional blunting, depression, increasing anxiety, physical symptoms and dependence. All benzodiazepines can produce these effects whether taken as sleeping pills or anti-anxiety drugs. The social and economic consequences of chronic benzodiazepine use are summarised in Table 3 (above).
Furthermore, the evidence suggests that benzodiazepines are no longer effective after a few weeks or months of regular use. They lose much of their efficacy because of the development of tolerance. When tolerance develops, "withdrawal" symptoms can appear even though the user continues to take the drug. Thus the symptoms suffered by many long-term users are a mixture of adverse effects of the drugs and "withdrawal" effects due to tolerance. The Committee on Safety of Medicines and the Royal College of Psychiatrists in the UK concluded in various statements (1988 and 1992) that benzodiazepines are unsuitable for long-term use and that they should in general be prescribed for periods of 2-4 weeks only.
In addition, clinical experience shows that most long-term benzodiazepine users actually feel better after coming off the drugs. Many users have remarked that it was not until they came off their drugs that they realised they had been operating below par for all the years they had been taking them. It was as though a net curtain or veil had been lifted from their eyes: slowly, sometimes suddenly, colours became brighter, grass greener, mind clearer, fears vanished, mood lifted, and physical vigour returned.
Thus there are good reasons for long-term users to stop their benzodiazepines if they feel unhappy about the medication. Many people are frightened of withdrawal, but reports of having to "go through hell" can be greatly exaggerated. With a sufficiently gradual and individualised tapering schedule, as outlined below, withdrawal can be quite tolerable, even easy, especially when the user understands the cause and nature of any symptoms that do arise and is therefore not afraid. Many "withdrawal symptoms" are simply due to fear of withdrawal (or even fear of that fear). People who have had bad experiences have usually been withdrawn too quickly (often by doctors!) and without any explanation of the symptoms. At the other extreme, some people can stop their benzodiazepines with no symptoms at all: according to some authorities, this figure may be as high as 50% even after a year of chronic usage. Even if this figure is correct (which is arguable) it is unwise to stop benzodiazepines suddenly.
The advantages of discontinuing benzodiazepines do not necessarily mean that every long-term user should withdraw. Nobody should be forced or persuaded to withdraw against his or her will. In fact, people who are unwillingly pushed into withdrawal often do badly. On the other hand, the chances of success are very high for those sufficiently motivated. As mentioned before, almost anyone who really wants to come off can come off benzodiazepines. The option is up to you.
[h3]Do you want to detox? Why do you want to detox? What should you expect?[/h3]
If you have clear answers to these questions then skip this section. Otherwise, seriously addressing these issues can make a huge difference to your chance of success. There is no getting over the fact that a) state of mind is of paramount importance; far more so than the actual method of detox used and b) chances are you will be stretched close to breaking point unless you have success at one of the "painless" methods described below. It is important to realise that dependence and addiction are two separate things. Dependence is the need to take the drug to avoid unpleasant withdrawal symptoms, and addiction is the obsessive and compulsive use of a substance to the exclusion of other aspects of life and in particular relationships with others. All most detoxes will do is break the dependence on opiates. The detox per se will not help with the addiction, but is an essential first step. I think having some clear idea of why you want to detox is helpful. Self-motivation is all but vital.
The options of quitting are fairly limited, eessential there is no way around it. In the subsequent sections a few basic settings are described. Basically, SWIM would that if you are on a high dosage and/or have been addicted for a long time (1+ year) and/or have a hard time quitting and/or have a bad initial situation (family, home, friends) you should consider going to a treatment facility. If none or only one of these apply you might try to do it at home at first.
Either way, in SWIMs opinion (many would disagree) after withdrawal a follow-up Ibogaine Therapy at a hospital (available in Canada, Mexico, Europe) would greatly help if not heal any long lasting psychological problems such as Anxiety and Depression. Check the Ibogaine section in this article. Beware, Ibogaine is dangerous and can be deadly if not supervised by professionals. If any drugs are combined with it, i.e. if benzos are still in your system, it will be deadly. Do your research.
See Iboga/Ibogaine - I Began Again for more information.
Once you have made up your mind to withdraw, there are some steps to take before you start.
Making a decision
Eventually it is up to you. Also to your time, financial, family and living situation as well as other circumstances. You should do research and consider the different options. Professional care is especially recommended for longterm or high dosage dependence, especially if psychological problems are underlying.
Your doctor may have views on whether it is appropriate for you to stop your benzodiazepines. In a small number of cases withdrawal may be inadvisable. Some doctors, particularly in the US, believe that long-term benzodiazepines are indicated for some anxiety, panic and phobic disorders and some psychiatric conditions. However, medical opinions differ and, even if complete withdrawal is not advised, it may be beneficial to reduce the dosage or to take intermittent courses with benzodiazepine-free intervals.
Unless you don't get your stuff from (a) doctor(s) your doctor's agreement and co-operation is necessary since he/she will be prescribing the medication. Many doctors are uncertain how to manage benzodiazepine withdrawal and hesitate to undertake it. But you can reassure your doctor that you intend to be in charge of your own program and will proceed at whatever pace you find comfortable, although you may value his advice from time to time. It is important for you to be in control of your own schedule. Do not let your doctor impose a deadline. Leave yourself free to "proceed as the way openeth", as the Quakers say.
It is a good idea to make out a dosage reduction schedule for the initial stages (see below) and to give your doctor a copy. You may need to mention the importance of flexibility, so that the rate of dosage tapering can be amended at any time. There may even be circumstances when you need to stop for a while at a certain stage. A continuation schedule can follow later depending upon how you get on, and the doctor can continue prescribing in accordance with the new schedule. (All this is explained later in this chapter).
Finally, your doctor may appreciate receiving some literature on benzodiazepine withdrawal, for example this whole article.
Make sure you have adequate psychological support
Support could come from your spouse, partner, family or close friend. An understanding doctor may also be the one to offer support as well as advice. Ideally, your mentor should be someone who understands about benzodiazepine withdrawal or is prepared to read about it and learn. It need not be someone who has gone through withdrawal - sometimes ex-users who have had a bad experience can frighten others by dwelling on their own symptoms. Often the help of a clinical psychologist, trained counsellor, or other therapist is valuable, especially for teaching relaxation techniques, deep breathing, how to deal with a panic attack etc. Some people find alternative techniques such as aromatherapy, acupuncture or yoga helpful, but these probably act only as an aid to relaxation. In my experience, hypnotherapy has not been helpful in long-term benzodiazepine users. Relaxation techniques are described in a few sections later.
Rather than (or in addition to) expensive therapists, you need someone reliable, who will support you frequently and regularly, long-term, both during withdrawal and for some months afterwards. Voluntary tranquilliser support groups (self-help groups) can be extremely helpful. They are usually run by people who have been through withdrawal and therefore understand the time and patience required, and can provide information about benzodiazepines. It can be encouraging to find that you are not alone, that there are plenty of others with similar problems to yours. However, do not be misled into fearing that you will get all the symptoms described by the others. Everyone is different and some people, with the right schedule and the right support, get no untoward symptoms at all. Many people in fact have managed to come off on their own without any outside help.
Get into the right frame of mind
• Be confident - you can do it. If in doubt, try a very small reduction in dosage for a few days (for example, try reducing your daily dosage by about one tenth or one eighth; you may be able to achieve this by halving or quartering one of your tablets). You will probably find that you notice no difference. If still in doubt, aim at first for dosage reduction rather than complete withdrawal. You will probably wish to continue once you have started.
• Be patient. There is no need to hurry withdrawal. Your body (and brain) may need time to readjust after years of being on benzodiazepines. Many people have taken a year or more to complete the withdrawal. So don't rush, and, above all, do not try to stop suddenly.
• Choose your own way - don't expect a "quick fix". It may be possible to enter a hospital or special centre for "detoxification". Such an approach usually involves a fairly rapid withdrawal, is medically "safe" and may provide psychological support. Such centres may be suitable for a small minority of people with difficult psychological problems. However, they often remove the control of withdrawal from the patient and setbacks on returning home are common, largely because there has been no time to build up alternative living skills. Slow withdrawal in your own environment allows time for physical and psychological adjustments, permits you to continue with your normal life, to tailor your withdrawal to your own lifestyle, and to build up alternative strategies for living without benzodiazepines.
• Burn Bridges: If you are depended because of a prescription drug habit, talk to your doc about the dosage, educate yourself beforehand and impress him with your knowledge and hope for his support - it's likely you will get support. However, if you did doctor-shopping, i.e. going to several doctors at the same time to satisfy your needs you should end the relationships to all except one (just in case). Burn the bridge. If you don't want to tell them about the addiction, tell them you made some awful experiences, predent you had paradoxical effects or whatever - just make sure you won't get Benzos again. At best no doctor should be left that easily hands out scripts. If you get your stuff illegally, also: burn bridges!
• Educate yourself! Read a lot beforehand, read experiences in forums, talk to people (consider NA meetings), maybe talk to a doctor or pharmacist. Read books on the topic of addiction (addiction to other drugs as well, if interested in it, as there are many similar patterns). Read this whole post
• Be ready to change your life! Look into the Aftercare section of this guide, as you may want to make up your mind before the withdrawal
Supplements & Things to consider
• Prepare supplements
• place to stay, hlidays ??
• doctor at hand, just in case, emergency nuber
• prepare schedule beforehand
• consider giving the dosages to a friend who always only gives out the dosage for a couple of days - throw every left over away
• disconnect from drugs (forums e.g. by temporary expulsion on request)/wrong friends/triggers (this also relates a lot to the Relapse section as well as the Aftercare section. Whatever preparatory you might find in there, consider it)
Withdrawal in older people
Older people can withdraw from benzodiazepines as successfully as younger people, even if they have taken the drugs for years. A recent trial with an elderly population of 273 general practice patients on long-term (mean 15 years) benzodiazepines showed that voluntary dosage reduction and total withdrawal of benzodiazepines was accompanied by better sleep, improvement in psychological and physical health and fewer visits to doctors. These findings have been repeated in several other studies of elderly patients taking benzodiazepines long-term.
There are particularly compelling reasons why older people should withdraw from benzodiazepines since, as age advances, they become more prone to falls and fractures, confusion, memory loss and psychiatric problems (see beginning of article).
Methods of benzodiazepine withdrawal in older people are similar to those recommended above for younger adults. A slow tapering regimen, in my experience, is easily tolerated, even by people in their 80s who have taken benzodiazepines for 20 or more years. The schedule may include the use of liquid preparations if available and judicious stepwise substitution with diazepam (Valium) if necessary. There is, of course, a great deal of variation in the age at which individuals become "older" - perhaps 65-70 years would fit the definition in most cases.
[h1]A word of caution - The Dangers of Stopping Cold Turkey (Don't do it!)[/h1]
fatal reaction if cold turkey + section about cold turkey symptoms (in appropriate category ) + link to it
In cases one feels seriously sick or feels like loosing control or is unsure about his safety and health he should seek professional help immediately!
Also see the Medical disclaimer at the end of the post.
[h2]Coming off Benzos[/h2]
Also see the Medical disclaimer at the end of the post.
[h3]Dosage tapering[/h3] There is absolutely no doubt that anyone withdrawing from long-term benzodiazepines must reduce the dosage slowly.
Abrupt or over-rapid withdrawal, especially from high dosage, can give rise to severe symptoms (convulsions, psychotic reactions, acute anxiety states) and may increase the risk of protracted withdrawal symptoms (see chapter on symptoms below). Slow withdrawal means tapering dosage gradually, usually over a period of some months. The aim is to obtain a smooth, steady and slow decline in blood and tissue concentrations of benzodiazepines so that the natural systems in the brain can recover their normal state. As explained in the beginning, long-term benzodiazepines take over many of the functions of the body's natural tranquilliser system, mediated by the neurotransmitter GABA. As a result, GABA receptors in the brain reduce in numbers and GABA function decreases. Sudden withdrawal from benzodiazepines leaves the brain in a state of GABA-underactivity, resulting in hyperexcitability of the nervous system. This hyperexcitability is the root cause of most of the withdrawal symptoms discussed in the next chapter. However, a sufficiently slow, and smooth, departure of benzodiazepines from the body permits the natural systems to regain control of the functions which have been damped down by their presence. There is scientific evidence that reinstatement of brain function takes a long time. Recovery after long-term benzodiazepine use is not unlike the gradual recuperation of the body after a major surgical operation. Healing, of body or mind, is a slow process.
The precise rate of withdrawal is an individual matter. It depends on many factors including the dose and type of benzodiazepine used, duration of use, personality, lifestyle, previous experience, specific vulnerabilities, and the (perhaps genetically determined) speed of your recovery systems. Usually the best judge is you, yourself; you must be in control and must proceed at the pace that is comfortable for you. You may need to resist attempts from outsiders (clinics, doctors) to persuade you into a rapid withdrawal. The classic six weeks withdrawal period adopted by many clinics and doctors is much too fast for many long-term users. Actually, the rate of withdrawal, as long as it is slow enough, is not critical. Whether it takes 6 months, 12 months or 18 months is of little significance if you have taken benzodiazepines for a matter of years.
It is sometimes claimed that very slow withdrawal from benzodiazepines "merely prolongs the agony" and it is better to get it over with as quickly as possible. However, the experience of most patients is that slow withdrawal is greatly preferable, especially when the subject dictates the pace. Indeed, many patients find that there is little or no "agony" involved. Nevertheless there is no magic rate of withdrawal and each person must find the pace that suits him best. People who have been on low doses of benzodiazepine for a relatively short time (less than a year) can usually withdraw fairly rapidly. Those who have been on high doses of potent benzodiazepines such as Xanax and Klonopin are likely to need more time.
Examples of slow withdrawal schedules are given at the end of this chapter. As a very rough guide, a person taking 40mg diazepam a day (or its equivalent) might be able to reduce the daily dosage by 2mg every 1-2 weeks until a dose of 20mg diazepam a day is reached. This would take 10-20 weeks. From 20mg diazepam a day, reductions of 1 mg in daily dosage every week or two might be preferable. This would take a further 20-40 weeks, so the total withdrawal might last 30-60 weeks. Yet some people might prefer to reduce faster and some might go even slower. (See next section for further details).
However, it is important in withdrawal always to go forwards. If you reach a difficult point, you can stop there for a few weeks if necessary, but you should try to avoid going backwards and increasing your dosage again. Some doctors advocate the use of "escape pills" (an extra dose of benzodiazepines) in particularly stressful situations. This is probably not a good idea as it interrupts the smooth decline in benzodiazepine concentrations and also disrupts the process of learning to cope without drugs which is an essential part of the adaptation to withdrawal. If the withdrawal is slow enough, "escape pills" should not be necessary.
(2) Switching to a long-acting benzodiazepine. With relatively short-acting benzodiazepines such as alprazolam (Xanax) and lorazepam (Ativan) (Table 1, at the beginning), it is not possible to achieve a smooth decline in blood and tissue concentrations. These drugs are eliminated fairly rapidly with the result that concentrations fluctuate with peaks and troughs between each dose. It is necessary to take the tablets several times a day and many people experience a "mini-withdrawal", sometimes a craving, between each dose.
For people withdrawing from these potent, short-acting drugs it is advisable to switch to a long-acting, slowly metabolised benzodiazepine such as diazepam. Diazepam (Valium) is one of the most slowly eliminated benzodiazepines. It has a half-life of up to 200 hours, which means that the blood level for each dose falls by only half in about 8.3 days. The only other benzodiazepines with similar half-lives are chlordiazepoxide (Librium), flunitrazepam (Rohypnol) and flurazepam (Dalmane), all of which are converted to a diazepam metabolite in the body. The slow elimination of diazepam allows a smooth, gradual fall in blood level, allowing the body to adjust slowly to a decreasing concentration of the benzodiazepines. The switch-over process needs to be carried out gradually, usually in stepwise fashion, substituting one dose at a time. There are several factors to consider. One is the difference in potency between different benzodiazepines. Many people have suffered because they have been switched suddenly to a different, less potent drug in inadequate dosage because the doctor has not adequately considered this factor. Equivalent potencies of benzodiazepines are shown in Table 1, but these are only approximate and differ between individuals.
A second factor to bear in mind is that the various benzodiazepines, though broadly similar, have slightly different profiles of action. For example, lorazepam (Ativan) seems to have less hypnotic activity than diazepam (probably because it is shorter acting). Thus if someone on, say, 2mg Ativan three times a day is directly switched to 60mg diazepam (the equivalent dose for anxiety) he is liable to become extremely sleepy, but if he is switched suddenly onto a much smaller dose of diazepam, he will probably get withdrawal symptoms. Making the changeover one dose (or part of dose) at a time avoids this difficulty and also helps to find the equivalent dosage for that individual. It is also helpful to make the first substitution in the night-time dose, and the substitution may not always need to be complete. For example, if the evening dose was 2mg Ativan, this could in some cases be changed to 1 mg Ativan plus 8mg diazepam. A full substitution for the dropped 1 mg of Ativan would have been 10mg diazepam. However, the patient may actually sleep well on this combination and he will have already made a dosage reduction - a first step in withdrawal. (Examples of step-wise substitutions are given in the schedules at the end of this chapter.)
A third important practical factor is the available dosage formulations of the various benzodiazepines. In withdrawal you need a long-acting drug which can be reduced in very small steps. Diazepam (Valium) is the only benzodiazepine that is ideal for this purpose since it comes in 2mg tablets, which are scored down the middle and easily halved into 1 mg doses. By contrast, the smallest available tablet of lorazepam (Ativan) is 0.5mg (equivalent to 5mg diazepam) [in the UK the lowest available dosage form for lorazepam is 1mg]; the smallest tablet of alprazolam (Xanax) is 0.25mg (also equivalent to 5mg diazepam). Even by halving these tablets the smallest reduction one could easily make is the equivalent of 2.5mg diazepam. (Some patients become very adept at shaving small portions off their tablets). Because of limited dose formulations, it may be necessary to switch to diazepam even if you are on a fairly long-acting benzodiazepine of relatively low potency (e.g. flurazepam [Dalmane]). Liquid preparations of some benzodiazepines are available and if desired slow reduction from these can be accomplished by decreasing the volume of each dose, using a graduated syringe.
Some doctors in the US switch patients onto clonazepam (Klonopin, [Rivotril in Canada]), believing that it will be easier to withdraw from than say alprazolam (Xanax) or lorazepam (Ativan) because it is more slowly eliminated. However, Klonopin is far from ideal for this purpose. It is an extremely potent drug, is eliminated much faster than diazepam (See Table 1), and the smallest available tablet in the US is 0.5mg (equivalent to 10mg diazepam) and 0.25mg in Canada (equivalent to 5mg Valium). It is difficult with this drug to achieve a smooth, slow fall in blood concentration, and there is some evidence that withdrawal is particularly difficult from high potency benzodiazepines, including Klonopin. Some people, however, appear to have particular difficulty in switching from Klonopin to diazepam. In such cases it is possible to have special capsules made up containing small doses, e.g. an eighth or a sixteenth of a milligram or less, which can be used to make gradual dosage reductions straight from Klonopin. These capsules require a doctor's prescription and can be made up by hospital pharmacists and some chemists in the UK, and by compounding pharmacists in North America. A similar technique can be used for those on other benzodiazepines who find it hard to substitute diazepam. Care must be taken to ensure that the compounding pharmacist can guarantee the same formula on each prescription renewal. It should be noted, however, that this approach to benzodiazepine withdrawal can be troublesome and is not recommended for general use.
[h3]Designing and following the withdrawal schedule[/h3] It basically comes down to tapering off slowly. As slowly as possible, basically. Every day a diny bit less, you may even just scrape of a little dust of each tablet every day (every day a little more).
Some examples of withdrawal schedules are given on later. Most of them are actual schedules which have been used and found to work by real people who withdrew successfully. But each schedule must be tailored to individual needs; no two schedules are necessarily the same. Below is a summary of points to consider when drawing up your own schedule.
1. Design the schedule around your own symptoms. For example, if insomnia is a major problem, take most of your dosage at bedtime; if getting out of the house in the morning is a difficulty, take some of the dose first thing (but not a large enough dose to make you sleepy or incompetent at driving!).
2. When switching over to diazepam, substitute one dose at a time, usually starting with the evening or night-time dose, then replace the other doses, one by one, at intervals of a few days or a week. Unless you are starting from very large doses, there is no need to aim for a reduction at this stage; simply aim for an approximately equivalent dosage. When you have done this, you can start reducing the diazepam slowly. If, however, you are on a high dose, such as 6mg alprazolam (equivalent to 120mg diazepam), you may need to undertake some reduction while switching over, and may need to switch only part of the dosage at a time (see Schedule 1). The aim is to find a dose of diazepam which largely prevents withdrawal symptoms but is not so excessive as to make you sleepy.
3. Diazepam is very slowly eliminated and needs only, at most, twice daily administration to achieve smooth blood concentrations. If you are taking benzodiazepines three or four times a day it is advisable to space out your dosage to twice daily once you are on diazepam. The less often you take tablets the less your day will revolve around your medication.
4. The larger the dose you are taking initially, the greater the size of each dose reduction can be. You could aim at reducing dosage by up to one tenth at each decrement. For example, if you are taking 40mg diazepam equivalent you could reduce at first by 2-4mg every week or two. When you are down to 20mg, reductions could be 1-2mg weekly or fortnightly. When you are down to 10mg, 1mg reductions are probably indicated. From 5mg diazepam some people prefer to reduce by 0.5mg every week or two.
5. There is no need to draw up your withdrawal schedule right up to the end. It is usually sensible to plan the first few weeks and then review and if necessary amend your schedule according to your progress. Prepare your doctor to be flexible and to be ready for your schedule to be adjusted to a slower (or faster) pace at any time.
6. As far as possible, never go backwards. You can stand still at a certain stage in your schedule and have a vacation from further withdrawal for a few weeks if circumstances change (if for instance there is a family crisis), but try to avoid ever increasing the dosage again. You don't want to back over ground you have already covered.
7. Avoid taking extra tablets in times of stress. Learn to gain control over your symptoms. This will give you extra confidence that you can cope without benzodiazepines (see Withdrawal Symptoms).
8. Avoid compensating for benzodiazepines by increasing your intake of alcohol, cannabis or non-prescription drugs. Occasionally your doctor may suggest other drugs for particular symptoms (see Withdrawal Symptoms), but do not take the sleeping tablets zolpidem (Ambien), zopiclone (Zimovane, Imovane) or zaleplon (Sonata) as they have the same actions as benzodiazepines.
9. Getting off the last tablet: Stopping the last few milligrams is often viewed as particularly difficult. This is mainly due to fear of how you will cope without any drug at all. In fact, the final parting is surprisingly easy. People are usually delighted by the new sense of freedom gained. In any case the 1mg or 0.5mg diazepam per day which you are taking at the end of your schedule is having little effect apart from keeping the dependence going. Do not be tempted to spin out the withdrawal to a ridiculously slow rate towards the end (such as 0.25mg each month). Take the plunge when you reach 0.5mg daily; full recovery cannot begin until you have got off your tablets completely. Some people after completing withdrawal like to carry around a few tablets with them for security "just in case", but find that they rarely if ever use them.
10. Do not become obsessed with your withdrawal schedule. Let it just become a normal way of life for the next few months. Okay, you are withdrawing from your benzodiazepines; so are many others. It's no big deal.
11. If for any reason you do not (or did not) succeed at your first attempt at benzodiazepine withdrawal, you can always try again. They say that most smokers make 7 or 8 attempts before they finally give up cigarettes. The good news is that most long-term benzodiazepine users are successful after the first attempt. Those who need a second try have usually been withdrawn too quickly the first time. A slow and steady benzodiazepine withdrawal, with you in control, is nearly always successful.
[h3]Examples of slow withdrawal schedules[/h3] These a examples for tapering schedules. They maybe be looked at to get the general idea. Most of these deal with substitution whatever you use with diazepam. In case that isnt available, just follow an equivalent schedule. Taper off slowly. Especially at the end you wanna make sure to take your time, as the last mgs are always the hardest.
A variety of withdrawal schedules from several benzodiazepines are illustrated below. Schedules such as these have worked on real people, but you may need to adapt them for your own needs. Reference to Table 1, which shows the equivalent strengths of different benzodiazepines, should enable you to work out your own programme and to devise an appropriate schedule for benzodiazepines such as prazepam (Centrax) and quazepam (Doral) and others which are not illustrated.
In my experience, the only exception to the general rule of slow reduction is triazolam (Halcion). This benzodiazepine is eliminated so quickly (half-life 2 hours) that you are practically withdrawn each day, after a dose the night before. For this reason, triazolam can be stopped abruptly without substitution of a long-acting benzodiazepine. If withdrawal symptoms occur, you could take a short course of diazepam starting at about 10mg, decreasing the dosage as shown on Schedule 2. The same approach applies to the non-benzodiazepines zolpidem and zaleplon which both have half-lives of 2 hours.
The following schedules are examples for specific situations, but can as well serve general purposes and be a guideline for creating your own schedule. Basically: taper off slowly
also see: Benzodiazepine withdrawal schedules
Schedules for withdrawal from: alprazolam; diazepam, lorazepam, nitrazepam, clonazepam, tempazepam, oxazepam, chlordiazepoxide, zopiclone:
In the following tables are several schedules for withdrawing from different types of Benzos.
Schedule 1 - Simple withdrawal from alprazolam(Xanax) daily with diazepam (Valium) substitution. (6mg alprazolam
is approximately equivalent to 120mg diazepam)
Continue as on Schedule 2, reducing from diazepam 40mg
Schedule 1 Notes:
1.There is no actual withdrawal (only diazepam substitution) in Stages 1-4, so these could be undertaken at weekly intervals (but you could take 2 weeks for each stage if preferred).
2. The evening dose of diazepam could be taken at bed-time, rather than with the alprazolam if that is usually taken earlier. (Do not take any other sleeping tablet).
3. Some dosage reduction occurs in later stages of the diazepam switchover (Stages 5-11), so these stages could be undertaken at two week intervals. Even at reducing doses, the diazepam should cover withdrawal from alprazolam, because by this time it has had time to work through the body and will be acting smoothly both day and night. The aim is to obtain a dose of diazepam which avoids withdrawal symptoms but is not so great as to make you sleepy.
4. At Stage 12 it would be sensible to move to twice daily dosage. Diazepam is long-acting and there is no need to take it more than twice a day. There is no reduction in dosage while you make this change (Stages 11 and 12).
Schedule 2 - Simple withdrawal from diazepam
...(Valium) 40mg daily
(follow this schedule to complete Schedule 1)
1. Schedule 2 Notes:
2. You could probably manage Stages 1-5 (or even Stages 1-10) in weekly intervals (but take 2 weeks between stages if you prefer).
3. The later stages are probably better taken in 2 week intervals.
4. When you get down to a dose of 5mg daily, you could begin to decrease in 0.5mg doses, but most people manage with 1mg reductions.
5. You will need to utilise a mixture of 10mg, 5mg, and 2mg diazepam tablets to obtain the required dosages. Halve the (scored) 2mg tablet to obtain 1mg doses.
6. If your starting dose is 20mg diazepam daily, you could begin at Stage 10, but in this case you could reduce by 1mg every 2 weeks.
7. If starting from Schedule 1 (alprazolam 6mg daily) continue your reduction using this schedule.
Schedule 3 - Withdrawal from lorazepam
...(Ativan) 6mg daily with diazepam (Valium) substitution. (6mg lorazepam is approximately equivalent to 60mg diazepam)
1. Schedule 3 Notes:
2. There is no actual withdrawal (only diazepam substitution) in Stages 1-5, so these could be undertaken at weekly intervals (but you could take 2 weeks if preferred).
3. The evening dose of diazepam could be taken at bed-time, rather than with the lorazepam if that is usually taken earlier. (Do not take any other sleeping tablet).
4. Some dosage reduction occurs during the later stages of the diazepam switchover (Stages 6-11), so these stages could be undertaken at two week intervals. Even at reducing doses, the diazepam should cover withdrawal from lorazepam, because by this time it has had time to work through the body and will be acting smoothly both day and night. The aim is to obtain a dose of diazepam which avoids withdrawal symptoms but is not so great as to make you sleepy.
5. Day-time doses of diazepam are gradually phased out (Stages 17-25); in succeeding stages you only need to phase out the night-time dose by 1mg every week or two.
6. A mixture of 10mg, 5mg and 2mg diazepam tablets will be needed to obtain the required doses. Halve the (scored) 2mg tablets to obtain 1mg doses.
Schedule 4 - Withdrawal from nitrazepam
...(Mogadon) 10mg at night with diazepam (Valium) substitution. (Nitrazepam is approximately the same strength as diazepam)
Schedule 4 Notes:
If you are taking more than 10mg nitrazepam, replace each 5mg nitrazepam, one at a time, with 5mg diazepam, then reduce the diazepam in 1mg or 2mg stages.
Schedule 5 - Withdrawal from clonazepam
...(Klonopin) 1.5mg daily with substitution of diazepam (Valium). (0.5mg clonazepam is approximately equivalent to 10mg diazepam)
Schedule 6 - Withdrawal from clonazepam
...(Klonopin) 3mg daily with substitution of diazepam (Valium).
(1 mg clonazepam is equivalent to 20mg diazepam)
Schedule 6 Notes:
The small reduction (27.5mg to 27mg) between Stages 9 and 10 is to allow you to adjust to twice daily dose.
Schedule 7 - Withdrawal from alprazolam
...(Xanax) 4mg daily with diazepam (Valium) substitution (4mg alprazolam is
approximately equivalent to 80mg diazepam)
Schedule 7 Notes:
The evening diazepam dose can be taken at bed-time, rather than with alprazolam if that is usually taken earlier.
Schedule 8 - Withdrawal from lorazepam
...(Ativan) 3mg daily with diazepam (Valium) substitution. (3mg lorazepam
is approximately equivalent to 30mg diazepam)
Schedule 9 - Withdrawal from temazepam
...(Restoril) 30mg nightly with diazepam substitution. (30mg temazepam is
approximately equivalent to 15mg diazepam)
Schedule 10 - Withdrawal from oxazepam
...(Serax) 20mg three times daily (60mg) with diazepam (Valium) substitution. (20mg) oxazepam is approximately equivalent to 10mg diazepam)
1. Schedule 10 Notes:
2. Oxazepam is short-acting (half-life 4-15 hrs) so substitution to diazepam (long-acting) is recommended.
3. Diazepam need only be taken twice a day.
4. A change from 5mg to 2mg diazepam tablets is necessary from Stage 4 onwards.
Schedule 11 -Withdrawal from chlordiazepoxide
...(Librium) 25mg three times daily (75mg). (25mg chlordiazepoxide is approximately equivalent to 10mg diazepam)
1. Schedule 11 Notes:
2. Chlordiazepoxide is long-acting so there is no need to take it more frequently than twice a day (hence Stages 4 and 5).
3. Because chlordiazepoxide is long-acting, there is no need for diazepam substitution.
4. If you are taking chlordiazepoxide capsules, change to tablets which can be halved for stages 14 onwards.
Schedule 12 - Withdrawal from zopiclone
...(Zimovane) 15mg with diazepam (Valium) substitution. (15mg zopiclone is approximately equivalent to 10mg diazepam)
1. Schedule 12 Notes:
2. It is possible to withdraw directly from zopiclone using the smallest available tablets (3.75mg), but this dose of zopiclone is equivalent to 2.5mg diazepam making for rather abrupt dosage reductions.
3. This method can also be used for withdrawing from loprazolam and lormetazepam. 1mg of each of these is approximately equivalent to 10mg diazepam; their half-lives are 6-12 and 10-12 hrs respectively.
[h1]Mechanisms & Stages of Withdrawal[/h1]
People who develop severe symptoms on benzodiazepine withdrawal have usually come off the drugs too rapidly. Lack of explanation of the symptoms has often added to their distress and has introduced fears ("Am I going mad?") which themselves magnify the symptoms. A few, because of these frightening experiences, have ended up with a condition akin to post-traumatic stress disorder (PTSD). But a proper understanding of the reasons for and nature of any symptoms that arise can do much to allay the bewilderment and fear associated with benzodiazepine withdrawal and can also help prevent long-term sequelae. Withdrawal reactions are in fact a normal response to the discontinuation of many chronically used drugs including alcohol, opiates, antipsychotics, antidepressants, and even some medications for angina and hypertension.
Mechanisms of withdrawal reactions
Drug withdrawal reactions in general tend to consist of a mirror image of the drugs' initial effects. In the case of benzodiazepines, sudden cessation after chronic use may result in dreamless sleep being replaced by insomnia and nightmares; muscle relaxation by increased tension and muscle spasms; tranquillity by anxiety and panic; anticonvulsant effects by epileptic seizures. These reactions are caused by the abrupt exposure of adaptations that have occurred in the nervous system in response to the chronic presence of the drug. Rapid removal of the drug opens the floodgates, resulting in rebound overactivity of all the systems which have been damped down by the benzodiazepine and are now no longer opposed. Nearly all the excitatory mechanisms in the nervous system go into overdrive and, until new adaptations to the drug-free state develop, the brain and peripheral nervous system are in a hyperexcitable state, and extremely vulnerable to stress.
Course of withdrawal
As a brief explaination, Withdrawals can be separated into:
The immediate effects on the body of stopping the drug
Post Withdrawal Symptoms
Symptoms such as craving and lasting depression immediately after the bodily withdrawal.
Protracted Withdrawal Symptoms
Long last symptoms, mostly psychological, that require special care or long term recovery.
During benzodiazepine withdrawal, symptoms characteristically wax and wane, varying in severity and type from day to day, week to week, and even during the course of a day. Some symptoms come and go; others may take their place. There is no need to be discouraged by these wave-like recurrences; the waves become less severe and less frequent as time passes. Typically "Windows" of normality, when you feel positively well for a few hours or days, appear after some weeks; gradually the "Windows" become more frequent and last longer, while any intervening discomfort ebbs away.
It is impossible to give an exact time for the duration of withdrawal symptoms. It depends on where you start from, how much support you need and receive, how you manage your taper and many other factors. With slow tapering, some long-term users have virtually lost all their symptoms by the time they take their last tablet, and in the majority symptoms disappear within a few months. Vulnerability to extra stress may last somewhat longer and a severe stress may - temporarily - bring back some symptoms. Whatever your symptoms, it is best not to dwell on them. Symptoms are just symptoms after all and most of them in withdrawal are not signs of illness but signals of recovery. Furthermore, as your mind clears, you can work out more and more effective ways to deal with them so that they become less significant.
One reassuring finding from many clinical studies is that eventual success in withdrawal is not affected by duration of use, dosage or type of benzodiazepine, rate of withdrawal, severity of symptoms, psychiatric diagnosis, or previous attempts at withdrawal. Thus from almost any starting point, the motivated long-term user can proceed in good heart.
[h1]The withdrawal - Shit hits the fan[/h1]
The most prominent effect of benzodiazepines is an anti-anxiety effect - that is why they were developed as tranquillisers. As a consequence, nearly all the acute symptoms of withdrawal are those of anxiety. They have been described in anxiety states in people who have never touched a benzodiazepine and were recognised as psychological and physical symptoms of anxiety long before benzodiazepines were discovered. However, certain symptom clusters are particularly characteristic of benzodiazepine withdrawal. These include hypersensitivity to sensory stimuli (sound, light, touch, taste and smell) and perceptual distortions (for example sensation of the floor undulating, feeling of motion, impressions of walls or floors tilting, sensation of walking on cotton wool). There also appears to be a higher incidence than usually seen in anxiety states of depersonalisation, feelings of unreality, and tingling and numbness. Visual hallucinations, distortion of the body image ("my head feels like a football/balloon"), feelings of insects crawling on the skin, muscle twitching and weight loss are not uncommon in benzodiazepine withdrawal but unusual in anxiety states.
As a brief explaination, Withdrawals can be separated into:
The immediate effects on the body of stopping the drug
Post Withdrawal Symptoms
Symptoms such as craving and lasting depression immediately after the bodily withdrawal.
Protracted Withdrawal Symptoms
Long last symptoms, mostly psychological, that require special care or long term recovery.
The recovery for most symptoms is similar in the different stages and can be applied to the different stages. Only few are specific. So in case one or a few specific problems occur make sure to check the several sections in this guide as information is partly spread and to avoid repetition is sometimes only posted in one section or a totally different part of this guide. SWIM suggests using the search function of the browser in such a case.
In case SWIY feels seriously sick or feels like loosing control or is unsure about his safety and health he should seek professional help immediately!
Also see the Medical disclaimer at the end of the post.
[h2]Acute Withdrawal Symptoms[/h2]
[h3]The main symptoms listed & explained[/h3]
Table 1 gives a list of symptoms which were spontaneously described by patients in my withdrawal clinic. It is clearly a long list and is probably not inclusive. Of course, not all patients get all the symptoms, and none of the symptoms are inevitable. Withdrawal often seems to seek out the individual's most vulnerable points: if he is prone to headaches, worse headaches may feature in withdrawal; if he is prone to "irritable bowel", digestive symptoms may be aggravated. Such symptoms are nearly always temporary and can be minimised. They are less frightening and seem less important or bizarre if their cause is understood. Furthermore, patients can learn techniques to alleviate or control many of the symptoms: there is a lot they can do to help themselves.
This list includes mostly short term related withdrawal symptoms. However, long-term symptoms also do occur, especially psychologically, such as Depression and Anxiety, loss of memory to name a few.
These symptoms have all been described by patients withdrawing from benzodiazepines; they are not arranged in any particular order, and few if any are specific to benzodiazepine withdrawal. The list is not inclusive. Different individuals experience different combinations of symptoms. Do not expect to get all these symptoms, but prepare for the worst. Lots of these ailments can be lessened in certain ways described further below.
Symptoms explained: Insomnia, nightmares, sleep disturbance
The sleep engendered by benzodiazepines, though it may seem refreshing at first, is not a normal sleep. Benzodiazepines inhibit both dreaming sleep (rapid eye movement sleep, REMS) and deep sleep (slow wave sleep, SWS). The extra sleep time that benzodiazepines provide is spent mainly in light sleep, termed Stage 2 sleep. REM and SWS are the two most important stages of sleep and are essential to health. Sleep deprivation studies show that any deficit is quickly made up by a rebound to above normal levels as soon as circumstances permit.
In regular benzodiazepine users REMS and SWS tend to return to pre-drug levels (because of tolerance) but the initial deficit remains. On withdrawal, even after years of benzodiazepine use, there is a marked rebound increase in REMS which also becomes more intense. As a result, dreams become more vivid, nightmares may occur and cause frequent awakenings during the night. This is a normal reaction to benzodiazepine withdrawal and, though unpleasant, it is a sign that recovery is beginning to take place. When the deficit of REMS is made up, usually after about 4-6 weeks, the nightmares become less frequent and gradually fade away.
Return of SWS seems to take longer after withdrawal, probably because anxiety levels are high, the brain is overactive and it is hard to relax completely. Subjects may have difficulty in getting off to sleep and may experience "restless legs syndrome", sudden muscle jerks (myoclonus) just as they are dropping off or be jolted suddenly by a hallucination of a loud bang (hypnagogic hallucination) which wakes them up again. These disturbances may also last for several weeks, sometimes months.
However, all these symptoms do settle in time. The need for sleep is so powerful that normal sleep will eventually reassert itself. Meanwhile, attention to sleep hygiene measures including avoiding tea, coffee, other stimulants or alcohol near bedtime, relaxation tapes, anxiety management techniques and physical exercise may be helpful. Taking all or most of the dose of benzodiazepine at night during the reduction period may also help.
A fascinating symptom in patients undergoing benzodiazepine withdrawal is that they often mention the occurrence of what seem to be intrusive memories. Their minds will suddenly conjure up a vivid memory of someone they have not thought about or seen for years. Sometimes the other person's face will appear when looking in the mirror. The memory seems uncalled for and may recur, intruding on other thoughts. The interesting thing about these memories is that they often start to occur at the same time that vivid dreams appear; these may be delayed until one or more weeks after the dosage tapering has started. Since recent sleep research indicates that certain stages of sleep (REMS and SWS) are important for memory functions, it is likely that the dreams and the memories are connected. In both cases the phenomena may herald the beginning of a return in normal memory functions and, although sometimes disturbing, can be welcomed as a sign of a step towards recovery.
Certain supplements may also help, see the list further below.
Poor memory and concentration
... are also features of benzodiazepine withdrawal, and are probably due to continued effects of the drug. Mentors should be prepared to repeat encouragements again and again, week after week, as their words are soon forgotten.
Also this will pass with time, however in certain cases memory/brain-supporting supplements, Nootropics, may be considered. But one has to bear in mind that some of them may cause anxiety and restlessness themselves.
Panic attacks may appear for the first time during withdrawal, although some patients have long experience with this distressing symptom. The actress Glenda Jackson, who was not on benzodiazepines, described them as follows: "God, those panic attacks. You think you're dying; your heart pounds so strongly it feels like it's going to jump out of your chest; you choke and begin to feel you can't breathe - and all this is accompanied by terrible shaking and tremor, and feeling freezing cold" (Sunday Times Magazine p.15, October 17, 1999). These attacks are characteristic of some anxiety states and are the result of storms of central and peripheral nervous system hyperactivity, especially the centres normally concerned with fear and flight reactions in response to emergencies. The brain centres that control these fear reactions have been damped down by benzodiazepines and may rebound with renewed vigour as the benzodiazepines leave the body.
Distressing as they are, panic attacks are never fatal and usually last little more than 30 minutes. What is more, it is possible to learn to exercise control over them. Various approaches are described below. Learning to control a panic attack is a skill that improves with practice and needs to be worked on at home. However, panic attacks (and other withdrawal symptoms) have a knack of coming on at inappropriate moments away from home. In such circumstances it is important to stand your ground, resisting the impulse to run away. Dr Peter Tyrer suggests the following manoeuvre when a severe withdrawal symptom such as a panic attack comes on when you are pushing a trolley round a supermarket:
"Take much slower and deeper breaths, making sure that you get air deep down into the lungs instead of just at the top of the chest."
"As you do this you will find that your arms and hands relax so that the whites of your knuckles no longer show as you grip the supermarket trolley."
"Do not move on until you feel the tension flowing out of your hands. With each deep breath you should feel your tension flowing away and, as it does, your symptoms will lessen or disappear."
(Peter Tyrer, How to Stop Taking Tranquillisers, Sheldon Press, London 1986, p.63.)
The discovery that a panic attack can be controlled without resorting to a tablet is a great boost to self-confidence, and the development of new stress-coping strategies is often the key to successful benzodiazepine withdrawal. Panic attacks usually disappear within six weeks of withdrawal.
Panic attacks also can disappear or at least become less frequent and easier to overcome with both or either an Antidepressant or Psychological help such as Cognitive Behavioural Therapy (CBT).
Generalised anxiety, panics and phobias
There are many non-pharmacological techniques for helping people with anxiety. Some of these are listed below, but it is beyond the scope of this booklet to give details of each technique or to mention all of them. None of them are essential for everybody coming off tranquillisers, but can be helpful for those having difficulty.
These are not exclusive to anxiety problems, but also can possible ease the problem of addiction as well as withdrawal in general.
A characteristic feature of benzodiazepine withdrawal is a heightened sensitivity to all sensations - hearing, sight, touch, taste and smell. When extreme, these sensations can be disturbing. One lady had to stop all the clocks in the house because their ticking sounded unbearably loud; many have had to don dark glasses because ordinary light seemed dazzlingly bright. Some find that the skin and scalp becomes so sensitive that it feels as if insects are crawling over them. Heartbeats become audible and there may be a hissing or ringing sound in the ears (tinnitus - see below). Many people complain of a metallic taste in the mouth and several notice strange, unpleasant, smells which seem to emanate from the body. These sensations, including an unpleasant smell (which usually no-one else can detect) have been described in anxiety states in the absence of benzodiazepines. Like insomnia and panics, they are probably reflections of heightened activity in the central nervous system. Such hypervigilance is part of the normal fear and flight response which is damped down by benzodiazepines but undergoes a rebound during withdrawal.
These sensations return towards normal as withdrawal progresses, and some people are pleased with the new, seemingly extraordinary, clarity of their perceptions. Only in withdrawal do they realise how much their senses have been obscured by benzodiazepines. One lady described how thrilled she was when she could suddenly see individual blades of grass in her newly bright green lawn; it was like the lifting of a veil. Thus, these sensations need not give rise to fear; they can be viewed as signs of recovery.
Feelings of depersonalisation and of unreality are associated with benzodiazepine withdrawal, although they also occur in anxiety states. They occur most often during over-rapid withdrawal from potent benzodiazepines and are, anecdotally, particularly marked on withdrawal from clonazepam (Klonopin). In these states, the person seems detached from his body and seems almost to be observing it from the outside. Similar experiences are described in near-death states when the individual feels that he is hovering above his body, detached from the events occurring below. They are also described by people involved in extreme emergencies and in individuals subjected to torture. They are clearly not specific to benzodiazepines.
Such experiences probably represent a normal defensive reaction evolved as a protection against intolerable suffering. They may involve a primitive brain mechanism similar to the "freezing" of some animals when presented with an inescapable danger. Like other benzodiazepine withdrawal symptoms, these feelings resolve in time and should not be interpreted as abnormal or crazy.
Hallucinations, illusions, perceptual distortions
The benzodiazepine withdrawal symptom that raises most fear of going mad is hallucination. Terrifying hallucinations have occurred in people undergoing rapid or abrupt withdrawal from high doses, but the reader can be reassured that they are exceedingly rare with slow dosage tapering as outlined earlier. If hallucinations occur, they are usually visual - patients have described hallucinations of a large bat sitting on the shoulder, or the appearance of horns sprouting from a human head - but auditory, olfactory and tactile hallucinations can also occur. Somewhat less frightening are hallucinations of small creatures, usually insects, which may be associated with the sensations of insects crawling on the skin (similar hallucinations occur in cocaine and amphetaminewithdrawal). Sometimes hallucinations merge with illusions and misperceptions. For example, a coat hanging on the door may give the illusion of being a person. Floors apparently tilting and walls that seem to slope inwards are perceptual distortions.
The mechanisms of these bizarre symptoms are probably similar to those which cause delirium tremens (hallucinations, classically of pink elephants or rats, in the "DTs" of alcohol withdrawal). Benzodiazepines cause profound perturbations throughout the brain, and abrupt withdrawal may be accompanied by uncontrolled release of dopamine, serotonin and other neurotransmitters which cause hallucinations in psychotic disorders as well as in alcohol withdrawal and cocaine, amphetamine and LSD abuse.
Once the hallucinations, which seem real at the time, are recognised as "merely" hallucinations, they quickly become less alarming. They do not herald the onset of madness; they are simply instances of benzodiazepines playing tricks on the brain which will right itself in time. A good mentor can usually reassure and "talk down" a person suffering from benzodiazepine withdrawal-induced hallucinations. In any case they should not worry anyone undergoing slow withdrawal.
Depression, aggression, obsessions
Depressive symptoms are common both during long-term benzodiazepine use and in withdrawal. It is not surprising that some patients feel depressed considering the amalgam of other psychological and physical symptoms that may assail them. Sometimes the depression becomes severe enough to qualify as a "major depressive disorder", to use the psychiatric term. This disorder includes the risk of suicide and may require treatment with psychotherapy and/or antidepressant drugs.
Severe depression may result from biochemical changes in the brain induced by benzodiazepines. Benzodiazepines are known to decrease the activity of serotonin and norepinephrine (noradrenaline), neurotransmitters believed to be closely involved in depression. Antidepressant drugs including the selective serotonin reuptake inhibitors (SSRIs such as Prozac) are thought to act by increasing the activity of such neurotransmitters.
Depression in withdrawal may become protracted (see section on protracted symptoms) and if it does not lift within a few weeks and is unresponsive to simple reassurance and encouragement, it is worth seeking a medical opinion and possibly taking an antidepressant drug (see section on adjuvant medication). Depression in withdrawal responds to antidepressant drugs in the same way as depressive disorders where benzodiazepines are not involved. If, as in many cases, an antidepressant drug is already being taken along with the benzodiazepine, it is important to continue the antidepressant until after benzodiazepine withdrawal is complete. Withdrawal from the antidepressant can be considered separately at a later stage.
Also see supplements below as well as the section on Anxiety above for treatment of Depression.
Aggressive disorders are also associated with low serotonin activity (among other factors) and the appearance of anger and irritability during benzodiazepine withdrawal may involve similar mechanisms as depression. However, these symptoms usually disappear spontaneously and do not last very long. Obsessive disorders (Obsessive Compulsive Disorder, OCD) also respond to SSRIs, suggesting a similar mechanism. Obsessive traits may be temporarily increased during withdrawal and seem to reflect a mixture of anxiety and depression. These tend to settle spontaneously as anxiety levels decline.
Benzodiazepines are efficient muscle relaxants and are used clinically for spastic conditions ranging from spinal cord disease or injury to the excruciating muscle spasms of tetanus or rabies. It is therefore not surprising that their discontinuation after long-term use is associated with a rebound increase in muscle tension. This rebound accounts for many of the symptoms observed in benzodiazepine withdrawal. Muscle stiffness affecting the limbs, back, neck and jaw are commonly reported, and the constant muscle tension probably accounts for the muscle pains which have a similar distribution. Headaches are usually of the "tension headache" type, due to contraction of muscles at the back of the neck, scalp and forehead - often described as a "tight band around the head". Pain in the jaw and teeth is probably due to involuntary jaw clenching, which often occurs unconsciously during sleep.
At the same time, the nerves to the muscles are hyperexcitable, leading to tremor, tics, jerks, spasm and twitching, and jumping at the smallest stimulus. All this constant activity contributes to a feeling of fatigue and weakness ("jelly-legs"). In addition, the muscles, especially the small muscles of the eye, are not well co-ordinated, which may lead to blurred or double vision or even eyelid spasms (blepharospasm).
None of these symptoms is harmful, and they need not be a cause of worry once they are understood. The muscle pain and stiffness is actually little different from what is regarded as normal after an unaccustomed bout of exercise, and would be positively expected, even by a well-trained athlete, after running a marathon.
There are many measures that will alleviate these symptoms, such as muscle stretching exercises as taught in most gyms, moderate exercise, hot baths, massage and general relaxation exercises. Such measures may give only temporary relief at first, but if practised regularly can speed the recovery of normal muscle tone - which will eventually occur spontaneously.
All sorts of strange tinglings, pins and needles, patches of numbness, feelings of electric shocks, sensations of hot and cold, itching, and deep burning pain are not uncommon during benzodiazepine withdrawal. It is difficult to give an exact explanation for these sensations but, like motor nerves, the sensory nerves, along with their connections in the spinal cord and brain, become hyperexcitable during withdrawal. It is possible that sensory receptors in skin and muscle, and in the tissue sheaths around bones, may fire off impulses chaotically in response to stimuli that do not normally affect them.
Nerve conduction studies in patients with such symptoms usually revealed nothing abnormal - for example, there was no evidence of peripheral neuritis. However, the symptoms were sometimes enough to puzzle neurologists. Three patients with a combination of numbness, muscle spasms and double vision were diagnosed as having multiple sclerosis. This diagnosis, and all the symptoms, disappeared soon after the patients stopped their benzodiazepines.
Thus these sensory symptoms, though disconcerting, are usually nothing to worry about. Very occasionally, they may persist (see section on protracted symptoms). Meanwhile, the same measures suggested under muscle symptoms (above) can do much to alleviate them, and they usually disappear after withdrawal.
Heart and lungs
Palpitations, pounding heart, rapid pulse, flushing, sweating, and breathlessness are usual accompaniments of panic attacks, but may occur without panics. They do not signify heart or lung disease but are simply the expression of an overactive autonomic nervous system. Slow deep breathing and relaxation, as described under panic attacks, can do much to control these symptoms. Do not worry about them: they would be accepted as normal if you were running for a bus, and will do no more harm than if you really were!
Problems with balance
Some people during benzodiazepine withdrawal report feeling unsteady on their feet; sometimes they feel they are being pushed to one side or feel giddy, as if things were going round and round. An important organ in controlling motor stability and maintaining equilibrium is a part of the brain called the cerebellum. This organ is densely packed with GABA and benzodiazepine receptors and is a prime site of action of benzodiazepines. Excessive doses of benzodiazepines, like alcohol, cause unsteadiness of gait, slurred speech and general incoordination, including inability to walk in a straight line. It may take some time for the cerebellar systems to restabilise after benzodiazepine withdrawal and the symptoms can last until this process is complete. Exercises, such as standing on one leg, first with eyes open, then with eyes closed, can speed recovery.
Some people have no problems at all with their digestive systems during or after withdrawal, and may even notice that they are enjoying their food more. Others, perhaps more prone constitutionally, may complain of a range of symptoms associated with "irritable bowel syndrome" (IBS). These can include nausea, vomiting, diarrhoea, constipation, abdominal pain, flatulence, gaseous distension and heartburn. Quite a few have found these symptoms so uncomfortable that they have undergone hospital gastrointestinal investigations, but usually no abnormality is found. The symptoms may be partly due to overactivity in the autonomic nervous system, which controls the motility and secretions of the gut and is very reactive to stress, including the stress of benzodiazepine withdrawal. In addition, there are benzodiazepine receptors in the gut. It is not clear what the functions of these receptors are or how they are affected by benzodiazepines or benzodiazepine withdrawal, but alterations in these receptors may play some part in increasing gut irritability.
Considerable loss of weight (8-10lb or more) sometimes occurs in withdrawal. This may be due to a rebound effect on appetite, since benzodiazepines have been shown to increase appetite in animals. On the other hand, some people gain weight in withdrawal. In any case, weight changes are not severe enough to worry about and normal weight is soon regained after withdrawal. A few people have difficulty in swallowing food - the throat seems to tighten up especially if eating in company. This is usually a sign of anxiety and is well-known in anxiety states. Practising relaxation, eating alone, taking small well chewed mouthfuls with sips of liquid and not hurrying make things easier and the symptom settles as anxiety levels decline.
Most digestive symptoms get better after withdrawal but in a few people they persist and become a protracted symptom, raising fears of food allergy or candida infection. These questions are discussed further in the section on protracted symptoms.
"Why do I get so many infections?" This question is commonly asked by patients withdrawing from benzodiazepines. They seem to be prone to colds, sinusitis, ear infections, cystitis, oral and vaginal thrush (candida), other fungal infections of the skin and nails, cracked lips, mouth ulcers and influenza. Also common are complaints of adverse reactions to antibiotics used to treat some of the bacterial infections.
It is not clear whether there really is an increased incidence of infections in people undergoing benzodiazepine withdrawal, because there have been no comparisons with otherwise similar populations who have not been exposed to benzodiazepines. However, many factors affect the immune system. One of these is stress, with increased output of the stress hormone, cortisol, which inhibits immune responses. Another factor is depression, also related to stress and associated with increased cortisol secretion. Increased cortisol levels can reduce resistance to infection and also cause flare-ups of incipient infection. Benzodiazepine withdrawal can clearly be stressful but, strangely, in patients that I have tested, blood cortisol concentrations have been low. So this subject remains a mystery and probably merits further research. The message for people undergoing benzodiazepine withdrawal is to try to lead a healthy lifestyle, which includes a balanced diet, plenty of exercise and rest, and avoidance of extra stress where possible. Slow dosage tapering is the best way to reduce the stress of withdrawal.
Benzodiazepines undoubtedly have effects on the endocrine system, but these have not been closely studied in humans, either during long-term benzodiazepine use or in withdrawal. Many women complain of menstrual problems but these are common in the general population and there is no clear evidence that they are directly attributable to benzodiazepines. A proportion of female long-term benzodiazepine users have had hysterectomies, but again there is no evidence of a direct link with benzodiazepine use. Occasionally both men and women on benzodiazepines complain of breast swelling or engorgement and it is possible that benzodiazepines affect secretion of the hormone prolactin. Endocrine symptoms that are due to benzodiazepines improve after withdrawal.
Benzodiazepines are potent anticonvulsants. They can be life-saving in status epilepticus (repeated fits, one after another) and in fits caused by overdose of certain drugs (for example, tricyclic antidepressants).
Such an occurrence is extremely rare with slowly eliminated benzodiazepines (e.g. diazepam) or with slow dosage tapering. If a fit does occur in these circumstances, it is usually only a single fit and causes no lasting damage. Other phenomena seen in rapid withdrawal are psychotic symptoms, severe confusion and delirium, but again these hardly ever occur with slow dosage tapering. By following the withdrawal schedules outlined before, you can be confident of avoiding these complications.
Again: One should never attempt to go cold turkey, not even if in care of a doctor or in a hospital. It is of the utmost importance and well known to medical professionals that Cold Turkey quitting of medium and high dosages of Benzodiazepines is potentially life threatening.
[h3]General Recovery Aid (not only) for Acute W/D[/h3]
Some unsorted tools and recovery aids. A lot of this may also be of help in later stages of withdrawal, or post-withdrawal or long-term problems such as anxiety and depression. Some things may actually not work for everyone during withdrawal, e.g. meditation, as most people are at that time psychologically not capable of such intense exercises.
Eat well, sleep lots, get a good strong B vitamin complex and a calcium/magnesium supplement on top of any multivits you get. Selenium and 5htp won't hurt either for keeping your mood on a level through what could be a dark period ahead.
Force yourself to do normal every day things:
*Get up, out of bed and dressed every morning.
*Do not sleep during the day
*Do dishes every day/Distract yourself
*Do laundry as soon as there is enough for a load
*Take care of yourself
*Cook healthy meals
*Drink lots of water
Another issue is finding fun things to do that do not involve drugs. She has found that even going out dancing, alcohol is usually served and that leads to cravings in her case for the old doc.
Counseling is a good one, usually there are underlying reasons that addicts have to deal with to be whole again and not go back to negative patterns.
Swim agrees relapses are to be learned from and just don't stay in the relapse. They are very common with meth addicts she knows. One just has to readjust and discover what was the trigger that caused the relapse so they can avoid it.
Number 1: Try to work out why SWIY uses
Number 2: Cut off all SWIY's conections (This is probably the hardest one)
Number 3: Indentify triggers in your life, this could be anything personal to you. It could be something as silly as a phonebox SWIY uses to ring his dealer that gives you the urge to use. Write these down and avoid.
Number 4: Identify high risk situations in which you would normally use. Write these down. Avoid them. These could be places your friends/aquaintances houses/flats for example.
[h4]Diets, Fluids, Exercise[/h4]
There has been increasing interest in the question of diet in benzodiazepine withdrawal, particularly in North America. What food/drinks should be excluded? What supplements should be added? These are frequent questions. In my opinion there is no need to be over-obsessive about diet. Some people advise that caffeine and alcohol should be completely ruled out. However, the point about gradual dosage tapering at home is that people should get used to living a normal lifestyle without drugs. In my experience, coffee or tea in moderation (about two cups a day), or reasonable amounts of cocoa, chocolate or coca cola, are perfectly compatible with benzodiazepine withdrawal - except in the few individuals who are exquisitely sensitive to caffeine or those with very high anxiety levels. Clearly one should not take caffeine late in the evening or drink cups of tea/coffee (unless decaffeinated) in the middle of the night if insomniac, but to prohibit a cup of tea/coffee at breakfast is in general unduly restrictive. One is, after all, striving to be normal and sociable, not fussy.
Similarly with alcohol: a glass or two of wine is perfectly permissible (and even said by some to be advisable for health). Although it is important not to substitute increasing doses of alcohol for decreasing doses of benzodiazepines, there is no need to deny oneself small pleasures. Moderation is the key: there is no call to be puritanical.
The same principles apply to food. Humans are singularly well adapted through evolution to obtain the nutrients they need from a wide variety of diets and to eliminate unwanted products. A normal healthy diet which includes generous amounts of fruit and vegetables and a source of protein and fats (from meat or vegetables), and not too much pure sugar or "junk foods", provides all the nutrients a person needs. There is no general need for dietary supplements or extra vitamins or minerals or for "detoxifying" measures. All these can be harmful in excess. Advice to cut out white flour, white sugar etc. may help certain individuals but I have also observed that overly restrictive diets can have adverse effects. Some people say they have felt much better after going on a particular diet - this makes one wonder what sort of diet they were eating before!
Individuals may find they are intolerant of certain foods although this is not usually a true allergy. In this case, let common sense prevail and avoid such foods for a while. If in doubt, get the advice of a reliable and unbiased nutritionist, but in general stick to a normal healthy diet without food fads. Before diets became "fashionable" thousands of people successfully came off their benzodiazepines in many different countries with widely varying dietary habits without restriction - and this continues today.
A normal diet includes a normal amount of fluid consumption. Requirements for water and salt vary with body size, environmental temperature, amount of exercise, etc. so cannot be stated categorically. However, there is no need to drink extra amounts of fluid during withdrawal with the idea of "flushing out impurities/toxins". The body is very good at doing this, even at minimal fluid consumption, and surplus water is simply excreted.
Regular moderate exercise is recommended during withdrawal as it maintains general fitness, builds up stamina, increases the circulation to brain, muscle and skin and improves mood, but there is no point in slavishly doing exercises that you hate. The aim is to lead a healthy lifestyle which by definition includes some exercise in a form that is enjoyable for you.
Increase the right proteins!!!! Proteins are the building blocks for neurotransmitters and neurotransmitter receptors…as well as the building blocks for your natural opiate receptors.
For 3 weeks you must remove all red meats from your diet. Red meat has chemical components that increase inflammation and pain. Fish, chicken, eggs are good sources of protein. If you are having a hard time taking in solid foods go to a health food store and buy protein powders that can be made into smoothies or drinks. You absolutely must have increased protein intake…proteins are the building blocks for all enzymes, neurotransmitters, and enzyme receptors in the body. No chemical works in the body without receptors. Just like benzos have to have GABA receptors this is the reason people have long-lasting anxiety and insomnia coming off Benzos…this isn’t much of a problem with Benzo use because of it’s short half-life…proteins are essential for the repair work in recovery…I now use a formulation made by Neuroresearch…their Neuroreplete/D-5 protein formulas works well for those coming off of methadone, methamphetamines and benzodiazepines or any drug for that matter…for more information on this product go to xxxxxxxxx or xxxxxxxxxx and try to find a doctor close to you that will help you get his product…in fact I treat all my methadone withdrawal patients with this formula.
Increase your intake of raw fruits and vegetables…you get little or nothing from canned foods…fresh fruits and veges are loaded with fiber which help bind and remove toxins from your body…they also normalize gut function.
Stay off candy, and other sugar heavy foods.
Drink lots of good water, green teas are good for the antioxidants and anti-inflammatory properties…no cokes or soda waters for three weeks.
When capable you must start exercising…swimming is best because it is low impact exercise…yoga…tai chi…walking daily…detoxing or otherwise…exercise is a normal component of good health.
Remember to take in enough good fruits and vegetables. Vitamines, minerals, antioxidants etc are essential.
Supplements: Some need less and some more…remember the efficacy of all nutrition and supplement use is ultimately guided by your genetics…and we are all different to some degree…This is the value of seeing a good Naturopathic physician in the state you are in…The fact is that very few Medical Doctors know anything about nutrition…70%-75% of the standard medical schools in this country have absolutely no nutritional classes what-so-ever…in the other 25 %--nutrition is often a 14-20 hour block of education and this is commonly an elective…Naturopathic physicians that are educated in a medical school environment are taught nutrition extensively with the associated biochemistry. For supplements and off-label drugs see further down below.
[h3]Psycho-Therapy & Techniques[/h3] Behaviour therapy
# aims to replace anxiety-related behaviours with better adapted behaviours
# Progressive muscular relaxation (reduces muscle tension and anxiety)
# Diaphragmatic breathing (many anxious people hyperventilate)
# Guided imaging (focus on pleasant, relaxing situations; relaxation tapes with music and calm words can also be used at home)
# Controlled exposure to frightening situations, gradually increasing till anxiety diminishes
# Teaches patients to understand their thinking patterns so that they can react differently to anxiety-provoking situations. This is one of the best, fastest and most effective therapies as it does not deal as much with the past, but focuses on preventing problems in the present.
# Coping skills therapy/anxiety management (learning techniques) to avoid anxiety-provoking situations and to deal with anxiety (if it occurs)
[h3]Meditation[/h3] I think this topic deserves its own section as for some people meditation can be immensly helpful and can be so powerful that one recovery competely and that it helps more than Antidepressants and Benzos and all drugs together.
If one has the interst and discipline after getting of drugs to pursue this he will be greatly rewarded and his life will change automatically. No need for all the hustle of trying to change this that aren't possible to change for oneself. They will change automatically.
SWIM made the experience that two things are of importane:
1. Patience: One has to practices regularly, at best 2x a day for 30 minutes
2. I really recommend going deeper into (Buddhist) philosophy and Ethics as this may also greatly help developing a different view of oneself, his/her problems and society in relation to that. Also it can keep one motivated to stay clean and to be productive, happy and to keep on Meditating.
There are various methods and techniques, schools and approaches, Buddhist and non-Buddhist. SWIM considers the Buddhist ones Superior as they often are more in-depth, while for SWIM many other techniques were good as a relaxation but eventually never left that stadium. SWIM might as well have laid down everyday, listening to relaxing music.. Having said that, everyone reacts differently.
Also intersting after a withdrawal maybe a temporary retreat. One of the posts below deals with that.
(I wrote this a while ago, in the meantime I found that the Zen technique is not for me, but that i prefer various Mahayana/Tibetan practices and philsophies. Check the link list to below to make your own impressions).
The are also posts from various DF members from this thread:
I'd like to start off with a Zen technique, i'm new to this whole thing but really ambitious. I'm just gonna give a short summary of the technique described in Zen Mind, Beginner's Mind by Shunryu Suzuki.
(i copied most of it from the wiki page on Zazen, which is a very good text about zazen)
Philosophy: Zazen is at the heart of ZenBuddhist practice. The aim of zazen is just sitting, opening the hand of thought. Once the mind is able to not be hindered by its many layers, one will then be able to realize one's true Buddha nature. In Zen Buddhism, zazen (literally "seated meditation") is a discipline practitioners perform to calm the body and the mind and experience insight into the nature of existence and thereby gain enlightenment
The technique: The posture of zazen is seated, with folded legs and hands, and an erect but settled spine. The legs are folded in one of the standard sitting styles. Beginners might also just sit on their legs, with their knees touching the ground. The hands are folded together into a simple mudra over the belly (the fingers of one hand over the others, while the thumbs touch each other, the hands forming a circle). In many practices, one breathes from the hara (the center of gravity in the belly) and the eyelids are half-lowered, the eyes being neither fully open nor shut so that the practitioner is not distracted by outside objects but at the same time is kept awake.
Once you've attained a proper posture, you will be ready to begin your zazen practice.Your practice will evolve over time, and may involve a number of different methods over the years.
Begin by breathing fully, deeply, and naturally. Breathe through your nose and from your abdomen, not from your chest, feeling your abdomen expand and contract. You should feel your center of energy shift to your abdomen as it becomes the focal point of both your posture and your breath.
Once your breathing is relaxed and regular, you can (if you want to, it might be easier for beginners) silently count each exhalation, counting up to ten and then starting over at one. Each count should last the full exhalation; instead of a short "One", you should count "Ooooooooone", "Twoooooooo", etc.
This practice will help you focus and relax your mind. You'll soon discover that your mind wanders or is busy with other thoughts. You'll suddenly realize that you've stopped counting/concentrating on the breathing and started daydreaming or thinking about something that's troubling you, or you may still be counting but have no idea what number you're on. When this happens, just go back to one or start over concentrating. Don't get angry or frustrated with yourself, just start again. Every time you get lost, go back to the beginning, without blame. Thoughts and feelings will come; just let them go, and take yourself back to one. If you return to counting your breaths again and again and again, everything else will settle down and stop bothering you quite naturally. Always gently and firmly come back to the practice with all your energy. That's pretty much it.
I found that method very easy, for you don't have to have any special equipment or any preparation (except for the sitting, which might be not taken too seriously at the beginning) and it's possible to practice your concentration in all kinds of situations during the day. You'll almost immeaditly feel how it improves your mood and how you psych. is getting balanced out.
I'm a huge fan of Qigong (pronounced Chee-gong) which is a Chinese meditative practice which often uses slow graceful movements and controlled breathing techniques to promote the circulation of qi within the human body, and enhance a practitioner's overall health. There are also many forms of Qigong that are done with little or no movement at all, in standing, sitting and supine positions; likewise, not all forms of Qigong use breath control techniques.
I run an acupuncture drop in where I use 5 finger Qigong and it always goes down well with my clients. It is very simple to do, you can even do it last thing at night when wanting to go to sleep. Here is a basic version:
Five ﬁnger qigong is an exercise often used for calming the mind and easing anxiety.
To begin sit down in a comfortable position and make an o shaped ring with the thumb and index ﬁnger of both your hands.
Rest your hands lightly on your lap, with your palms facing upwards and breathe deeply becoming aware of the cooling sensation as the air enters your nose. Remain like this breathing calmly for a few moments.
Focus on your breath and the slightest, lightest pressure between your thumbs and index ﬁngers.
Now move your thumbs to connect lightly with your middle ﬁngers and continue to breath slowly and deeply for the next minute.
When a minute has passed move your thumbs lightly onto your ring ﬁngers and keep breathing deeply and calmly for the next few moments.
And when another minute has passed, move your thumbs to make contact with you little ﬁngers - keep your posture and your breathing relaxed and remain, breathing deeply and calmly, for another minute.
Try it out and hopefully you will enjoy! )
I am a really big fan of combining multiple techniques into one experience. My methods are dictated by what my purpose is or what I am simply hoping to get out of it. Relaxing, stability, contemplation, healing, and cleansing will be call for one method and if I am purely trying to attain a state of higher consciousness I will use other methods. Of course with every session will come different goals so the methods are always customized even further.
No matter what my purpose for meditation is I always like to start with QiGong (also pronounced 'Chi-Kung' sometimes).
I really emphasize the Guanqifa (Qi-cultivation/permeating) movements to gather energy. Mixed with those I will throw in techniques specific to my purpose.
I am a big fan of Brainwave Entrainment so a lot of times I will have the headphones on during my Qigong, and will always have the headphones on and tuned to Theta during meditation.
If I am not trying to necessarily attain higher consciousness and am focusing more on 'this realm' I will meditate in either the Lotus or Half-Lotus position. I curl in my perinium a little bit, keep my Crown aligned with spine and perinium and tuck in my chin a bit and keep it aligned with spine and perinium as well.
I may then go in to the Microcosmic Orbit Meditation or a specific Khundalini position then my intentions go to my 'purpose'.
If I am trying to attain higher consciousness, Astral Projection, I will go through the Qigong but then lay down, flat on my back, hands to my side and palms up. I know a lot of people find it easier to leave their body in a sitting position but It has been much easier for me to control the 'phases' while laying down.
I am very intrigued by Magick and Alchemy so I am also really in to the idea of the ritual and the use of sigil's. If you are looking for knowledge or health or anything make something that represents a conglomeration of your purpose. Anything, and I mean anything that has relativity to your purpose should go in to this. If there is a color associated with it include that in your representation, same goes for anything else.
Do not go over board with it though. While creating this representation, consciously put your specific intentions in to the representation the entire time you are creating it. Perform Qigong before preparing the Sigil. Feel the energies flowing in to the Sigil whilst creating it, you will know when it is finished. When it is complete you must somehow make the Sigil public. It does not matter how you do this but, people MUST experience the Sigil. If it is sound they must hear it, if an image, it must be seen.
Give your Sigil ample time to be experienced, again, do not go overboard, you will know when it is time. If you dont get the feeling it is time, then it is time.
After the Sigil has been experienced it is time to meditate, or probably even better yet, to Astral Project and 'ask for' the sigil to guide you.
I also find it very good to make your intentions verbal beforehand. There is a reason people pray. Relax yourself thoroughly, kneel or get into a comfortable position and while focusing deeply on your intentions, make them verbal. It may even help to 'sing' them with the music if you have some playing.
I hope that maybe I have given someone some ideas, and am eager to hear more about people's methods and experiences
Monkey once went to one of those 10 day vipassana meditation retreats where you basically live like a buddhist monk for the duration--no talking, limited eating, meditating from four am until around eleven pm, etc.
The technique used was simple and monkey found it to be very refreshing, increasing body awareness and vitility, relaxing and clearing the mind.
Sit and focus on breath, going into nostrils, down into lungs, causing stomach to protrude, and back up in reverse. This is done for several minutes.
Next focus awareness at top of head and feel the sensations there without thinking anything, just awareness of sensation. Now scan over your body--down face, head, neck, chest, back, shoulders, arms (one by one), et cetera, right down to the tip of each individual toe. Let attention rest at each little part of the body until you feel the sensations there (some places you will find difficult to be aware of at first). Then you move back up from toes to crown of head.
This can be kind of tedious and it takes quite a while (should take at least 20 minutes each direction), but is worthwhile if you can force yourself to sit and do it.
I find the technique Zazen to be an excellent one for Indian and Japanese people, who are very used to the sitting position involved, while western people are not at all, they feel numbness, discomfort, and anxiety while meditating in such a position, it destroys their body rather than relax it.
The key is not to sit in a specific position, but to provide the ultimate comfort for your body, my recommendations are to sit relaxed with your back on a comfortable couch or chair (a bed will most likely make you fall to sleep), and think of the duality of life and death, how the body dies, the mind dies, and the heart dies after you die, watch and see what remains there.
Consciousness is sure of its immortality, it is your body that is afraid to die.
I speak a lot on the subject in my personal blog, focusing on my inward journey and how I came to realize the things any intelligent person has the potential to realize, if you consider yourself smart enough you can enjoy the experiences and even surpass me and teach me! I don't believe in masters and students, we are all catalysts, it is only you who is responsible for your experience.
The information is too big to be shared here, if you are interested in mind expansion and self-exploration, you should read it, but unfortunately I cannot post the link, you'll have to ask me in a personal message for me to share it.
But you can also serach yourself for relaxing Buddhist music e.g. from tibet through piratebay or other torrent website. Feel free to PM me on this! I am convinced that, if done regularly and with the right intention and mindfulness, Buddhism and Meditation is THE solution to all problems. And no, i does not take "years"! Its more like trying to learn and instrument. It takes some time to get the basics, but with the basics you can already do a lot. Of course, it takes years to be very good, but the first success won't take too long.
[h3]Complementary medicine techniques[/h3]
# Massage, reflexology
# Antidepressants (see list below)
#Non-addictive Anxiety drugs
#In bad cases: Anti-psychotics
#Other (herbal) supplements may also be tried, see the list further down.
[h3]Exercise and other techniques[/h3]
# Sports - aerobics, jogging, swimming, "pilates", walking and anything active that you find enjoyable
The choice of, and response to, each of these measures depends very much on the individual preference and the symptoms.
The various psychological techniques have been formally tested and give the best long-term results. However, the outcome depends largely on the skill of the therapist, including his/her knowledge of benzodiazepines, and the rapport between therapist and client.
Of the complementary medicine techniques, all can help with relaxation during the procedure but the effects tend to be short-lived. For example, patients who underwent a course of 12 acupuncture sessions by an acupuncturist trained in both Chinese and Western acupuncture enjoyed and felt relaxed by the sessions but they did not do any better in the long run than others who did not have acupuncture.
Certain individuals respond very well to yoga and meditation techniques. One particular patient who was confined to a wheelchair with a spastic paralysis and who was also blind, was able to come off all his benzodiazepines with the help of a meditation technique. His spasticity actually improved. However, not everyone is able to devote the mental and physical concentration required for these techniques. Physical exercise, within your own limitations, is good for everyone.
On the whole, different approaches suit different individuals and need to be personalized. If you believe in a certain approach, it will probably do you good. Find out what is good for you, by using common sense and seeking treatment for occuring symptoms. Consider professional help.
I hardly dare to mention smoking in view of present day attitudes to this unfortunate addiction, but for those who are smokers it is probably asking too much to attempt to stop smoking and withdraw benzodiazepines at the same time. Many people have found that giving up smoking is easier when they are off benzodiazepines, when the desire for nicotine may even wane somewhat. In general, excessive worrying over your undesirable habits (or your diet) can add to the stress of withdrawal. It is better to relax a bit and be gentle with yourself.
[h2]Post Acute Withdrawal Syndrome (PAWS)[/h2]
This overlaps witht the next section of Protracted W/D Symptoms. I suggest to read both, as they are very (but not completely) similar.
MissSparkles has put this together from various recovery sites and literature she uses herself. It's just a rough guide to PAWS, how it affects the recovering addict (not substance specific) and some strategies to enable a person to get through it. It's not AA/NA specific, (Sparkles has removed references to AA/NA) although some of the terms may be similar. To be honest if it helps someone who is struggling, that's all that counts.
Recovery is different for everyone, so take what's helpful and leave the rest.
There are several stages of withdrawal. The first stage is the acute stage, which usually lasts at most a few weeks. During this stage, you may experience physical withdrawal symptoms. But every drug is different, and every person is different.
The second stage of withdrawal is called the Post-Acute Withdrawal Syndrome (PAWS). During this stage you'll have fewer physical symptoms, but more emotional and psychological withdrawal symptoms.
Post-acute withdrawal occurs because your brain chemistry is gradually returning to normal. As your brain improves the levels of your brain chemicals fluctuate as they approach the new equilibrium causing post-acute withdrawal symptoms.
Most people experience some post-acute withdrawal symptoms. Whereas in the acute stage of withdrawal every person is different, in post-acute withdrawal most people have similar symptoms.
[h3]The symptoms of Post-Acute Withdrawals[/h3]
The most common post-acute withdrawal symptoms are:
Post-acute withdrawal feels like a rollercoaster of symptoms. In the beginning, your symptoms will change minute to minute and hour to hour. Later as you recover further they will disappear for a few weeks or months only to return again. As you continue to recover the good stretches will get longer and longer. But the bad periods of post-acute withdrawal can be just as intense and last just as long.
Each post-acute withdrawal episode can last for a few minutes to a few days. Once you've been in recovery for a while, you will find that each post-acute withdrawal episode usually last from minutes to days. There is no obvious trigger for most episodes. You will wake up one day feeling irritable and have low energy. If you hang on it will lift just as quickly as it started. After a while you'll develop confidence that you can get through post-acute withdrawal, because you'll know that each episode is time limited.
Post-acute withdrawal can last a couple of years. This is one of the most important things you need to remember, but you can get though this. If you think that post-acute withdrawal will only last for a few months, then you'll get caught off guard, and when you're disappointed you're more likely to relapse. Some people do get through this stage quicker than others, but it takes time to dismantle the beliefs, behaviour and thinking that addiction brings with it.
See the section on How to treat/prevent PAWS for further information.
Also see the supplements (especially Iboga/Ibogaine and Antidepressants) and other parts of this guide for further Recovery Aid and consider professional help in the long term if problems dont go away themselves.
Almost all symptoms go away by just enough time, while some long-term symptoms really can take a long time.
Bear in mind that the following list regarding both symptoms and treatments is not exclusive and that the suggested treatments in one category also often help with problems of another category or withdrawal symptoms in general! The categories are just indicators for which treatment may be especially beneficially for a certain problem, however, by using common sense SWIY can see that each of the treatment options have many benefits and may be used in different situations.
[h3]Recovery Aid for Post-Acute Withdrawal Syndrome (PAWS)[/h3] How to survive Post-Acute Withdrawal. Be patient. It can feel like a long time if you're in a rush to get through it. You can't hurry recovery. But you can get through it one day at a time.
If you try to rush your recovery, or resent post-acute withdrawal, or try to bulldoze your way through, you'll become exhausted. And when you're exhausted you'll think of using to escape.
Post-acute withdrawal symptoms are a sign that your brain is recovering. They are the result of your brain chemistry gradually going back to normal. Therefore don't resent them. But remember, even a year on, you are still susceptible to PAWS.
Go with the flow.Withdrawal symptoms are uncomfortable. But the more you resent them the worse they'll seem. You'll have lots of good days, enjoy them. You'll also have bad days. On those days, don't try to do too much. Take care of yourself, focus on your recovery, and you'll get through this.
Practice self-care. Give yourself lots of little breaks, tell yourself "what I am doing is enough." Be good to yourself. That is what most addicts can't do, and that's what you must learn in recovery.
Sometimes you'll have little energy or enthusiasm for anything. Understand this and don't over book your life. Give yourself permission to focus on your recovery. Remember if you can get through these bad times without using your DOC (even if you do nothing else) it's a success.
Post-acute withdrawal can be a trigger for relapse. You'll go for weeks without any withdrawal symptoms, and then one day you'll wake up and your withdrawal will hit you like a ton of bricks. You'll have slept badly. You'll be in a bad mood. Your energy will be low. And if you're not prepared for it, if you think that post-acute withdrawal only lasts for a few months, or if you think that you'll be different and it won't be as bad for you, then you'll get caught off guard. But if you know what to expect you can get through this.
Being able to relax will help you through post-acute withdrawal.
Eventually, everything will go away with enough with time. The acute ones settle with in a few days to weeks, depending on the dosage and length of addiction. However, the long-term effects may take a lot longer, for some people even years and professional help may be needed in cases where Benzos suppressed anxiety/depression feelings that surfaced again after withdrawal and now cause trouble again.
Depending on the individual symptom of withdrawals, several methods or supplements are available to lessen or possibly even prevent their occurrence. This is basically dealt with on a case-to-case basis, it is good to be prepared for the worst, but not everything must occur. Some things are only short term related (especially physical), some things are most disturbing in the long term (especially psychological).
Having said that, I can again only stress the need to taper off. Tapering off Benzos will lessen withdrawal and most of these things will not happen. It will be a lot easier and also not life-threatening.
When you're tense you tend to dwell on your symptoms and make them worse. When you're relaxed it's easier to not get caught up in them. You aren't as triggered by your symptoms which means you're less likely to relapse. PAWS or "Post Acute Withdrawal Syndrome." This is the more drawn-out phase of withdrawal...as the body learns to cope without the drugs. includes boredom, insomnia, self-doubt, 'restless legs,' depression.
I believe from my own experience, combined with reports from recovering opiate addicts and the physiology involved that the initial withdrawal is the big, feared MONSTER associated with feelings of sickness and delirium, whereas PAWS can be extremely different for different people. PAWS seems to be more akin to a "waiting game" with fears of overwhelming boredom than an acute sickness. The most important thing to remember during PAWS is AWARENESS that PAWS IS ONLY TEMPORARY!
With time, PAWS will go away!! In fact, with few exceptions, it seems that with every passing week, PAWS symptoms can be demonstrated as improving--sometimes DRAMATICALLY compared to the weeks prior.
Some Reasons why PAWS takes several months to get over:
Behavioral changes are necessary in order to learn new and solid pathways for the brain's reward circuit, and
It takes MUCH LONGER for your effective neurotransmitter levels and nerve conduction parameters to return to normal, pre-addiction levels.
And depending on your expectations and how you approach these critical 're-building' and 're-organizing' phases, will go far in how well you'll feel during and after withdrawal.
What can be done to HELP your nerve conduction while re-equilibrating to life without benzos? (or--"How to Maximize Your Neuronal Signaling During Post Acute Withdrawal Syndrome.")
Boost the deficient neurotransmitters.
Maximize electrical conduction ALONG the nerve.
1. BOOSTING THE DEFICIENT NEUROTRANSMITTERS.
First, let's talk about boosting the neurotransmitters. For the benzo addict, this means SPECIFICALLY "GABA"---short for "gamma-aminobutyric acid (GABA)".
However, another thing that also helps one to recover faster are Endorphines. There are some things you should know about endorphins. They are responsibe for "feeling good", in a happy way. Endorphin is released naturally in response to pain, orgasm, exercise, laughter, positive thoughts, secondary messengers responsible for fevers & immune responses, and there are other potential triggers including prayer.
These tips may not seem like earth-shattering phenomena by themselves, but believe me, when these steps are clustered and performed regularly, THEY REALLY DO HELP!!!
Common activities known to boost endorphin levels/satisfy cravings:
Chocolate. Chocolate has a mild effect on endorphins.
Candy. Actually any kind of sugary candy boosts natural endorphin levels. Candy helps most with early stages of withdrawal. Lab mice experiments have shown sugary sweets appease craving after abruptly cessation of morphine. Swim practically LIVED on Reese's Pieces, sour candies, M&M's, and those 'tiny' Hershey Kisses for 8 TO 10 WEEKS! Note: he did not gain or lose weight during this time.
Exercise. This is #1. Force yourself to walk out the front door. FORCE YOURSELF to walk 2-3 blocks from your front door…then you turn around and get 2-3 additional blocks in for good measure. I CANNOT STRESS THIS ENOUGH!!! The best exercise is running/jogging/spinning/anything aerobic. Second best is walking or yoga. Somewhere in-between the two is weight lifting. Weight lifting or resistance-training can be done in a fraction of the time and there is evidence to show that this kind of exercise might benefit the MOST at the late stages of withdrawal (i.e. insomnia from 'restless legs').
some medical professionals believe the positive feeling you get when you meet a physical challenge, rather than the exertion itself, is what stimulates the endorphin release....(how much endorphin-release you get) is all about intensity and duration.
Accomplishment. That's right. Any kind of accomplishments. Small ones, big ones. Just be sure you're PLANNING and EXECUTING daily. Anything that fosters a feeling of self-accomplishment and PRIDE will cause your brain to squirt out some Endogenous Morphine.
Sex. Orgasms release endorphins. You've probably already figured this one out… OR--more likely, you've noticed that your sex drive has gone down to almost NOTHING while on opiates. This is normal. I can explain the hormones of it later if you're interested. The point is, you've replaced the endorphin-rush of sex with one that requires no build-up, no mess, and no chance of rejection. Do not feel embarrassed if you become a masturbation machine. This is also a normal part of recovery. Eventually, the sex act itself will be overshadowed by the LOVE aspect.
Love. Love is a complicated emotion. It's the fuel for poets, playwrights since recorded history and the need for it traces all the way back to the first man and woman. HOWEVER!! SEXUAL LOVE IS *NOT* WHAT I'M TALKING ABOUT HERE!!!! Ultimately, your most long-lasting, gratifying experiences outside of drugs will come from the experience of giving AND RECEIVING love. Get creative with this. Love your enemies. Remember people's names. Start remembering birthdays. Surprise someone with your generosity. Next time you mow the lawn, cut your neighbor's grass…and take his trash out to the street. Donate time to feeding the homeless. There's literally TENS OF THOUSANDS of small things you can do to put forth love out into the world. *THIS* is the true secret to learning how to live without opiates! And believe it or not, the rewards are MUCH GREATER than even the best heroin you'll ever do!!! But you've got to get up and DO SOMETHING!
Sleep. Eventually---like in 4-6 months from now--your body's autonomic nervous system will stop being 'revved-up' all the time. Eventually, you will be able to sleep again without having to knock yourself in the head with a sledgehammer! When this day comes, BE PREPARED! Start going to bed as early as possible, to allow yourself a good 7 or 8 hours of restful sleep. Your endorphin levels will naturally increase from the circadian rhythm, plus you'll allow yourself the luxury of copious dreaming--not only endorphin-releasing, but overall will make your days more relaxing and give your psyche plenty of time to play.
Eat a hot Chili Pepper. * Quote:
The rush you get after holding one on your tongue is likely due to your body's protective response. "Chewing a hot pepper can release endorphins centrally and on the tongue," says Dr. Hirsch. Why? To reduce pain, of course.
Think Positive Thoughts.* Placebos, prayer and positive thinking all trigger endorphin release according to Dr. Slotnick.
Get Emotionally Moved *
Dr. Fuhrman says that viewing beautiful art, watching a touching dramatic scene or even listening to an inspiring piece of music can produce endorphins. "A person who gets pleasure in life, from whatever source, will keep endorphins at a healthy level," he says.
Undergo Acupuncture.* Quote:
"Putting needles into the body is a release," says Dr. Fuhrman, "and it may trigger endorphin production." Also, acupuncture patients benefit from a placebo effect -- they believe that the process is working, so it really does, says Dr. Fuhrman. Talk about the brain's power.
Endorphin factor: 3 (NOTE: HIGHEST LEVEL). People who use acupuncture tend to be positive thinkers, which adds to the effects.
Be Afraid.* Quote:
Whether you're watching a horror movie... or feeling a rush of wind in your hair as you plummet down a steep incline on a roller coaster, fear causes endorphin release. Why do you think extreme sports are so popular? No one wants to get hurt; it's just fun (in a twisted kind of way) to cheat death. "The thrill of a high-speed ride induces a positive mood state that can leave you giddy," says Dr. Hirsch. And Freddy Krueger can do it for you too. Who knew he was such a heartthrob?
Watch a Funny Movie or TV Show. More specifically, research has proven that simply the expectation of watching one's favorite funny movie releases Beta-endorphin and human growth hormone.** Go ahead and buy the Seinfeld Box DVD.
2. MAXIMIZING NERVE CONDUCTION. or How to Increase Electrical Conductivity WITHIN Neurons.
The portion of your body that is re-learning its own equilibrium WITHOUT BENZOS is essentially an aquatic salt-water ecosystem that runs almost entirely off electrolytes (+ and - particles called "ions" dissolved in solution) and VERY THIN membranes. These membranes are "semi-permeable" which means that with some assistance from various proteins, these membranes allow your body to separate and partition off positively-charged & negatively-charged ions. This creates VOLTAGE--the difference in charges across a membrane or "potential energy."
You can imagine the separated + and - ions as being like a battery. As long as the membranes are intact and your body is able to separate positives from negatives, then your batteries are "charged." But, if you punch a hole in one of the membranes or stop actively separating out positives from negatives, you end up with a lifeless or DEAD battery. ions from
Anytime you 'fire' off a neuron, an "ON" signal is propagated from somewhere deep inside the brain, along a LOOOONG axon, that ends by terminating into either another neuron (inside the brain) or somewhere else outside the brain (like a muscle or a salivary gland, for example).
If you were to tell yourself, "I am now Lifting my right fore-finger," then a neuron in your brain's motor cortex will first "fire" using a neurotransmitter. But the signal actually travels all the way down on a single neuron from the brain to your right arm. All the way down a discrete "wire" found in a bundle of other wires (your spinal cord) until the single nerve cell finally ends on muscles in your forearm where ANOTHER neurotransmitter is released, cause you to LIFT YOUR RIGHT FOREFINGER.
Why the description? well, the FIRST step involved in this example involves a neurotransmitter. In this case, the neurotransmitter is called acetyl-choline... but there are plenty of other neurotransmitters whose functions are to transmit various ideas, emotions, reactions, reflexes, memories, etc.
The SPECIFIC neurotransmitter you're missing is GABA, but the whole system is out of Balance! Earlier in this post, I listed suggestions to help you SHOWER your brain with endorphin--and these will make you feel much better. If you can assimilate some or all of these activities into your daily routine, then you'll not only be back to normal very soon, BUT (swear to GOD) you'll actually FEEL MUCH BETTER.
The reason I went thru the whole explanation of the + and - ions, the function of cell membranes to partition off these charged particles, and how that nerves & thus your entire brain FUNCTIONS by using a continuous flow of ions in and out of various partitions is because I want you to really REALLY UNDERSTAND something about how our bodies work.
You see, all this fine detail about nerve transmission can ONLY take place under ONE condition. And this is one of the most convincing arguments for evolution that I've ever heard… The ONLY PERFECT ENVIRONMENT for the proper flow of electricity and nerve conduction is found---IN THE OCEAN!
Fortunately, our body's have a "waxy coat" of skin that traps the ocean INSIDE US!
So, whenever you hear someone say "SALT IS BAD FOR YOU", you can tell them they would be DEAD if it weren't for the salt they eat!
Without getting too involved in this, just know that your body has exquisite mechanisms for hanging onto precious minerals and filtering out 'excess' ions. This is mostly done by the kidneys. HOWEVER, your body has NO WAY of either DILUTING or CREATING electrolytes. (i.e. sodium, potassium, calcium, magnesium, & trace minerals)
So, HOW CAN YOU ASSIST YOUR BODY IN ACHIEVING THIS OPTIMUM AQUEOUS ENVIRONMENT???
Simple. Drink plenty of water.Plain water.Not colas, not coffee, not beer. Your body will utilize pure water to form the MOST PERFECT, EXACT ion levels in the various partitioned areas. Unlike what many people believe, drinking extra water does NOT go straight into your piss!! Rather, the water goes from your GI tract, into your bloodstream where it is then dispersed EVENLY throughout every single cell in your body!
That's right…when you drink a glass of pure water, that water becomes almost instantly available to EACH AND EVERY CELL IN YOUR BODY, in order beginning with those cells which NEED WATER THE MOST! So, those cells which urgently need this pure water will get 'first dibs', and so on until the water has been evenly dispersed.
What do the cells DO WITH this pure water??
Rejuvenate Cell Processes/Restore Cellular Health. First off, the new water allows overly-concentrated, sluggish, toxic (dehydrated) cells to return to their original healthy size, shape, & texture. You may recall from biology that a single water (H2O) molecule is generated in cellular energy generation (called respiration). Glucose and Oxygen are transformed into energy, releasing CO2, and H2O. Well, if your teachers were like mine, they neglected to teach how important pre-EXISTING H2O was for this energy to be produced in the first place! Without a surplus of pure H2O, NONE of this energy can be produced!!
Eliminate Toxins. This pure water is necessary for your muscles (and other cells) to mobilize their toxic byproducts for excretion in to the urine. Plus, the additional water will optimize sub-cellular activities that have become erratic or sub-optimal from dehydration, built-up waste materials, and are living in an overall unbalanced, unhealthy state. These molecular-level processes will be cleansed by way of excessive hydration, dilution of toxins, and toxic elimination when these toxins are absorbed along with excess water into the bloodstream and almost immediately filtered into the urine. This 'flooding' leads to a "clean slate" on a sub-cellular level, which then allows the cell's energy production to normalize, which translates into higher energy, more energy efficiency on the tissue & organ level which affects the energy and health that we "FEEL" as organisms!!
Enhance Normal Nerve Conduction Velocity. Remember all that talk about positive and negative ions being separated by membranes to form a 'biological battery'?? Well, one of the most vitally important pieces of the nerve-conduction puzzle is adequate hydration! Adequate hydration allows nerves to conduct their signals FASTER and also allows each nerve to 'reset itself' FASTER as well! So, in essence, adding pure water into your body will make your brain and muscles faster and more efficient--as though your neurotransmitter levels were actually HIGHER--when in reality, you haven't done anything to change your neurotransmitter levels!
When your urine has any yellow coloration or smells, this signifies waste products and toxins that your body must ELIMINATE in order to create this perfect aqueous environment for your nerve cells, muscles, and every tissue.
HOW MUCH WATER SHOULD YOU DRINK? honestly, everyone is different. People going through drug withdrawal require more water than someone whose tissues are already in equilibrium. Your need for 'extra' water during times of stress or drug detoxification will be obvious by the color and smell of your urine.
RULE OF THUMB REGARDING PURE WATER CONSUMPTION: Your urine should be clear and have no smell. This signifies optimal hydration.
Vitamins and Minerals. For fastest re-equalization, you should take ONE daily vitamin with minerals. These days, most every daily vitamin includes minerals as well as folate (aka folic acid). Don't waste your money on expensive vitamins or supplements. All you need are the basic RDA. The *REAL* secret to maximizing the absorption of vitamins is to simply take them WITH FOOD. Taking excess or "mega-dose" vitamins is just a waste of vitamins. 250mg to 500mg of Vitamin C per day is also encouraged, especially in the first few months of withdrawal.
The basic message is to take care of the things that you probably never even THOUGHT ABOUT while on the junk. Things like making sure to take vitamins, eat balanced meals to provide sustenance, exercising and drinking PLENTY OF WATER!
There are other threads which discuss supplements which can be taken to boost other neurotransmitters like norepinephrine, dopamine, and serotonin. Feel free to ask me if you have any questions...this is just WAY TOO HUGE of a topic to answer in a single post! good luck future smack quitters, and to all the Ex-Junkies--PEACE!
Mark Wilson...president of the Hudson Valley Triathlon Club and a triathlon coach. "It doesn't take much to enjoy the benefits of endorphins via exercise," he says. "Literally 10 to 20 minutes of activity can release the natural drugs into your system, which creates a sense of well-being and joy that cannot be felt by sedentary folks. Brief, quick efforts up stairways or down the block can trigger the release of endorphins and possibly keep you from buying that cup of joe on the way to work, not to mention the doughnut! Bottom line, keep moving your body; it likes that!"
Still, some of the best things in life are endorphin-friendly and generate many health and social benefits....Plus, as a drug of choice, endorphins are very safe, and you'll never run out.
"It feels so peaceful," says Dorothy Hamburg, an exercise physiologist and certified exercise trainer who owns Personal Strength and Training in Rhinebeck. "The runner's high, being in the zone, is real. I've been in races where I find myself struggling, then all of a sudden it just becomes easy, fun. Instead of 'oh, no, I've got to run another hour,' it becomes effortless. There is no struggle."
Hamburg, who has enjoyed endurance athletics and marathons for years, explains that endorphins are released when exercise level is moderate to high," at the point when you are going from aerobic to anaerobic exercise." A clue as to when that's happening is
"when you wouldn't be able to have a comfortable conversation while exercising." Short bursts of activity like weight-lifting or sprinting, don't trigger endorphins enough to be measured in the bloodstream, but might boost brain levels, and they help condition the body for more exertional activities.
Also, studies do show that an hour or more of even modest exercise can elevate endorphins. Most of Hamburg's personal training clients are women wanting to get exercise back into their lives as their bodies change in middle life. The endorphins are not a goal, but a perk, and the exercise can be just plain enjoyable for many reasons. "The most important thing is to find what you like doing. If you don't like it, you won't do it." It could include a combination of things, like gardening, walking, and yoga, for a total of half an hour a day. "Start with gentle effort. Learn the movement patterns, see how you feel, then increase in duration, intensity, and frequency."
Bruce Pomeranz, PhD, at the University of Toronto, was the first to propose that acupuncture, commonly undertaken to relieve pain, does so through endorphins. After attending a 1975 conference at which the discovery of endorphins was announced, he theorized that acupuncture needles inserted at key locations in the body (which correspond to points on the meridian) stimulate nerves that trigger endorphin release within the brain (d'ai chi, meaning twisting the needles, is key to the effect, he says). There, the endorphins block the brain from registering the sensation of pain.
He then spent 20 years collecting data to disprove that (as proper science is meant to proceed). But diverse studies of his and other researchers indeed support this "westernized" medical explanation of why acupuncture is analgesic (versus that of traditional Chinese medicine, which explains it in terms of chi energy flowing through meridians). Bottom line: Acupuncture works and endorphins help make it happen.
Chiropractic adjustmentreleases endorphins through its impact on the nervous system From my memory, I want to say that this has statement has actually been proven on animal and human models--on animals for sure--that the 'popping' of the vertebral joints actually induces small regional bursts of endorphin--hence the immediate pain-relief and sometimes-referred to as mildly-'addictive' nature of chiropractic adjustments.
Also SWIM finds it important to mention that one should try to not bring the neuro-chemical system out of balance. SWIM experienced, and tried & prooved this many times for himself. it might not be the same for everybody, but swim is sure that many are affected, especially if anxiety & depression are involved. try to avoid strong triggers and more imporantly avoid drugs/substances that work on the brain the way drugs to. so that means: no kratom (as it works the same receptors), no single-dose opiates, no benzodiazepnes if possible, swim found alcohol to be quite good at disturbing the chemical balance, no cocaine, no "drugs" in that direction (apart from maybe psychedelics), maybe even no thc, also avoid caffeine in the form of coffe (tea is good though).
[h2]Protracted Withdrawal Syndrome[/h2]
PAWS and Protracted Withdrawal Syndromes kind of overlap, but are not necessarily the same. In case of such trouble SWIM adivses to read both section. Similarly, the recovery tips on both overlap.
A minority of people who have withdrawn from benzodiazepines seem to suffer long-term effects - protracted symptoms that just don't go away after months or even years. It has been estimated that perhaps 10-15 per cent of long-term benzodiazepine users develop a "post-withdrawal syndrome". Many of these people have taken benzodiazepines for 20 years or more and/or have had bad experiences in withdrawal. The incidence of protracted symptoms in those who have undergone a slow taper under their own control is almost certainly very much lower.
[h3]Symptoms of Protracted Withdrawal[/h3]
Table 3 shows the symptoms most likely to be long-lasting. These include anxiety, insomnia, depression, various sensory and motor symptoms, gastrointestinal disturbances, and poor memory and cognition. The reasons why these symptoms persist in some people are not clear. Probably many factors are involved, some directly due to the drug and some to indirect or secondary effects (See Table 4).
TABLE 3. SOME PROTRACTED BENZODIAZEPINE WITHDRAWAL SYMPTOMS
TABLE 4. SOME POSSIBLE CAUSES OF PROTRACTED BENZODIAZEPINE WITHDRAWAL SYMPTOMS
(?) indicates possible mechanisms for which at present there is no scientific evidence
[h4]Symptoms Explained[/h4] Anxiety
Anxiety persisting after the acute phase of withdrawal may be partly due to the uncovering of a learning defect caused by the benzodiazepines. These drugs specifically impair the learning of new skills, including stress-coping strategies. Such skills are normally acquired continuously from childhood to middle age or later as experience of life accumulates. Their development may be blocked for a period of years during which benzodiazepines are taken. After withdrawal the ex-user is left in a vulnerable state with a decreased ability to deal with stressful situations. Full recovery may require many months of learning new stress-coping strategies to replace the years when this facility was blanketed by pills.
Secondly, benzodiazepine withdrawal may uncover life problems that have never been fully addressed. For example, the impairment of memory caused by benzodiazepines may prevent the normal resolution of personal stresses such as bereavement or a car crash. Such buried or half-forgotten experiences may have to be faced after withdrawal and may prolong both anxiety and depression. It is not uncommon for a widow or widower, first prescribed benzodiazepines on the death of the spouse, to go through the grieving process for the first time after withdrawal, even though the bereavement had occurred many years previously.
A third factor may operate in people who have had frightening experiences during withdrawal. This is not uncommon in those who have undergone rapid withdrawal without adequate explanation, often in hospital or detoxification centres but sometimes at home when their doctor has withdrawn prescriptions. Such people may develop symptoms of post-traumatic stress disorder (PTSD) in which their experiences are constantly repeated as flashbacks or nightmares and so prolong the anxiety.
In addition, many (though by no means all) long-term benzodiazepine users are constitutionally highly strung, sensitive people with relatively low self-esteem, whose anxiety problems have led to the prescription of benzodiazepines in the first place and whose continuing anxiety (possibly heightened by the benzodiazepines) has prompted the doctor to go on prescribing the drugs. It may take a long time for these people to regain, or attain, full confidence in themselves.
Despite these factors, protracted anxiety symptoms, including agoraphobia and panics, do tend to subside gradually and rarely last more than a year. The process may be hastened by good psychological support and by the measures described under acute anxiety symptoms. Believe it or not, people often feel more self-confident after withdrawal than they did before starting to take benzodiazepines.
Depression may be caused or aggravated by chronic benzodiazepine use, but is also a feature of the withdrawal syndrome. Depressive symptoms may appear for the first time after withdrawal, sometimes after a delay of a few weeks, and it can be severe and protracted for some months. It is not clear whether people who have had depression before, or have a family history of depression, are more prone to this complication, and its causes are not understood. As discussed in Chapters I and II, benzodiazepines disrupt the function of many neurotransmitters and hormones and depression could be the result, for example, of low serotonin activity combined with the stress of withdrawal. If severe enough to require definitive treatment, the depression in withdrawal responds to antidepressant drugs and/or cognitive therapy and usually diminishes gradually over 6-12 months.
Poor sleep is a common accompaniment of both anxiety and depression. In anxiety there is typically a difficulty in falling asleep, while depression is associated with early morning waking as well as frequent wakings during the night. Insomnia is also common as an acute withdrawal symptom along with nightmares and other sleep disturbances. Occasionally, however, insomnia (sometimes with "restless legs" and muscle jerks) persists as an isolated symptom after other symptoms have disappeared, and may last for many months. However, poor sleepers can be reassured that an adequate sleep pattern does return at last. There are powerful natural mechanisms in the body which ensure that the brain does not become severely sleep-deprived.
Craving for the drug can also be a long term problem. There are several thread about it in this forum and aid is given below.
Sensory and motor disturbances
There is no doubt that benzodiazepine withdrawal leaves in its wake a nervous system that is exquisitely sensitive to all sensory and motor stimuli. Usually this state settles in a few weeks but occasionally disturbing sensations persist.
One of the most distressing sensory symptoms is tinnitus, a constant ringing or hissing in the ears which has been noted in several studies of benzodiazepine withdrawal. One lady described her tinnitus as a "needle of sound" piercing deep inside her head. Tinnitus is often associated with a degree of hearing loss and is not uncommon in people with partial nerve deafness who have never taken benzodiazepines. Nevertheless, it often makes its first appearance during benzodiazepine withdrawal in people who have had hearing loss for years. Also, it may be unilateral or precisely localised, even in those with symmetrical bilateral hearing loss. Whether people who have taken long-term benzodiazepines are particularly prone to tinnitus and if so why, is not known. It can persist for years and does not always respond to the usual treatments for tinnitus (maskers, etc); nor is it always relieved by restarting benzodiazepines. However, people with persisting tinnitus after withdrawal should seek the advice of a hearing specialist and may be lucky enough to find a clinic which specialises in this symptom.
A number of unpleasant bodily sensations may persist after withdrawal including tingling, "pins and needles" or patches of numbness in the trunk, face, limbs and fingers. These may be accompanied by burning pain or aches that sometimes seem to originate deep in the muscles or bones. Some people complain of an "inner trembling" or a sense of vibration, and some have described bizarre sensations as of water or slime running over the body or a serpent-like writhing on the scalp. Motor symptoms that may persist include muscle tension, weakness, cramps, jerks, spasms and shaking attacks.
Possible mechanisms of persisting sensory and motor symptoms. Although the above symptoms are often made worse by stress, they are clearly not simply due to anxiety. They suggest a dysfunction in motor and sensory pathways in the spinal cord and/or brain. A possible clue to their mechanism is provided by a trial with flumazenil (Anexate, Romazicon) a benzodiazepine receptor antagonist, published by Lader and Morton (Journal of Psychopharmacology 1992, 6, 357-63). This drug, when infused intravenously brought rapid relief of protracted symptoms (muscle tension, "pins and needles", weakness, muscle cramps or jerks, burning, tremor or shaking) that had been present for 5-42 months post-withdrawal in 11 patients. The symptoms were improved by 27-82 percent and the greatest response occurred in patients with the lowest anxiety ratings. There was no response to infusions of saline solution.
Flumazenil is thought to act by "resetting" GABA/benzodiazepine receptors (See Chapter I) so that they are more receptive to the inhibitory actions of GABA. The results suggest that some protracted symptoms are due to the failure of the receptors to revert to their normal state after they have become unresponsive to GABA, due to the development of tolerance (See Chapter I). The response to flumazenil also shows that benzodiazepines can cause longer-lasting pharmacological effects than previously believed.
Unfortunately, flumazenil does not at present offer a practical cure for protracted symptoms. The drug has to be infused intravenously and is very short acting so that symptom relief is only temporary. The drug cannot be given to a person who is still taking benzodiazepines as it precipitates an acute withdrawal reaction. However, although protracted sensory and motor symptoms may sometimes seem to be almost permanent, they do in fact decline in severity over the years, even without flumazenil, and they do not signify a major neurological illness. Such symptoms may be partially alleviated by relaxation techniques; some motor and sensory systems may respond to carbamazepine (Tegretol) and motor symptoms may respond to propranolol (Inderal).
Poor memory and cognition
Although it is well known that benzodiazepines impair memory and some cognitive functions, particularly the ability to sustain attention, some long-term users complain of continued loss of intellectual abilities persisting after withdrawal. There have been several studies on this question which indicate that improvement may be very slow. The longest studies in therapeutic dose long-term users extend for only 10 months after withdrawal. Cognitive impairment, though slowly improving, persisted for at least this time and was not related to anxiety levels (Tata et al. Psychological Medicine 1994, 24, 203-213). Some Swedish studies have found that intellectual impairment, although improved, was still present 4-6 years after cessation of benzodiazepine use, but it was not clear whether high dosage and/or alcohol use were added factors.
Do benzodiazepines cause structural brain damage? These results have raised the question of whether benzodiazepines can cause structural brain damage. Like alcohol, benzodiazepines are fat soluble and are taken up by the fat-containing (lipid) membranes of brain cells. It has been suggested that their use over many years could cause physical changes such as shrinkage of the cerebral cortex, as has been shown in chronic alcoholics, and that such changes may be only partially reversible after withdrawal. However, despite several computed tomography (CT) scan studies, no signs of brain atrophy have been conclusively demonstrated in therapeutic dose users, and even the results in high dose abusers are inconclusive. It is possible that benzodiazepines can cause subtle changes which are not detected by present methods, but on the available evidence there is no reason to think that any such changes would be permanent.
Gastrointestinal symptoms may be prolonged after withdrawal, usually in people who have a previous history of digestive troubles. Such people may develop apparent intolerance to certain foods, although reliable tests for true food allergy (e.g. antibodies against specific food constituents) are nearly always negative. Nevertheless many sufferers feel that they have damage to the immune system or have developed intestinal candidiasis. There is at present no clear scientific evidence on these topics, though as mentioned before, benzodiazepine receptors are present in the gut and benzodiazepine use or withdrawal may affect immune responses. There is some evidence that chronic hyperventilation provokes the release of histamine (a substance released in allergic reactions) and that the incidence of food-intolerance and "pseudo-allergic" reactions is high in chronic hyperventilators. Advice on diet, breathing and candida infections is given in books by Shirley Trickett quoted at the end of this chapter. It is usually inadvisable to stick to a strict exclusion diet; with a normal balanced diet and sensible general health measures, including regular exercise, gastrointestinal symptoms due to withdrawal gradually abate.
Coping with protracted symptoms
A number of people are expressing fears that some benzodiazepine withdrawal symptoms last for ever, and that they can never completely recover. Particular concerns have been raised about impairment of cognitive functions (such as memory and reasoning) and other lingering problems such as muscle pains and gastrointestinal disturbances.
People with such worries can be reassured. All the evidence shows that a steady decline in symptoms almost invariably continues after withdrawal, though it can take a long time - even several years in some cases. Most people experience a definite improvement over time so that symptoms gradually decrease to levels nowhere near as intense as in the early days of withdrawal, and eventually almost entirely disappear. All the studies show steady, if slow, improvement in cognitive ability and physical symptoms. Although most studies have not extended beyond a year after withdrawal, the results suggest that improvement continues beyond this time. There is absolutely no evidence that benzodiazepines cause permanent damage to the brain, nervous system or body.
People bothered by long-term symptoms can do a lot to help themselves. Also check the supplements section as well as the general guidelines for withdrawal. Most things do still apply, even after the acute withdrawal. For example:
1. Exercise your body. Physical exercise improves the circulation and function of both brain and body. Find an exercise that you enjoy: start at low level, work up gradually and keep it up regularly. Exercise also helps depression, decreases fatigue and increases general fitness.
2. Exercise your brain. Use your brain to devise methods to improve its efficiency: make lists, do crossword puzzles, find out what bothers you most - there is always a way round it. Cognitive retraining helps people to find ways around their temporary impairment.
3. Increase your interests. Finding an outside interest which you have to work at employs the brain, increases motivation, diverts attention away from your own symptoms and may even help others.
4. Calm your emotions. Above all, stop worrying. Worry, fear and anxiety increase all withdrawal symptoms. Many of these symptoms are actually due to anxiety and not signs of brain or nervous system damage. People who fear withdrawal have more intense symptoms than those who just take it as it comes and think positively and confidently about recovery.
How long do benzodiazepines stay in the body after withdrawal? This question is often asked by people with long-term symptoms. Is it possible that one cause of protracted symptoms is that benzodiazepines remain in the body even after months, lurking perhaps deep in such tissues as brain and bones? Could slow elimination from these sites keep the withdrawal symptoms going?
Like many other issues concerning benzodiazepines, the answers to these questions are still unclear. Benzodiazepine concentrations in the blood have been measured and shown to reach undetectable levels in 3-4 weeks after cessation of use in people withdrawn from clinical doses. Information on benzodiazepine concentrations in the brain and other tissues is difficult to obtain, especially in humans. Benzodiazepines certainly enter the brain and also dissolve in all fatty (lipid-containing) tissues including fat deposits all over the body. It is possible that they linger in such tissues for some time after blood levels have become undetectable. However, most body tissues are in equilibrium with the blood that constantly perfuses them, and there is no known mechanism whereby benzodiazepines could be "locked up" in tissues such as the brain. There is no data on how long benzodiazepines remain in bones, which have a lower fat content but also a slower rate of cell turnover.
Nevertheless, the concentration of benzodiazepines remaining in body tissues after withdrawal must be very low, otherwise the drugs would leak back into the blood in discernible amounts. It is difficult to imagine that such concentrations would be sufficient to produce clinical effects or that any direct effects could last for months or years. However, it is not inconceivable that even low concentrations might be enough to prevent the return of GABA/benzodiazepine receptors in the brain to their pre-benzodiazepine state. If so, the receptors would continue to be resistant to the natural calming actions of GABA (See Chapter I), and the effect could be to prolong the state of nervous system hyperexcitability. Possible factors contributing to protracted symptoms are outlined in Table 4.
[h3]Stages of relapse[/h3]
Relapse is a process, it's not an event. In order to understand relapse prevention you have to understand the stages of relapse. Relapse starts weeks or even months before the event of physical relapse. There are three stages of relapse.
[h4]Emotional Relapse & Prevention[/h4]
In emotional relapse, you're not thinking about using. But your emotions and behaviors are setting you up for a possible relapse in the future.
The signs of emotional relapse are:
Not asking for help
Poor eating habits
Poor sleep habits
The signs of emotional relapse are also the symptoms of post-acute withdrawal. Understanding Post-Acute Withdrawal makes it easier to avoid relapse, because the early stage of relapse is easiest to pull back from. In the later stages the pull of relapse gets stronger and the sequence of events moves faster.
Early Relapse Prevention Relapse prevention at this stage means recognizing that you're in emotional relapse and changing your behavior. Recognize that you're isolating and remind yourself to ask for help. Recognize that you're anxious and practice relaxation techniques. Recognize that your sleep and eating habits are slipping and practice self-care.
If you don't change your behavior at this stage and you live too long in the stage of emotional relapse you'll become exhausted, and when you're exhausted you will want to escape, which will move you into mental relapse.
Practice self-care. The most important thing you can do to prevent relapse at this stage is take better care of yourself. Think about why you use. You use drugs or alcohol to escape, relax, or reward yourself. Therefore you relapse when you don't take care of yourself and create situations that are mentally and emotionally draining that make you want to escape.
For example, if you don't take care of yourself and eat poorly or have poor sleep habits, you'll feel exhausted and want to escape. If you don't let go of your resentments and fears through some form of relaxation, they will build to the point where you'll feel uncomfortable in your own skin. If you don't ask for help, you'll feel isolated. If any of those situations continues for too long, you will begin to think about using. But if you practice self-care, you can avoid those feelings from growing and avoid relapse.
[h4]Mental Relapse & Techniques for handling it[/h4] In mental relapse there's a war going on in your mind. Part of you wants to use, but part of you doesn't. In the early phase of mental relapse you're just idly thinking about using. But in the later phase you're definitely thinking about using.
The signs of mental relapse are:
Thinking about people, places, and things you used with
Glamorizing your past use
Hanging out with old using friends
Fantasizing about using
Thinking about relapsing
Planning your relapse around other people's schedules
It gets harder to make the right choices as the pull of addiction gets stronger.
Techniques for Dealing with Mental Urges Play the tape through. When you think about using, the fantasy is that you'll be able to control your use this time. Using once usually leads to more than once. You'll wake up the next day feeling disappointed in yourself. You may not be able to stop the next day, and you'll get caught in the same vicious cycle. When you play that tape through to its logical conclusion, using doesn't seem so appealing.
A common mental urge is that you can get away with using, because no one will know if you relapse. Perhaps your spouse is away for the weekend, or you're away on a trip. That's when your addiction will try to convince you that you don't have a big problem, and that you're really doing your recovery for someone or something else. Play the tape through. Remind yourself of the negative consequences you've already suffered, and the potential consequences that lie around the corner if you relapse again. If you could control your use, you would have done it by now.
Tell someone that you're having urges to use. Call a friend, a support, or someone in recovery. Share with them what you're going through. The magic of sharing is that the minute you start to talk about what you're thinking and feeling, your urges begin to disappear. They don't seem quite as big and you don't feel as alone.
Distract yourself. When you think about using, do something to occupy yourself. Call a friend. Get up and go for a walk. Do anything to occupy yourself. If you just sit there with your urge and don't do anything, you're giving your mental relapse room to grow.
Wait for 30 minutes. Most urges usually last for less than 15 to 30 minutes. When you're in an urge, it feels like an eternity. But if you can keep yourself busy and do the things you're supposed to do, it'll quickly be gone.
Maintain your recovery one day at a time. Don't think about whether you can stay "clean" forever. That's a paralyzing thought. It's overwhelming even for people who've been in recovery for a long time.
One day at a time, means you should match your goals to your emotional strength. When you feel strong and you're motivated to not use, then tell yourself that you won't use for the next week or the next month. But when you're struggling and having lots of urges, and those times will happen often, tell yourself that you won't use for today or for the next 30 minutes.
Deal with recovery in bite-sized chunks and don't sabotage yourself by thinking too far ahead.
Make relaxation part of your recovery. Relaxation is an important part of relapse prevention, because when you're tense you tend to do what’s familiar and wrong, instead of what's new and right. When you're tense you tend to repeat the same mistakes you made before. When you're relaxed you are more open to change.
[h4] Physical Relapse[/h4]
Once you start thinking about relapse, if you don't use some of the techniques mentioned above, it doesn't take long to go from there to physical relapse. Going to the shop/store where you used to buy your alcohol. Going to your dealer.
It's hard to stop the process of relapse at that point. That's not where you should focus your efforts in recovery. That's achieving a substance free life through brute force. This is not recovery. If you recognize the early warning signs of relapse, and understand the symptoms of post-acute withdrawal, you'll be able to catch yourself before it's too late.
[h3]Recovery Skills and Coping Strategies[/h3]
[h4]The first rule of recovery[/h4] You don't recover from an addiction by stopping using. You recover by creating a new life where it is easier to not use. If you don't create a new life, then all the factors that brought you to your addiction will eventually catch up with you again.
You don't have to change everything in your life. But there are a few things and behaviors that have been getting you into trouble, and they will continue to get you into trouble until you let them go. The more you try to hold onto your old life in recovery, the less well you will do.
Here are the three most common things that people need to change in order to achieve recovery.
[h4] Avoid High Risk Situations[/h4]
Some common high-risk situations are described by the acronym, HALT:
Although this term is used by AA/NA it's a good rule of thumb for anyone wanting to succeed in recovery.
How do you feel at the end of the day? You're probably hungry because you haven't eaten well. You're probably angry because you've had a tough day at work or a tough commute home. You may feel lonely because you're isolated. You don't have to be physically alone to feel lonely. And you're tired. That's why your strongest cravings usually occur at the end of the day. Here's another way of looking at high-risk situations:
People. (People who you use with or who are related to your use. People who you have conflicts with, and who make you want to use. People who you celebrate with by using. People who encourage you to use either directly or indirectly.)
Places. (Places where you use or where you get your drugs or alcohol.)
Things. (Things that remind you of your using.)
How can you avoid high-risk situations? Of course, you can't always avoid these situations. But if you're aware of them, they won't catch you off guard, and you can prevent little craving from turning into major urges.
Take better care of yourself. Eat a healthier lunch so you're not as hungry at the end of the day. Join a support group so that you don't feel isolated. Learn how to relax so that you can let go of your anger and resentments. Develop better sleep habits so that you're less tired.
Avoid your drinking/using friends, your favorite bar, and having alcohol in the house. Avoid people who you used drugs with, your dealer's neighborhood, and drug paraphernalia.
Recovery isn't about one big change. It's about lots of little changes.
Avoiding those high-risk situations helps you create a new life where it's easier to not use.
Make a list of your high-risk situations. Addiction is sneaky. Sometimes you won't see your high-risk situations until you're right in the middle of one. That's why it's important that you learn to look for them. Make a list of your high-risk situations and to keep it with you. Go over the list with someone in recovery so that can spot any situations that you might have missed. Make the list and keep it with you. Some day that list may save your life.
[h4]Learn to Relax[/h4] There are only a few reasons why people use drugs and alcohol.
The first rule of recovery is that you must change your life. What do you need to change? If you understood the previous paragraph, then you need to change the way you relieve tension. Everyone needs to escape, relax, and reward themselves. Those are essential coping skills for a happy life. But addicts don't know how to do those things without using.
If you manage to stop using for a while, but don't learn how to relax, your tension will build until you'll have to relapse just to escape again. Tension and the inability to relax are the most common causes of relapse.
There is only one reason why people don't relax – because they think they're too busy to relax. It goes something like this, "I know it makes sense, but I've got so many other things I have to do."
Ask yourself how much time you were prepared spend on your addiction. If you add up all the time it takes to get your drug, use it, deal with its consequences, you'll realize that relaxing for twenty to forty minutes a day is a bargain.
They use to escape, relax, and reward themselves. In other words, people use drugs and alcohol to relieve tension.
[h4] Be Honest[/h4] Relaxation is not an optional part of recovery. It's essential to recovery. There are many ways to relax. They range from simple techniques like going for a walk, to more structured techniques like meditation. Meditation is an important part of that mix because the simple techniques don't always work. If you're under a lot of stress, you may need something more reliable like meditation. Use any of these techniques, or any combination. But do something everyday to relax, escape, reward yourself, and turn off the chatter in your mind.
An addiction requires lying. You have to lie about getting your drug, using it, hiding its consequences, and planning your next relapse. An addiction is full of lying. By the time you've developed an addiction, lying comes easily to you. After a while you get so good at lying that you end up lying to yourself.
The other problem with lying is that you can't like yourself when you lie. You can't look yourself in the mirror. Lying traps you in your addiction. The more you lie, the less you like yourself, which makes you want to escape, which leads to more using and more lying.
Nothing changes, if if you change nothing. Ask yourself this: will more lying, more isolating, and more of the same make you feel better? If you don't change your life, then why would this time be any different? You need to create a new life where it's easier to not use.
Recovery requires complete honesty. You must be completely honest with the people who are your supports: your family, your doctor, your therapist. If you can't be honest with them, you won't do well in recovery.
When you're completely honest you don't give your addiction room to hide. When you lie you leave the door open to relapse.
One mistake people make in the early stages of recovery is they think that honesty means being honest about other people. They think they should share what's "wrong" with other people. But recovery isn't about fixing other people. It's about fixing yourself. Stick with your own recovery. Focusing on what you don't like about others is easy because it deflects attention from yourself.
Honesty won't come naturally in the beginning. You've spent so much time learning how to lie that telling the truth, no matter how good it is for you, won't feel natural. You'll have to practice telling the truth quite a few times before it comes a little easier. In the beginning, you'll have to stop yourself as you're telling a story, and say, "now that I think about it, it was more like this..." One lie, however harmless is a foundation for more lies to be built upon.
Show common sense.Not everybody is your best friend. And not everybody will be glad to know that you have an addiction or that you're doing something about it. There may be some people who you don't want to tell about your recovery. But don't be reluctant to tell the people close to you about your recovery. You should never feel ashamed that you're doing something about your addiction.
[h3] The Chance to Change Your Life[/h3]Your addiction has given you the opportunity to change your life. Changing your life is what makes recovery both difficult and rewarding. Recovery is difficult because you have to change your life, and all change is difficult, even good change. Recovery is rewarding because you get the chance to change your life. Most people sleepwalk through life. They don't think about who they are or what they want to be, and then one day they wake up and wonder why they aren't happy.
If you use this opportunity for change, you'll look back and think of your addiction as one of the best things that ever happened to you. People in recovery often describe themselves as grateful addicts. Why would someone be grateful to have an addiction? Because their addiction helped them find an inner peace and tranquility that most people crave. Recovery can help you change your life.
Remember recovery is the beginning of your new life. But life does have it's ups and downs, it's not perfect, (it wasn't perfect before you became addicted) but it is possible to deal with any problem life throws at you, without using. And the sense of achievement you'll feel can't be imagined or explained. There will be times when you feel desperate, but there are also times when you will feel bliss beyond anything you could everany substance, or as a result of any addiction.
[h1]Supplements & other Medication for Withdrawal Symptoms and Revoery Aid[/h1]
experience, on "Is there any medication I can take to help me through withdrawal?"
This question is sometimes asked by people embarking on a benzodiazepine tapering program. In contrast, others are so against drugs when they decide on withdrawal that they are loth to take anything, even the simplest pain killer.
[h2]Aftercare - I'm clean, what now?[/h2] Change your Environment
Change your Life
This is something quite controversial. Some people swear by it, while other demonize it. You'll have to find out for yourself.
Swim would recommend you go to NA meetings. The people there all have been in your shoes before and can help by giving swim a support system - people who she can call 24 hours a day for advice. Plus they probably can give you leads on open-minded doctors who will prescribe the medication to you, however it is a lot less expensive getting it from India. Copy and print out the post to show the doctor why you need the medication and be honest.
Oh, Some at NA are anti-drugs (all drugs, except cigs), but many are not and are on medication from their doctors. That is what swim would do if she/he was you. Go today, look up Narcotics Anonymous, go to the meeting talk to other addicts and ask them for a doctor who believes in "dual diagnosis." In other words a Doctors who believes that one can treat addiction with other drugs. These recovering addicts will help you find a doctor that will prescribe you the medicine.
Drugs to avoid
[h2]Drugs/Medication that can support recovery[/h2]
However, there are some drugs which may help to control particular symptoms in withdrawal and which deserve consideration in certain situations though not recommended for routine use. Usually they will only be required temporarily, but they can sometimes ease a difficult situation and enable the user to proceed with the withdrawal program.
For all of these: If one thing sounds like it may help, do your research! Find out the suggested dosage, possible side effects, possible benefits. Don't rely only on this list, these are just hints.
[h3]Antidepressants[/h3] Antidepressants are among the most important adjuvant drugs to consider in withdrawal.(also see the DF section on Antidepressants).
A small introduction to the brain's chemistry:
A person’s sense of well-being is due to the action of key neurotransmitters working in a cascade fashion in the brain. The final site of action of these neurotransmitters is in the limbic system located near the center of the brain. The most important transmitters are serotonin (our natural antidepressant), enkephalins (along with endorphins, our natural pain killers), GABA (our natural sedative) and dopamine (along with norepinephrine, our natural stimulant) working in concert to bring about a feeling of well-being and stress reduction. Certainly we know the importance of increasing well-being and reducing stress in preventing relapse.
The nucleus accumbens, the “reward site,” in the brain is the master of simple but powerful drives. When all of the neurotransmitters, working in harmony and in conjunction with one another, stimulate the production, transportation, and reception of dopamine at the “reward site,” a person is calm, at ease and satisfied. This process of the neurotransmitters working in harmony and in conjunction with one another has been termed the “Brain Reward Cascade.” In the hypothalamus, serotonin stimulates the enkephalins, which in turn inhibits GABA in the substania nigra, which in turn fine tunes dopamine in the ventral tegmental area causing the release of dopamine at the nucleus accumbens.
So you target serotonin levels in order to prevent/correct dopamine depletion, for example high levels of serotonin, which occur when you take Ecstasy, make you feel happy, euphoric. When serotonin and noradrenaline are released from nerve cells in the brain they act to "lighten mood". When they are reabsorbed into the nerve cells, they no longer have an effect on mood. It is thought that when depression occurs, there may be a decreased amount of serotonin and noradrenaline released from nerve cells in the brain.
Hands down, of most drugs that give relief an AD is potentially the best, given that one finds an AD that (a) works well and (b) doesn't cause many side-effects. An AD can considerably lower problems with benzowithdrawal and even help with the sleep troubles if the right one is taken or two are taken together (e.g. one for the anxiety/depression, one for sleep).
As mentioned before, depression and anxiety can be a real problem in withdrawal and can sometimes be severe enough to pose a risk of suicide, though this is unusual with slow tapering. Like any other depression, the depression in withdrawal responds to antidepressant drugs and is probably caused by the same chemical changes in the brain. The "old fashioned" tricyclic antidepressants as well as tetracyclic (especially Mirtazapine) as well as "modern" SSRIs, SSNRIs, SNRIs or other special ADs can be effective and an antidepressant drug may be indicated if depression is severe.
If depression is severe during benzodiazepine withdrawal as in any other situation, it seems foolhardy to leave it untreated. ADs are also known to partly alleviate certain anxiety symptoms, lessen panic attacks, possibly calming one down, some even make a great sleep-aid. They may be started before the withdrawal, as they may have side effects that can take a few weeks till they disappear.
One of the other problems is that taking ADs is often like playing russian roulette. It is not exactly known how they work and while one works for a person, it may not work for someone else and they other way round. Its more of a tryout, hoping to get one that works. ADs affect different people differently. A doctor, or even better a psychiatrist may have the experience to see certain thing that point to possible advantages of one or the other, so professional help should be sough here. This should not be a problem, even without mentioning a withdrawal, as they prescribe 'em like candy.
There are, however, some more disadvantages with antidepressants. One is that they take 2-4 weeks or more to become really effective. TThe second drawback is that anxiety or depression may be temporarily worsened at the start of treatment either with tricyclics or SSRIs. This is a particular risk during benzodiazepine withdrawal when anxiety levels are usually high, thus ADs should be started before withdrawak. To avoid aggravation of anxiety, it is important to start with the lowest possible dose of an antidepressant and then work up slowly, over two or three weeks. Do not be persuaded by your doctor to start immediately on the "therapeutic" dose for depression. There are also fears that antidepressants such as Prozac may in some patients induce an agitated, violent or suicidal state at the start of treatment; low initial dosage and careful monitoring may avoid this risk.
It is usually possible to continue with slow benzodiazepine tapering while starting on an antidepressant, although some may prefer to halt their programme for 2-3 weeks until the antidepressant has "taken hold" (but increasing the benzodiazepine dose should be strenuously avoided). Antidepressants not only alleviate depression but also, after 2-3 weeks, have anti-anxiety effects. They are in fact a better long-term treatment than benzodiazepines for anxiety, panic and phobic disorders, and may in some cases actively help the benzodiazepine withdrawal process.
Once started on an antidepressant for depression, the treatment should be continued for some months (usually about 6 months or more) to avoid recurrence of the depression, also after the withdrawal of Benzos. Benzodiazepine tapering can continue during this time, and the antidepressant will sometimes act as a welcome umbrella during the last stages of withdrawal. It is important to finish the benzodiazepine withdrawal before starting to withdraw the antidepressant. Quite often, people taking long-term benzodiazepines are already taking an antidepressant as well. In this case they should stay on the antidepressant until the benzodiazepine withdrawal is complete.
Another drawback of antidepressants is that they, too, cause withdrawal reactions if they are stopped suddenly, a fact which has not always been appreciated by doctors. Antidepressant withdrawal symptoms include increased anxiety, sleep difficulties, influenza-like symptoms, gastrointestinal symptoms, irritability and tearfulness - not much different, in fact, from benzodiazepine withdrawal symptoms in theory, however, usually described as being a lot easier to handle if tapered down slowly and causing no craving at all. Many individuals do not even experiences withdrawal, while a few experiences very strong symptoms. Nevertheless, one can say that generally they are a lot easier to stop than Benzos. Reactions can be prevented by slow tapering of the antidepressant dosage over about 1-3 months . Most people who have withdrawn from benzodiazepines will be experts at tapering dosages when the time comes to stop the antidepressant and will be able to work out a rate of withdrawal that suits them.
Apart from their therapeutic effects in depression and anxiety, some antidepressants have a sedative effect which patients who are particularly plagued with insomnia have found helpful. Low doses (10-50mg) of amitriptyline or doxepin are remarkably effective in promoting sleep if taken at bed-time. These can be taken for short periods of a few weeks and stopped by reducing the dosage stepwise or taking the drug every other night. Withdrawal is not a problem when small doses are taken for short periods or intermittently. If sleep is really a problem, a small dose of a tricyclic antidepressant with sedative effects or Mirtazapine (see antidepressants, above) is a possible and effective option.
Personally, SWIM can recommend Citalopram as it seems to be, supported by studies and personal experience, the most potent and effective in comparison to its very low side effects profile. The cost/benefits calculation is pretty good (of course, some people react differently). This should suffice for dealing with depression and a big part of anxiety problems, in a dosage at 20 to 60mg. To avoid problems, start slow, SWIM'd recommend to go 1mg up each day (e.g. by scraping of parts of tablets and measuring by the eye.. doesn't have to be exact) and going up like this all the way to 20. Then wait for 2 more weeks (as 20 days already passed) and depending on the remission go up further or not. In case you experience sexual and/or too much sedative/fatigue effects (although citalopram is considered to be one of the more "activating" SSRIs, this may happen) consider adding Bupropion (e.g. 150mg and playing around from that point. start slowly again) or Venlafaxine.. Thats a pretty individual choice as both are known to cause anxiety and other problems in many people while others find them great. As an augmentation to citalopram a lower than usual dose suffices. Talk to your doctor.
[h3]Beta-blockers[/h3]In a few cases, severe palpitations, muscle tremors or motor jerks develop during benzodiazepine withdrawal and hinder progress. These symptoms can be controlled or ameliorated by beta-blocking drugs such as propranolol or metoprolol.
Drugs of this type inhibit the effects of excess epinephrine and norepinephrine (adrenaline and noradrenaline) released by an overactive sympathetic nervous system. They slow the heart and prevent excess muscle activity and also have a potentially calming effect on the body. Although they have little effect on psychological symptoms, they can cut the vicious circle in which palpitations or tremor create anxiety which leads to yet more palpitations. Some people in benzodiazepine withdrawal take small doses of these drugs (10-20mg Inderal three times daily) regularly, while others reserve them to take only if the physical symptoms of a panic attack seem uncontrollable. They are not a cure, but can sometimes help people through a difficult situation. In larger doses, beta-blockers are used for raised blood pressure and angina, but such doses are not advised in benzodiazepine withdrawal. They should not be taken by anyone who has asthma as they can cause constriction of the bronchial tubes. If beta-blockers have been used regularly for any length of time, they should be withdrawn slowly by tapering the dosage, as they too can cause a withdrawal reaction of increased heart rate and palpitations.
Questions regarding Beta-Blockers can be asked here: Various drugs not covered by other forums
If sleep is really a problem, apart from TCA antidepressents another option may work: Antihistamines. They regularly do send one into the land of dreams, however, they may be too weak in cases of severe insomnia due to withdrawal. They are well worth a try though, considering their relatively high safety and low abuse potential. Watch out for ODs though, as their may cause (unpleasant) hallucinations and other uncomfortable side effects.
Alternatively, an antihistamine with sedative effects (e.g. DPH, DHM, promethazine, Doxylamine) may be used. They generally do not cause physical addiction as far as SWIM is aware, at least not in the short term. Neither antidepressants nor antihistamines act by the same mechanisms as benzodiazepines. For further question on Antihistamines see Deleriant antihistamines.
They also have possible Anti-anxiety effects, but in high doses cause some nasty side effects so their main purpose is really only falling asleep. In case of acute withdrawal they may not be strong enough and only cause side effects and sedating ADs may be the better option or other drugs.
L-Theanine (gamma-ethylamino-L-glutamic acid) is an unique amino acid found in trace amounts in green tea. It converts in the brain into GABA, the neurochemical involved in inhibiting over active mental activities, such as stress, anxiety, worrying, and nervousness. Unlike herbs theanine protects & enhances Cognition, without causing sleepy or drowsiness.
- Instant relaxation due to its potent effects on raising GABA
- Unlike the supplement GABA it passes through the blood brain barrier readily and has superior GABA raising effects.
- Has been studied compared to Paxil.
-Able to cross the blood-brain barrier, theanine has psychoactive properties. Theanine has been shown to reduce mental and physical stress, and improves cognition and mood.
While structurally related to the excitatory neurotransmitter glutamate, theanine only has weak affinity for the glutamate receptor on post-synaptic cells. Rather, its primary effect seems to increase the overall level of the brain inhibitory transmitter GABA. Theanine also increases brain dopamine levels and has micromolar affinities for AMPA, Kainate and NMDA receptors. Its effect on serotonin is still a matter of debate in the scientific community, with studies showing increases and decreases in brain serotonin levels using similar experimental protocols. It has also been found that injecting spontaneously hypertensive mice with theanine significantly lowered levels of 5-hydroxyindoles in the brain. Researchers also speculate that it may inhibit glutamic acid excitotoxicity. Theanine also promotes alpha wave production in the brain.
-When can I feel it? Works within a few hours. Effects are relatively minor. Can be used as a sleep aid or as slight mood lifter.
- converted to glutamic acid, the brain's emergency source of
energy when glucose is in short supply.
- precursor to the neurotransmitter GABA
- neutralizes excess ammonia (which can inhibit proper
- improves intelligence
- helps to control alcoholism
- helps to speed ulcer healing
- alleviates fatigue, depression, impotence,
Inositol is a simple polyol precursor in a second messenger system important in the brain. Cerebrospinal fluid inositol has been reported as decreased in depression. A double-blind controlled trial of 12 g daily of inositol in 28 depressed patients for four weeks was performed. Significant overall benefit for inositol compared to placebo was found at week 4 on the Hamilton Depression Scale. No changes were noted in hematology, kidney or liver function. Since many antidepressants are effective in panic disorder, twenty-one patients with panic disorder with or without agoraphobia completed a double-blind, placebo-controlled, four week, random-assignment crossover treatment trial of inositol 12 g per day. Frequency and severity of panic attacks and severity of agoraphobia declined significantly with inositol compared to placebo. Side-effects were minimal. Since serotonin re-uptake inhibitors benefit obsessive compulsive disorder (OCD) and inositol is reported to reverse desensitization of serotonin receptors, thirteen patients with OCD completed a double-blind controlled crossover trial of 18 g inositol or placebo for six weeks each. Inositol significantly reduced scores of OCD symptoms compared with placebo[/b]. A controlled double-blind crossover [b]trial of 12 g daily of inositol for a month in twelve anergic schizophrenic patients, did not show any beneficial effects. A double-blind controlled crossover trial of 6 g of inositol daily vs. glucose for one month each was carried out in eleven Alzheimer patients, with on clearly significant therapeutic effects. Antidepressant drugs have been reported to improve attention deficit disorder (ADDH) with hyperactivity symptomatology. We studied oral inositol in children with ADDH in a double-blind, crossover, placebo-controlled manner. Eleven children, mean age 8.9 +/- 3.6 years were enrolled in an eight week trial of inositol or placebo at a dose of 200 mg/kg body weight. Results show a trend for aggravation of the syndrome with myo-inositol as compared to placebo. Recent studies suggest that serotonin re-uptake inhibitors are helpful in at least some symptoms of autism. However a controlled double-blind crossover trial of inositol 200 mg/kg per day showed no benefit in nine children with autism. Cholinergic agonists have been reported to ameliorate electroconvulsive therapy (ECT)-induced memory impairment. Inositol metabolism is involved in the second messenger system for several muscarinic cholinergic receptors. Inositol 6 g daily was given in a crossover-double-blind manner for five days before the fifth or sixth ECT to a series of twelve patients, without effect. These results suggest that inositol has therapeutic effects in the spectrum of illness responsive to serotonin selective re-uptake inhibitors, including depression, panic and OCD, and is not beneficial in schizophrenia, Alzheimer's ADDH, autism or ECT-induced cognitive impairment.
generally.. good diet and/or multivitamine.. bla
"All proteins in the body are made from amino acids. It is for this reason that amino acids are often referred to as the "building blocks" of proteins. Phenylalanine is one of the eight amino acids indispens-able (essential) in the diet of man. It comes in two forms, called "D" and "L." L (laevo, or left-handed) Phenylalanine is the form most commonly found in the high protein foods we eat, and is the form the body uses to make its own proteins. D -(dextro, or right-handed) Phenylalanine is a nearly identical molecule to the L form, but is an exact mirror image of it. D-Phenylalanine is found most abundantly in bacteria and plant tissue. The human body slowly converts D-Phenylalanine to L-Phenylalanine before it is utilized in known bodily functions."
DLPA has been around since the 70s but has recently been noticed. Many people use it for chronic pain and mood elevation but it can help with w/d symptoms too.
" DLPA taken orally in 375 mg. tablets, is a powerful analgesic. Its effect often equals or exceeds those of morphine or other opiate derivatives. It differs from the usual prescription drugs and over-the counter medicines in several critical ways:
* DLPA is non-addictive.
* DLPA's effects become stronger over time - patients do not de-velop tolerance to the pain-relieving effect.
* No adverse side effects, mental or physical, are associated with DLPA's use.
* Toxic overdose is impossible, and there is generally a lack of potential for abuse.
* DLPA can be combined with any other existing therapy - drugs, aspirin, acupuncture, chiropractic, etc., without adverse interac-tions, and often with benefits greater than could be obtained from either therapy alone.
* DLPA also has a strong antidepressant action - extremely important in the common instance where the sufferer of chronic pain is also a victim of depression.
* Perhaps most amazingly, the pain relief produced by DLPA can last far beyond the period in which it is taken. Some patients have reported that, following a week of DLPA use, pain relief continues for up to a month without additional medication of any kind. Pain control using DLPA can be very economical.
[h3]Nootropics[/h3] Nootropics, also referred to as smart drugs, memory enhancers, and cognitive enhancers, are drugs, supplements, nutraceuticals, and functional foods that are purported to improve mental functions such as cognition, memory, intelligence, motivation, attention, and concentration. Nootropics are thought to work by altering the availability of the brain's supply of neurochemicals (neurotransmitters, enzymes, and hormones) by improving the brain's oxygen supply or by stimulating nerve growth. However the efficacy of nootropic substances in most cases has not been conclusively determined. This is complicated by the difficulty of defining and quantifying cognition and intelligence.
For more Information See wikipedia and Nootropics <- the DF section on Nootropics.
WHAT IS TAURINE?
Taurine is an amino acid which plays a major role in the brain as an "inhibitory" neurotransmitter & neuromodulator. It is similiar in structure to the amino acids GABA & L-Glycine, which are also neuroinhibitory. This means it helps to calm or stabilize an excited brain.
Taurine stabilizes nerve cell membranes thus depressing the firing of brain cells & dampening the nerve cell action of the excitatory amino acids, glutamate, aspartate, & quinolinate.
Taurine acts by regulating the sodium & potassium concentration in the cells & the magnesium level between the cells. This has everything to do with the electrical activity of the cells & subsequent communication between cells.
By this mechanism, it has anti-anxiety & anti-convulsant activity. It has also been found useful in some cases of migraine, insomnia, agitation, restlessness, irritability, alcoholism, obsessions, depression, hypomania/mania.
Dosage is from 500 mg twice daily to a total of 5000 mg daily in 3-4 divided doses, though I rarely recommend that high a dose. The total ideal body pool of taurine for adults is 12,000- 18,000 mg.
Since taurine also affects the hypothalamus to help regulate body temperature, a higher dose can decrease your temperature & give chilliness, so be aware of that.
Taurine also plays a role in memory & increases the level of a memory neurotransmitter, acetylcholine, in the brain (in animal studies).
HOW DO YOU GET TAURINE?
Taurine is highly concentrated in animal & fish protein or organ meats. Strict vegetarians can be at risk for taurine deficiency. Your body can make taurine in the liver & brain from the amino acids, L-Cysteine, & L-Methionine. Three enzymes are involved in the conversion, all requiring the pyridoxal-5-phosphate form of Vitamin B6 for this conversion. A B6 deficiency can thus cause a taurine deficiency.
Some studies suggest humans are dependent upon dietary taurine to maintain "adequate" taurine reserves. Females tend toward lower taurine levels than males as their production pathways don't work as efficiently.
Taurine is closely bound to zinc & manganese so deficiencies of either of these can interfere with its' utilization. Likewise, zinc & manganese enhance the effects of taurine.
Taurine is the amino acid present in highest concentration of all amino acids in the fetal & newborn brain, which is the most dependent upon taurine & the least able to synthesize it.. The developing infant must derive taurine from the placenta, the newborn, from breast milk or taurine fortified formula. It is low in cow's milk. Taurine is essential for proper development of the central nervous system & the eyes. Nursing mothers especially need taurine as it stimulates prolactin to promote lactation, which is an interesting twist of nature, since infants need it so much. ( We could speculate that a mother unable to lactate may be taurine deficient, among other possibilites, & the infant is thus protected from receiving taurine deficient breast milk) Premature infants are especially prone to taurine deficiency.
WHAT ELSE INFLUENCES TAURINE LEVELS?
MSG can decrease taurine. Trauma, surgery, radiation therapy, burns, muscle diseases, steroid use, intestinal dysfunction with bacterial overgrowth of the small bowel can all lead to excess loss of taurine in the urine & subsequent deficiency.
The medications Thorazine (a major tranquilizer) & Chloroquine (an antimalarial) can reduce taurine levels. Some depressed patients have decreased taurine.
WHAT ELSE DOES TAURINE DO?
EYES: It is in high concentration in the eyes where it has multiple functions to maintain normal retinal structure & function. Depletion leads to degeneration of the photoreceptor cells. Degenerative changes in the retinas of taurine deficient cats & dogs resemble retinitis pigmentosa. Taurine may be helpful in preventing cataracts. Age related macular degeneration has responded favorably to "injected" taurine as reported by American Biologics Mexico Hospital.
CARDIOVASCULAR: Taurine is the most abundant amino acid in the heart, a particularly electrically excitable tissue, as are the brain & eye. Since taurine participates in electrical stabilization of the cell membranes & the normal regulation of nerve-muscle interaction, it is useful in heart irregularities & mitral valve prolapse, acting similarly to a calcium channel blocker (a class of drugs used in CV Disease) Taurine also helps control high blood pressure & is useful in congestive heart failure.
DIABETES: Taurine affects carbohydrate metabolism. It potentiates the effect of insulin, enhances glucose utilization & glycogen (stored glucose) synthesis.
FAT METABOLISM: Taurine reduces cholesterol by forming bile acids which are the end products of cholesterol breakdown & are the only route for eliminating cholesterol from the body. This action requires a functioning gall bladder. Taurine has an inhibitory effect on the formation of cholesterol gall stones. It is required for efficient fat absorption & solubilization. It is helpful in states of fat malabsorption such as with cystic fibrosis & other pancreatic deficiency syndromes.
DETOXIFICATION: Taurine conjugates & detoxifies various internal & external toxic compounds & may help chemical sensitivities.
ANTIOXIDANT: Taurine plays a major role in protecting cell membranes from oxidative attack.
STRESS: It can inhibit the release of adrenalin & thus help with anxiety in this way, as well as protecting from other adverse effects of too much adrenalin.
MISC: Acts as an immune stimulant to increase Natural Killer Cell Activity & Interleukin 2. Controls cell volume & osmolality. Is involved in the regulation of iron metabolism. Modulates levels of serum copper.
TAURINE CAN ALSO STIMULATE RELEASE OF STOMACH ACID SO YOU SHOULD AVOID IF YOU HAVE ULCERS OR GASTRITIS.
see nootropics section
[h3]SAMe or L-Methionine[/h3]
Helps liver detox metabolites of methadone…Detoxing agents can be found in many products…most in combinations…
[h3]Milk Thistle with alpha-Lipoic Acid[/h3]
is one combination that I use extensively---for liver repair and detoxification…1200 to 1500 mg of milk thistle and 400 mg of lipoic acid per day in split doses
This is the basics. There is absolutely no way to eliminate all the problems associated with withdrawal from methadone...one must have a supportive environment and often with daily visits from a compassionate health care provider…This will not kill you…it will be a miserable event…what kills most is the movement back to street drugs to ward off the side effects of withdrawal. If fact, cold turkey deaths coming off opioids and methadone are rare and usually associated with other health problems, or overdosing on prescription medications…withdrawal from methadone is much less of a risk than total withdrawal from alcohol. I wish you all luck on this endeavor…My compassion and empathy goes out to you…Ultimately, I know that you can do this…after all…it has to be done.
[h2] Iboga/Ibogaine - I Began Again[/h2]
Slow Withdrawing prior to Ibogaine/Iboga treatment is a must! Do not take it after coming off Benzos Cold Turkey! Never get off Benzos Cold Turkey! You can DIE if you go Cold Turkey and then take Iboga(ine)!!!!!!!! Also see the Medical Disclaimer at the end of this post.
Valerian Root has been used as a sleep aid for over 1,000 years. It's ability to help relax the central nervous system, promote feelings of calm, decrease levels of anxiety and stress, and enhance sleep are known to millions the world over. Valerian is not known to cause morning grogginess and is non-addictive.
You can help your body and mind relax by taking Valerian Root which aids relaxation and promotes sleep.
It is a mild antidepressant, with very low side-effects and works well for mild depression. However, it is important to use & find a good product (for suggestions see the FAQ) as the potency varies a lot
A brief introduction:
St. John's wort has recently come to popular attention primarily because of its scientifically documented antidepressant action.
As a result, many of the less scrupulous herb distributors have started marketing St. John's wort as "nature's Prozac" or even "nutritional support for depression". While St. John's wort does indeed appear effective in the treatment of certain cases of depression, the real situation is considerably more complex. It's not at all clear whether St. John's wort works in the same manner as Prozac, if it works more like dopamine stimulating agents such as bupropion (marketed as Wellbutrin in the U.S.), if it is more similar in action to tricyclic or other heterocyclic antidepressants or if a brand new mechanism of action is present.
The most striking thing about St. John's wort is the fact that sexual dysfunction from St. John's wort has never been reported in the scientific literature. It is commonly used for: Psychogenic disturbances, depressive states, sleep disorders, anxiety and/or nervous excitement, particularly those associated with menopause.
Oily Hypericum preparations are approved for stomach and gastrointestinal complaints and have anti-diarrheal activity.
Rhodiola is a well known and commonly used adaptogen, effective as a mild antidepressent, antioxidant, anxiety and stress relief. It can be taken alongside "real" antidepressants.
his is a perennial plant with red, pink, or yellowish flowers. One of the greatest things Rhodiola does is enhance mental and physical performance. It has been widely used by Russian athletes to increase energy. Rhodiola is cardio-protective, normalizing the heart rate immediately after intense exercise. It improves nervous system and mental functions such as memory by increasing blood-supply to the muscles and brain, and also increases protein synthesis (1,2,3). Rhodiola Rosea has extraordinary pharmacological properties as an anti-mutagen and anti-depressive agent. In this respect Rhodiola Rosea is much more powerful than other adaptogens. In one study done by O.M. Duhan and colleagues, the anti-mutagenic activity of Panax Ginseng and of Rhodiola Rosea was compared (4). It appeared that the extracts of Rhodiola Rosea have a higher capacity to counteract gene mutations induced by various mutagens (up to about 90 percent inhibition in some cases). The anti-depressive and anti-stress activity of Golden Root is higher than that of St. John's Wort, Ginkgo biloba and Panax Ginseng. In one clinical trial, 150 individuals who suffered from depression took Rhodiola Rosea extracts for one month. At the end of that period, two-thirds of them had full remission of clinical manifestations of depression, and had become more active and more sociable.Daytime weakness and general weakness disappeared. Furthermore, Rhodiola rosea is four times less toxic than Panax ginseng. The main active components that are responsible for the extraordinary potency of Rhodiola Rosea are rosavin, salidroside, rosin, and rosarin. Quality Rhodiola Rosea extract should contain at least 2 percent rosavin and 0.8 percent salidroside.
Rhodiola rosea is a popular plant in traditional medical systems in Eastern Europe and Asia with a reputation for stimulating the nervous system, decreasing depression, enhancing work performance, eliminating fatigue, and preventing high altitude sickness. Rhodiola rosea has been categorized as an adaptogen by Russian researchers due to its observed ability to increase resistance to a variety of chemical, biological, and physical stressors. Its claimed benefits include antidepressant, anticancer, cardioprotective, and central nervous system enhancement. Research also indicates great utility in asthenic conditions (decline in work performance, sleep difficulties, poor appetite, irritability, hypertension, headaches, and fatigue) developing subsequent to intense physical or intellectual strain. The adaptogenic, cardiopulmonary protective, and central nervous system activities of Rhodiola rosea have been attributed primarily to its ability to influence levels and activity of monoamines and opioid peptides such as beta-endorphins.
(Altern Med Rev 2001;6(3):293-302)
Rhodiola rosea ("golden root" or "Arctic root") is widely distributed at high altitudes in Arctic and mountainous regions throughout Europe and Asia. It is a popular plant in traditional medical systems in Eastern Europe and Asia, with a reputation for stimulating the nervous system, decreasing depression, enhancing work performance, eliminating fatigue, and preventing high altitude sickness.1 In addition to Rhodiola rosea, over 200 different species of Rhodiola have been identified and at least 20 are used in traditional medical systems in Asia, including R. alterna, R. brevipetiolata, R. crenulata, R. kirilowii, R. quadrifida, R. sachalinensis, and R. sacra.
Rhodiola rosea has been intensively studied in Russia and Scandinavia for more than 35 years. Although the majority of this research on Rhodiola rosea is unavailable for review, available literature is supportive of its adaptogenic properties. Similar to other plant adaptogens investigated by Russian researchers, such as Eleutherococcus senticosus (Siberian ginseng) and Panax ginseng (Korean ginseng), extracts of this plant produce favorable changes in a variety of diverse areas of physiological function, including neurotransmitter levels, central nervous system activity, and cardiovascular function.
Rhodiola rosea has been categorized as an adaptogen by Russian researchers due to its observed ability to increase resistance to a variety of chemical, biological, and physical stressors. Origination of the term adaptogen has been dated to 1947 and credited to a Russian scientist, Lazarev. He defined an "adaptogen" as an agent that allows an organism to counteract adverse physical, chemical, or biological stressors by generating non-specific resistance. Inherent in his definition is the concept that administration of the adaptogenic agent allows an organism to pre-adapt itself in a manner that allows it to be more capable of responding appropriately when diverse demands are eventually placed on it. In 1969, Brekhman and Dardymov proposed specific criteria that need to be fulfilled in order for a substance to qualify as an adaptogen.
Subjecting animals and humans to a period of stress produces characteristic changes in several hormones and parameters associated with the central nervous system and the hypothalamic-pituitary-adrenal axis (HPA). HPA changes include an increase in cortisol, a reduced sensitivity of the HPA to feedback down-regulation, and a disruption in the circadian rhythm of cortisol secretion. Central nervous system changes include the stress-induced depletion of catecholamine neurotransmitters such as norepinephrine and dopamine. An acute increase in beta-endorphin levels is also observed under stressful conditions.
To successfully combat stress and stressful situations, adaptation is required. Adaptation might be best thought of as the ability to be exposed to a stressor, while responding with either decreased or no characteristic hormonal perturbations. Adaptation also implies being prepared to and capable of rapidly reassuming homeostasis after the stressor is withdrawn. As an example, a well-trained athlete can participate in an event that would induce a large HPA perturbation (stress response) in a sedentary person, and yet the athlete will be relatively unaffected. This is a result of adaptation that has occurred during the athlete's training process. Additionally, if athletes are exposed to stressors they were not trained for, hormonal perturbations characteristic of a stress response would be expected; however, this response might not be as great as that found in less fit individuals. Furthermore, after the stress ended, their physiology would be expected to re-establish homeostasis rapidly. This is a result of non-specific resistance to stress gained by virtue of a training-induced higher level of fitness.
The utility of plant adaptogens is analogous to the training an athlete undergoes in order to prepare for competition. Plant adaptogens cause our physiology to begin the adaptation process to stress. When a stressful situation occurs, consuming adaptogens generates a degree of generalized adaptation (or non-specific resistance) that allows our physiology to handle the stressful situation in a more resourceful manner.
As an example of this process, Rhodiola rosea administration promotes a moderate increase in the amount of serum immunoreactive beta-endorphin in rats under basal conditions. This moderate increase is similar to that found when rats are adapted to exercise. When Rhodiola rosea-treated rats were subjected to a 4-hour period of non-specific stress, the expected elevation in beta-endorphin was either not observed or substantially decreased. Consequently, the characteristic perturbations of the HPA were decreased or totally prevented.3 In these rats administration of Rhodiola rosea appears to have generated non-specific resistance and prepared the rats to respond more appropriately to the eventual stressful situation.
The chemical composition and physiological properties of Rhodiola species are to a degree species-dependent, although some overlap in constituents and physiological properties does exist in many Rhodiola species.
Twenty-eight compounds have been isolated from the roots and above-ground parts of Rhodiola rosea, including 12 novel compounds. The roots contain a range of biologically active substances including organic acids, flavonoids, tannins, and phenolic glycosides. The stimulating and adaptogenic properties of Rhodiola rosea were originally attributed to two compounds isolated from its roots, identified as p-tyrosol and the phenolic glycoside rhodioloside. Rhodioloside was later determined to be structurally similar to the known glycoside salidroside found in several other plant species. Salidroside, rhodioloside, and occasionally rhodosin are used to describe this compound and are considered to be synonyms. Additional glycoside compounds isolated from the root include rhodioniside, rhodiolin, rosin, rosavin, rosarin, and rosiridin. These glycoside compounds are also thought to be critical for the plant's observed adaptogenic properties.1,4
A range of antioxidant compounds have been identified in Rhodiola rosea and related species, including p-tyrosol, organic acids (gallic acid, caffeic acid, and chlorogenic acid), and flavonoids (catechins and proanthocyanidins).5,6 Significant free-radical scavenging activity has been demonstrated for alcohol and water extracts of Rhodiola sp. and is attributed to the variety of antioxidant compounds.5,6 p-Tyrosol has been shown to be readily and dose-dependently absorbed after an oral dose,7,8 and appears to produce a significant antioxidant8 and modest 5-lipoxygenase inhibitory activity9 in vivo.
Salidroside (rhodioloside), the additional salidroside-like glycoside compounds (rhodiolin, rosin, rosavin, rosarin, and rosiridin), and p-tyrosol are thought to be the most critical plant constituents needed for therapeutic activity.1,2 The contents of salidroside and p-tyrosol in root samples gathered from various areas in China have been shown to range from 1.3-11.1 mg/g and 0.3-2.2 mg/g, respectively.4 These two compounds have been found in all studied species of Rhodiola; however, the other active glycosides, including rosavin, rosin, and rosarin, have not been found in all examined Rhodiola species.5,6 Because of this variation within the Rhodiola genus, verification of Rhodiola rosea by high performance liquid chromatography (HPLC) is dependent on the content of the additional glycosides (rather than salidroside and p-tyrosol); rosavin is the constituent currently selected for standardization of extracts.10
The adaptogenic properties, cardio-pulmonary protective effects, and central nervous system activities of Rhodiola rosea have been attributed primarily to its ability to influence levels and activity of monoamines and opioid peptides such as beta-endorphins. Oral administration of a water extract of Rhodiola rosea to rats for 10 days modulated biogenic monoamines in the cerebral cortex, brain stem, and hypothalamus. In the cerebral cortex and brain stem, levels of nor-epinephrine and dopamine decreased, while the amount of serotonin increased substantially. In the hypothalamus, the results were reversed with a 3-fold increase in the amount of norepinephrine and dopamine, and a trend toward reduced serotonin levels. It is believed these changes in monoamine levels are a result of Rhodiola rosea inhibiting the activity of the enzymes responsible for monoamine degradation, monoamine oxidase and catechol-O-methyltransferase. It is also believed Rhodiola rosea facilitates the transport of neurotransmitters within the brain.11 In addition to these central effects on monoamines, Rhodiola rosea has been reported to prevent both catecholamine release and subsequent cAMP elevation in the myocardium, and the depletion of adrenal catecholamines induced by acute stress.12
Abstracts of untranslated Russian research indicate that a great deal of the activity of Rhodiola rosea might be secondary to an ability to induce opioid peptide biosynthesis and through the activation of both central and peripheral opioid receptors.3,13-15 Lack of current availability of the complete text of these articles make verification of these effects impossible.
Rhodiola rosea appears to offer generalized resistance against physical, chemical, and biological stressors in rats and other animals studied. Evidence also suggests cardioprotective and anticancer benefits in animals.
In the test of swimming "to the limit," Rhodiola rosea administration increased the swimming time of rats 135-159 percent. Working capacity of the rats consistently improved throughout the supplementation period.16
Eggs from the freshwater snail Lymnaea stagnalis were incubated in water extracts of Rhodiola rosea and subsequently exposed to a variety of environmental stressors, including heat shock (43Â°C for four minutes), oxidative stress (600 ÂµM menadione for two hours), and heavy metal-induced stress (one-hour exposure to 150 ÂµM copper sulphate or 20 ÂµM cadmium chloride). Exposure to these environmental stressors kills 80-90 percent of larvae within four days post-exposure. Pre-incubation with Rhodiola rosea extract afforded a significant degree of non-specific resistance against each of these environmental stressors as measured by rate of survival. While only nine percent of the control population survived exposure to heat shock, approximately 90 percent of snail larvae pre-incubated with Rhodiola rosea (40.5 Âµg/ml) survived. Pre-incubation with Rhodiola resulted in non-specific resistance to oxidative stress (survival of approximately 68 percent) and heavy metal stress (approximately 28-35 percent of larvae survived depending on the metal exposure).10
Two experiments have suggested possible benefit on various aspects of learning and memory in rats under certain experimental conditions. Rhodiola rosea extract administered orally at a dose of 0.1 mL/day for 10 days resulted in a non-significant trend toward protection against impairments in memory, as assessed by step-down passive avoidance, induced by electroshock in rats.17 Rhodiola rosea extract was administered in a single dose of 0.10 mL. Improvements in both learning and memory retention, as determined by using a maze test with negative reinforcement, were observed. Repeated dosing with the same quantity of the extract over a 10-day period generated significant improvement in long-term memory as assessed by the maze test with negative enforcement and the "staircase" method with positive enforcement. However, in this experiment two other doses were tested (0.02 and 1.0 mL) and were found to have no substantial effect on learning and memory.1
This suggests the possibility of an efficacious dose of Rhodiola rosea administration, above and below which beneficial physiological effects might be less likely. In the other experimental conditions investigated (active avoidance with negative reinforcement using a "shuttle box" and passive avoidance using "step down" and "step through") no beneficial effects on either learning or memory were observed with any of the administered doses of Rhodiola rosea.1
Rhodiola rosea has been shown to moderate against stress-induced damage and dysfunction in cardiovascular tissue. Treatment with Rhodiola rosea extract prevents the decrease in cardiac contractile force secondary to environmental stress in the form of acute cooling and contributes to stable contractility. In animals, acute cooling leads to a decrease in myocardial contractile activity that partially recovers during the first 18 hours after the cold-stress is removed. This recovery is viewed as only partial, since the heart tissue is incapable of stable contractility during perfusion. Pretreatment with Rhodiola rosea extracts appears to create a beneficial adaptive response in this type of stress. When Rhodiola pretreated rats were exposed to acute cooling, the decrease in contractility was prevented and stable contractility of heart tissue occurred during perfusion.18
Other reports suggest administration of Rhodiola rosea protects cardiovascular tissue from stress-induced catecholamine release12 and mitigates against adrenaline-induced arrhythmias in rats.13,14,19 The antiarrhythmic effect of Rhodiola rosea is suggested to be secondary to an ability to induce opioid peptide biosynthesis13 and related to the stimulation of peripheral kappa-opioid receptors.14
Administration of Rhodiola rosea appears to have potential as an anticancer agent, and might be useful in conjunction with some pharmaceutical antitumor agents. In rats with transplanted solid Ehrlich adenocarcinoma and metastasizing rat Pliss lymphosarcoma, supplementation with Rhodiola rosea extract inhibited the growth of both tumor types, decreased metastasis to the liver, and extended survival times.20 Administration of Rhodiola rosea extract also directly suppressed the growth of and the extent of metastasis from transplanted Lewis lung carcinomas.21 When Rhodiola rosea extract was combined with the antitumor agent cyclophosphamide in these same tumor models, the antitumor and antimetastatic efficacy of drug treatment was enhanced. The authors also commented that, "complete abrogation of the haematotoxicity of cyclophosphamide" was observed.21 The chemotherapeutic drug Adriamycin is known to induce pronounced liver dysfunction, generally reflected by an increase in transaminase levels. In animal experiments, adding Rhodiola rosea extract to a protocol with Adriamycin resulted in an improved inhibition of tumor dissemination (as compared to that found with Adriamycin alone), and the combined protocol prevented liver toxicity.22
Although Rhodiola rosea has been studied in the former Soviet Union for more than 35 years, this research is presently unavailable for review. This makes it impossible to verify the Russian claims of its antidepressant, anticancer, cardioprotective, and central nervous system enhancing properties.23 Available animal evidence seems supportive of a possible role for this plant adaptogen in many of these conditions. Table 2 outlines the conditions suggested to benefit from Rhodiola supplementation.
colds and flu
sexual dysfunction (male)
There have also been claims that this plant has great utility as a therapy in asthenic conditions (decline in work performance, sleep disturbances, poor appetite, irritability, hypertension, headaches, and fatigue) developing subsequent to intense physical or intellectual strain, influenza and other viral exposures, and other illness. 23 Two randomized, double-blind, placebo-controlled trials of the standardized extract of Rhodiola rosea root (SHR-5) provide a degree of support for these claimed adaptogenic properties and indicate possible utility in asthenic conditions induced by overwork or over study. SHR-5 is standardized to contain rosavin (3.6%), salidroside (1.6%), and p-tyrosol 0.1%).10
Darbinyan et al evaluated the effect of chronic administration of 170 mg of SHR-5 for 14 days on aspects of mental performance and fatigue on 56 healthy male and female physicians (age 24-35) on night duty. Mental performance was evaluated using tests to determine speed of visual and auditory perception, attention capacity, and short-term memory. Based on the results of the battery of tests used, a Fatigue Index was calculated. The trial was divided into three periods: (1) a two-week test period of one SHR-5 or placebo tablet daily; (2) a two-week washout period; and (3) a third two-week cross-over period of one placebo or SHR-5 tablet daily. A statistically significant improvement in Fatigue Index was observed during the first two-week period in the SHR-5 group, and the improved mental performance reverted toward baseline values during the washout period. Administration of SHR-5 for the final two weeks of the six-week night duty period was unable to significantly offset declines in mental performance.24
Spasov et al investigated the effects of SHR-5 on male medical students during an exam period. Forty students were randomized to receive either 50 mg SHR-5 or placebo twice daily for a period of 20 days. The students receiving the standardized extract of Rhodiola rosea demonstrated significant improvements in physical fitness, psychomotor function, mental performance, and general wellbeing. Subjects receiving the Rhodiola rosea extract also reported statistically significant reductions in mental fatigue, improved sleep patterns, a reduced need for sleep, greater mood stability, and a greater motivation to study. The average exam scores between students receiving the Rhodiola rosea extract and placebo were 3.47 and 3.20, respectively. 25
In the two double-blind clinical trials, the dose of a standardized Rhodiola rosea extract ranged from 100-170 mg per day. The content of rosavin consumed in these daily doses is approximately 3.6-6.14 mg. The therapeutic dose of available Rhodiola rosea preparations will vary depending on degree of standardization; however, for chronic administration rosavin content within the above range seems prudent. This would suggest a dose of approximately 360-600 mg Rhodiola rosea daily of an extract standardized for one-percent rosavin, 180-300 mg of an extract standardized for two-percent rosavin, or the dose of between 100-170 mg for an extract standardized for 3.6-percent rosavin. As an adaptogen, chronic administration is normally begun several weeks prior to a period of expected increased physiological, chemical, or biological strain, and continued throughout the duration of the challenging event or activity. When using Rhodiola rosea as a single dose for acute purposes (e.g., for an exam or athletic competition), the suggested dose is three times the dose used for chronic supplementation.
The Russian approach to long-term supplementation with adaptogens generally calls for repeating cycles characterized by short periods of adaptogen administration, followed by an interval with no supplementation.26 Rhodiola rosea has been administered for periods ranging from as little as one day (acute administration) up to four months. Until more specific information is available, a dosing regime following the established patterns used with other plant adaptogens, with periodic intervals of abstinence, seems warranted when Rhodiola rosea is being used chronically.
At the doses administered in the clinical trials, a complete absence of all side effects has been reported. However, preliminary clinical feedback indicates that at doses of 1.5-2.0 grams and above of Rhodiola rosea extract standardized for two-percent rosavin, some individuals might experience an increase in irritability and insomnia within several days. It is possible that other physiological parameters that benefit from a lower dose of Rhodiola rosea extract might be exacerbated by a dose that is inappropriately high and/or sustained for prolonged periods of time.
Evidence on the safety and appropriateness of Rhodiola rosea supplementation during pregnancy and lactation is currently unavailable.
Consistent with benefits found with other adaptogenic substances, Rhodiola rosea appears to offer generalized resistance to physical, chemical, and biological stressors. Available evidence suggests it can be a suitable substitute in conditions where other adaptogens might be considered. However, Rhodiola rosea also appears to be unique among the currently available adaptogenic herbs and might offer an advantage in some clinical conditions and stressful circumstances. Unlike Korean and Siberian ginseng, which are thought to exert their adaptogenic activity primarily at the level of HPA function,27-29 Rhodiola rosea appears to exert its adaptogenic effects by working centrally and peripherally on monoamine and opioid synthesis, transport, and receptor activity. If this is in fact the case in humans, it suggests the potential for therapeutic utility of Rhodiola rosea in conditions not particularly responsive to administration of ginseng products. It also suggests the possibility of potential synergistic interactions among Rhodiola rosea and other plant adaptogens.
Based on the proposed mechanism of action and available experimental data, Rhodiola rosea appears to offer an advantage over other adaptogens in circumstances of acute stress. A single dose of Rhodiola rosea prior to acute stress produces favorable results and prevents stress-induced disruptions in function and performance. Acute stress tends to initially impact monoamine levels and endorphins, while chronic stress places greater demands on the HPA axis. While this is a generalization and there is obvious overlap in the stress response, Rhodiola does seem to exert a pronounced effect on aspects of the acute stress response. Since many stressful situations are acute in nature, and sometimes unexpected, an adaptogen that can be taken acutely in these circumstances, rather than requiring chronic advance supplementation, could be very useful.
Rhodiola rosea also offers some cardioprotective benefits not associated with other adaptogens. Its proposed ability to moderate stress-induced damage and dysfunction in cardiovascular tissue might make Rhodiola rosea the adaptogen of choice among patients at higher risk for cardiovascular disease.
Since Rhodiola rosea administration appears to impact central monoamine levels, it might also provide benefits and be the adaptogen of choice in clinical conditions characterized by an imbalance of central nervous system monoamines. This is consistent with Russian claims for improvements in depression and schizophrenia. It also suggests that research in areas such as seasonal affective disorder, fibromyalgia, and chronic fatigue syndrome, to name a few clinical conditions, is warranted.
Administration of Rhodiola rosea appears to have potential as an anticancer agent, and might be useful in conjunction with some pharmaceutical antitumor agents. While available evidence is limited to animal models, results appear promising. This is an area that would benefit from additional research.
The clearest indication for Rhodiola rosea administration is for the asthenic condition resulting from acute or chronic overwork, which may manifest as decline in work performance, sleep disturbances, poor appetite, irritability, hypertension, headaches, and fatigue.
Some animal and preliminary clinical evidence suggests the need for a narrow range of therapeutic dosage of Rhodiola rosea, above and below which beneficial physiological effects might be less likely. Because of this, it seems prudent to keep doses at a moderate level both in terms of the quantity and duration of supplementation. While Rhodiola rosea appears to be a promising plant medicine, and has been investigated intensively in Russia, additional research is required before any conclusions with respect to its therapeutic utility can be made.
Latin name: Piper methysticum
A Remedy For
In the past, Kava Kava has been taken for a host of ailments on which it has no appreciable effect, including asthma, arthritis, indigestion, cystitis, syphilis, and gonorrhea. For tension and sleeplessness, however, it is now considered a proven remedy.
What It Is; Why It Works
One of the "new" herbs that have recently gained considerable media attention, Kava Kava has actually been around for centuries in the South Seas, where it's used as a ceremonial beverage. The plant's fleshy underground stem is mildly intoxicating when chewed. Prepared as a nonalcoholic drink, it is said to foster a sense of contentment and well-being, while sharpening the mind, memory, and senses.
Research shows that the active ingredients in Kava Kava (kava pyrones) do in fact have a calming, sedative effect. They also appear to relax the muscles, relieve spasms, and prevent convulsions. At least two scientific studies have confirmed the herb's ability to significantly reduce symptoms of anxiety. In a third study, researchers rated it as effective as prescription tranquilizers.
Do not use Kava Kava if you are pregnant or nursing. Also avoid it if you have a depressive disorder; it can deepen a depressed mood.
When first taking Kava Kava, you may notice a slightly tired feeling in the mornings.
In rare cases, Kava Kava can cause an allergic reaction, a slight yellowing of the skin, gastrointestinal complaints, impaired or abnormal movement, loss of balance, pupil dilation, and difficulty focusing. Because of the possibility of visual disturbances, drive with caution while using this herb.
High doses of the herb have been known to trigger hepatitis. Heavy long-term use can also cause an unusual scaly rash, and may lead to unwanted weight loss. Do not take this herb for more than 3 months without consulting a physician.
Possible Drug Interactions
Do not take Kava Kava when using other substances that act on the brain, such as alcohol, barbiturates, or other mood-altering drugs. It may increase their effect. Be especially wary of taking it with the tranquilizer Xanax; the combination has caused coma.
Kava Kava also has an antagonistic effect on dopamine. If you are taking a levodopa-based medication for Parkinson's disease, avoid this herb.
Special Information If You Are Pregnant or Breastfeeding
Remember, Kava Kava should be avoided during pregnancy and nursing.
How To Prepare
Commercial extracts are the predominant form of Kava Kava. The crushed root can also be used.
Daily doses delivering between 50 and 240 milligrams of the active ingredients are the customary recommendation. Commercial capsules containing between 150 and 300 milligrams of root extract may be taken twice a day. Because the potency of commercial preparations may vary, follow the manufacturer's directions whenever available.
An overdose is usually signaled by a lack of coordination, followed by tiredness and a tendency to sleep. If you suspect an overdose, seek medical attention immediately.
1. What is it and where does it come from?
Kava Kava is a member of the pepper family and is Native to several pacific islands. The herb has been used widely for over 3,000 years by pacific native populations, and has become popular in Europe and North America.
Kava Kava (Piper methysticum) supplements are produced by using the underground stem of the plant, and the substance in Kava responsible for its effects are Kavalactones.
Kava is also known as: Malohu, maluk, meruk, milik, kew, Rauschpfeffer, sakau, tonga, Wurzelstock, yagona, yangona, yaqona, yongona, ava, ava pepper, ava root, awa, gea, gi, intoxicating pepper, intoxicating long pepper, kao, Piper methysticum, Macropiper, Latifolium, Piper inebrians, kava, kava kava, kava-kava, kava root, kava-kava root, kavain, kava pepper, kavapipar, kawa, kawa kawa, kawa pepper, kawapfeffer, maori kava and rhizoma di kava-kava.
It is important to note that Kava is produced according to certain standards. The standard of highest quality is WS 1490. Not all brand names may meet this standard. When purchasing Kava products, look for this certification.
2. What does it do and what scientific studies give evidence to support this?
Kava is a diverse substance and performs many physiological actions. Kava is best known for its ability to induce relaxation. Kavalactones (the active ingredient), induce physical and mental relaxation, and feelings of well being. These Kava induced feelings of well being and relaxation relax muscles, and help induce sleep.
Learn more about the benefits of Kava Kava on Clayton South's Health Facts.
3. Who needs it and what are symptoms of deficiency?
Anyone in good health can benefit from supplementing with Kava. Because of its sedative properties, Kava is often used by persons who have anxiety3,4,5.
Bodybuilders may benefit from supplementing with Kava as it may offset overtraining. Bodybuilders using Kava should also supplement with Milk Thistle. Persons supplementing with Kava should be monitored by a qualified medical practitioner.
4. How much should be taken? Are there any side effects?
No rigid dosage procedures have yet been established, but it is recommended that dosage should not exceed 300mg daily.
Side effects of overdose can include: difficulties focusing and temporary dilation of the pupils, skin rashes, hypertension, reduced protein levels, blood cell abnormalities, liver damage, muscle weakness, visual impairment, dizziness and drying or a yellowing of the skin6. Persons experiencing these side effects should immediately discontinue the use of kava products. This product should not be used continuously for a period exceeding three months.
Because of its sedative effects kava should not be used by pregnant women or nursing women. Persons consuming alcohol should avoid Kava supplementation8 and, because of its sedative effect, Kava should not be consumed before driving or operating heavy machinery.
There have been safety concerns associated with Kava use. Because of a series of deaths linked with kava, German officials are considering banning the supplement9, although a study done on the cases in question showed that of the seventeen persons supplementing kava, five of those persons were shown to have no problems resulting from kava, while the other twelve cases were shown to be complicated by other factors, thus calling kavas causational role into question. 10
In addition, four case reports linking kava products to liver toxcitity have appeared in scientific literature. 11,12,13It should be noted, however, that all of the case study subjects were also taking other medications that have been linked to liver damage. 15 Thus, no conclusions can be reasonably reached based on the four case studies cited. In the United Kingdom there have been three cases of liver toxicity suspected to be due to kava, but as of this time further data is needed. 16
Breaking research (resulting from unfounded claims that kava is harmfull) has determined that persons suffering side effects from kava (about two in thirty-six) have immunologically mediated idiosyncratic mechanisms and that direct toxic mechanism is much less likely. 17 This suggests that the problems experienced from kava use by a very small segment of the population is due to an immune system dysfunction rather than the kava itself.
Evidence shows that toxicity can be eliminated if the product is manufactured correctly. 18 Further research established that kava rarely causes liver injury. 19 A study done on rats showed that kava extracts had no effect on liver function and were not at all harmfull. 20
The breaking scientific evidence on this product shows that it is safe. Persons considering using kava as a supplement should consult with a physican prior to use.
[h3]Eleutherococcus Senticosus (Siberian Ginseng)[/h3]
Known as the “King of Adaptogens,” this herb actually has as many beneficial properties as common Ginseng, but without being as stimulating. This herb has become very popular in Russia and in the United States. It has been extensively researched and tested on humans, and has proven to be very effective and safe. Eleutherococcus shrubs grow up to 9 feet tall; they have rough- edged arrays of leaves, and small white flowers which bear dark blue fruit. Siberian Ginseng contains seven active substances, referred to as eleutheroside A, B, C, D, E, F and G. Total eleutheroside content of the root is up to 2 percent. Certified potency of Siberian Ginseng extract is standardized for a minimum content of eleutheroside B of 300 mcg, and eleutheroside D — 400 mcg per 100 mg (One tablet may typically contain 100mg — 250mg of extract). These active ingredients are specific to Eleuthero and are not present in the Panax species (American, Chinese, Korean or Japanese Ginseng). Eleutherococcus has numerous clinically proven beneficial properties, such as relief of insomnia, various types of neuroses, hypertension, hypotension, acute pyelonephritis (kidney problems), chronic bronchitis, and even cancer. In numerous clinical trials it has been shown that Siberian Ginseng can increase the ability of humans to withstand many adverse physical conditions such as extra workload, motion, noise, or heat. It increases mental alertness and work output, improves the quality of work produced under stressful conditions, and improves athletic performance.
[h3]Schizandra Chinensis (Chinese Magnolia Vine)[/h3]
This is a creeping vine with small red berries that is native to Northern China. In ancient China, Schizandra was used as a staple food for hunting and gathering tribes. As a traditional medicinal herb, Schizandra, called Wu-wei-tzu in China, has been used as an astringent for treatment for dry cough, asthma, night sweats, nocturnal seminal emissions and chronic diarrhea. It is also used traditionally as a tonic for the treatment of chronic fatigue. During the early 1980’s, Chinese doctors began researching Schizandra as a possible treatment for hepatitis, based on its potential for liver-protective effects and the nature of its active constituents. As a result of that research, Schizandra is now a recognized adaptogen, capable of increasing the body's resistance to disease, stress, and other debilitating processes. Known active constituents include sesquicarene, lignans (schizandrin, gomisin), schizoandrol, citral, phytosterols (stigmasterol, beta-sitosterol), and Vitamins C and E. In Asia, this adaptogenic property is said to “stimulate immune defenses, balance body function, normalize body systems, boost recovery after surgery, protect against radiation, counteract the effects of sugar, optimize energy in times of stress, increase stamina, protect against motion sickness, normalize blood sugar and blood pressure, reduce high cholesterol, shield against infection, improve the health of the adrenals, energize RNA-DNA molecules to rebuild cells and produce energy comparable to that of a young athlete.” Studies conducted on Schizandra’s effects have noted that the herb has a stimulating effect in low doses, but this effect disappeared with larger doses. The compounds thought responsible for the liver- protective effects of Schizandra are lignans composed of 2 phenylpropanoid. More than 30 of these have been isolated in Schizandra, some 22 of which were tested in 1984 by the Japanese scientist H. Hikino for their ability to reduce the cytotoxic effects of carbon tetrachloride and galactosamine on cultured rat liver cells.
Most lignans were found to be effective, and some were extremely active (schizandrins A and B, gomisin A, B-bisabolne). Subsequent Japanese studies have found that two of the lignans, wuweizisu C and gomisin A, exert their liver protective effects by functioning as antioxidants to prevent the lipid peroxidation produced by harmful substances such as carbon tetrachloride. Since lipid peroxidation leads to the formation of liver damage, the two compounds did indeed exert a protective influence. Western herbalists commonly recommend Schizandra as support for the lungs, liver and kidneys, and to help with depression due to adrenergic exhaustion. In Russia, Schizandra is used to treat eye fatigue and increase acuity.
[h3]Avena Sativa (Fresh Wild Oat Seed)[/h3]
An excellent remedy for strengthening the entire nervous system, oats are used in treating nervous debility, exhaustion when associated with depression, and stress. Fresh Wild Oat Seed has been used to treat nervous exhaustion, insomnia and “weakness of the nerves.” This plant is a nerve-tonic, stimulant, and antispasmodic. It ranks among the most important restoratives for conditions depending upon nervous prostration, and for the nervous system. It has been used to treat a weak heart, spermatorrhoea, and insomnia. In weak states of the heart muscle it may act as a good tonic to improve the energy of the organ. Studies suggest Wild Oat Seed provides a normalizing effect from the avena-seed extract. Spasmodic conditions of the neck of the bladder are said to also be relieved by avena-seed extract.
[h2]Drugs to avoid[/h2]
The answer to the first question is that there is no medication which will substitute for a benzodiazepine, unless it is another benzodiazepine, or a drug with benzodiazepine-like properties.
The following somehow mimic the effects of benzodiazepines or act in similar ways and thus eventually substitute one addiction for another:
All such drugs should be avoided as they only substitute one type of dependence for another.
However, there is the possibility to use some as a temporary substitution as they may ease symptoms of withdrawal or as a substitution may be a chance in certain cases to switch to a drug that is easier to come off. This is a decision that should be well though through, as one addiction may easily be substituted for another - a lot easier than one may think. People tend do overestimate their abilities and psychological strength regarding addiction. In case a temporary or even longterm substitution is sought, please do research and inform yourself e.g. in the respective forums in the DF.
This chapter ends with many unknowns. Benzodiazepine withdrawal remains an unfinished story and several aspects need serious attention:
Education. All doctors and paramedicals need to acquire greater knowledge and to receive better training on the prescription of benzodiazepines (short-term only), their adverse effects (especially dependence), and methods of withdrawal (slow tapering of dosage combined with adequate support). Such education should include family physicians, psychiatrists, other specialists, staff in detoxification units, pharmacists, psychologists and other therapists and community nurses. Increased general awareness and pressure from the public could speed these measures.
Research. More research is needed on the effects of long-term benzodiazepine use. Particular areas include effects on the brain structures, using modern techniques such as magnetic resonance imaging (MRI) and brain blood flow (fMRI), combined with neuropsychological testing. Further work is also needed in the little researched fields of benzodiazepine actions on endocrine, gastroenterological and immune systems.
Treatment methods. Better methods for treatment of anxiety and insomnia need to be developed. It is doubtful if any drug will ever "cure" anxiety or insomnia but it may be possible to develop pharmacological agents with fewer side-effects. For example, rats treated with the benzodiazepine antagonist flumazenil along with a benzodiazepine do not develop tolerance but still apparently experience an anxiolytic effect. Such a combination might work in humans but long-acting benzodiazepine antagonists that can be taken by mouth have not been subjected to trials. Alternatively, mood-stabilising anticonvulsants such as gabapentin, tiagabine and pregabalin may hold promise since their mode of action is different from that of benzodiazepines. At the same time, psychological therapies for treating anxiety and insomnia could be improved and more widely taught. And it may well be possible to develop better methods than those described in this monograph for drug withdrawal in people who have become dependent on benzodiazepines.
Provision of facilities. Facilities for benzodiazepine dependent people need to be developed. Detoxification units, dealing with dependence on alcohol and illicit drugs, are not appropriate for prescribed benzodiazepine users who have unwittingly become dependent through no fault of their own. Such places usually withdraw the drugs too rapidly and apply rigid "contract" rules which are quite unsuitable for benzodiazepine patients struggling with withdrawal symptoms. Much needed are clinics specialising in benzodiazepine withdrawal where clients can receive individualised, flexible, understanding and supportive counselling. At present only too few voluntary support groups valiantly strive to fill this gap with minimal finances. Proper financing would also allow provision of residential accommodation where clients in need could go for short breaks in a supportive, non-hospital, atmosphere at crucial times during their withdrawal process.
Finally, it is a tragedy that in the 21st century millions of people worldwide are still suffering from the adverse effects of benzodiazepines. Nearly 50 years after benzodiazepines were introduced into medical practice in the 1950s there should be no need for a monograph such as this. However, I hope that the experience from many patients described in this book will help to raise awareness amongst the medical profession and the public of the problems associated with long-term benzodiazepine use and withdrawal.
If you feel seriously sick, seek professional help immediately.
The material published in this online Manual is for general health information to the public. The author and publisher are not engaged in rendering medical, health, psychological advice or any other kind of personal or professional services on this site.
The material should not be considered complete and does not cover all diseases, ailments, physical conditions or their treatment. The information about drugs contained on this site is general in nature. It does not cover all possible uses, actions, precautions, side effects, or interactions of the medicines mentioned.
The material provided on this site should not be used for diagnosing or treating a health problem or disease. It is not a substitute for professional care nor should it be used in place of a call or visit to a medical health or other competent professional, nor is the information intended as medical advice for individual problems or for making an evaluation as to the risks and benefits of taking a particular drug.
The author and the operator of this site do not assume responsibility for any inaccuracies or omissions or for consequences from use of material obtained on this site and the author and the operator of this site specifically disclaim all responsibility for any liability, loss or risk, personal or otherwise, which may be incurred as a consequence, directly or indirectly, of the use and application of any of the material on this site.
It is suggested that readers consult other sources of information as well as obtain direct consultation with a physician when making decisions about their health care. If you have, or suspect you may have, a health problem, you should consult your professional health care provider. The material on the site is in no way intended to replace medical advice offered by physicians or a complete medical history and physical examination by a physician. In any event and before adopting any of the suggestions in this Manual or drawing inferences from it, you should consult your professional health care provider
Last edited by 0utrider; 03-01-2010 at 06:16.
Reason: improving / adding
Absolutely fantastic FAQ article, and very thorough indeed. I love the title image too. I can't verify the data but at a glance the structure looks good.
Perhaps section 3 could be separated into one section about the process of withdrawing, then another about the symptoms associated? Not sure if this is necessary at all, it would reduce the size of section 3 though. Maybe supplements could have it's own as well. Not sure though, just some ideas.
yes im just thinking about restructuring it. initially it was ok, but now as more and more gets added the separation of symptoms and relief doesnt make sense anymore
In case you should already see (structural) mistakes or have things to add please do let me know
i wanna add a little more about GABA and the mechanisms in general, more about supplements and drugs that help and relief techniques
and somehow also stuff about GBL/GHB as it kinda also has its place but im not familiar with that stuff so if someone could point me in the right direction it would be nice..
also will have to fix some of the structure and make a intro + mini intro / outros
also a lot of unneccesary spaces are inbetween paragraphs.. that needs to get fixed
Also: I'm kinda unsatisfied with the title.. do you guys have any suggestions for the heading? Becaue its not that much about GABAergics and also that term is way too broad. On the other hand, it really does not only focus on Benzos but Much more, i even plan to add a GBL/GHB section..
I might split this into 2 and have one part in the general benzos forum, as certainly the start of the post seems better suited (or at least equally suited) to this part of the forum.
Guys, I als copied a lot of stuff from the DF. I would like to apologize in retrospect because at that time i for some reason did not think about mentioning the original authors! If you happen to find your post in here (quoted or not, as i didnt quote all) please let me know so i can add your name!
I also need to fix some of images.. There is a problem with the sizes as some tend to be too big if readable but not readable if they are of a good size...
i will probably create a separate thread for using ibogaine for Benzos as it may be too dangerous to throw around manuals on the treatment in such a general faq
there is still some editing to be done
univeristy started again, well continue in about 3 weeks