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medication assisted treatment for addiction

There is a big move in addictions treatment to utilize medications in an attempt to improve success rates in keeping people sober. The following are selections pulled from wikipedia on the most common medications for MAT (medication assisted treatment). Clinical literature and my own experience show that MATs can be a nice adjunct to counseling and social and spiritual supports but are not a replacement for a genuine recovery experience. There are approved MATs for alcohol and opiates with both agonists (activate receptor sites in a similar but safer way then the drug) and antagonists (block receptor sites). For alcohol there is also antabuse which prevents the usual breakdown of alcohol and massively increases the chemicals related to hangover resulting in an immediate negative experience upon consumption. There are significant side effects and contraindications with all of these approaches and everyone in the treatment field or who struggles with addiction would be well advised to do some homework on possible medication options.

Medication Assisted Treatment Medicines (from Wikipedia)

 

Acamprosate (brand name: Campral):Acamprosate is thought to stabilize the chemical balance in the brain that would otherwise be disrupted by alcoholism, possibly by blocking glutamatergic N-methyl-D-aspartate receptors, while gamma-aminobutyric acid (GABA) type A receptors are activated. Alcohol inhibits activity of biochemical receptors called N-methyl-D-aspartate receptors, or NMDARs, so that chronic alcohol consumption leads to the overproduction (upregulation) of these receptors . Thus, sudden alcohol abstinence causes these excessive numbers of NMDARs to be more active than normal and to produce the symptoms of delirium tremens and excitotoxic neuronal death.[9] Withdrawal from alcohol induces a surge in release of excitatory neurotransmitters like glutamate, which activates NMDARs.[10] Acamprosate reduces this glutamate surge.[11] The drug also protects cultured cells in excitotoxicity induced by ethanol withdrawal.[12] and by glutamate exposure combined with ethanol withdrawal.[13]In addition to its apparent ability to help patients refrain from drinking, some evidence suggests that acamprosate is neuroprotective (that is, it protects neurons from damage and death caused by effects of alcohol withdrawal and possibly other insults). Reports indicate that acamprosate only works with a combination of attending support groups and abstinence from alcohol.[3] Certain serious side effects include allergic reactions, irregular heartbeats, and low or high blood pressure, while less serious side effects include headaches, insomnia, and impotence.[4] Acamprosate should not be taken by people with kidney problems or allergies to the drug. FDA concluded: “Campral proved superior to placebo in maintaining abstinence (keeping patients off alcohol consumption), as indicated by a greater percentage of acamprosate-treated subjects being assessed as continuously abstinent throughout treatment. Campral is not addicting and was generally well-tolerated in clinical trials. The most common adverse events reported for patients taking Campral included headache, diarrhea, flatulence, and nausea.”

Buprenorphine (Subutex, Temgesic, or Suboxone [buprenorphine:naloxone 4:1 preparation] – sublingual tablets – Buprenex – for injection – and Norspan – transdermal patch) is a semi-synthetic opioid that is used to treat opioid addiction in higher dosages (>2 mg) and to control moderate pain in non-opioid tolerant individuals in lower dosages (~200 µg).

Disulfiram is a drug used to support the treatment of chronic alcoholism by producing an acute sensitivity to alcohol. Trade names for disulfiram in different countries are Antabuse and Antabus manufactured by Odyssey Pharmaceuticals. Disulfiram is also being studied as a treatment for cocaine dependence, as it prevents the breakdown of dopamine (a neurotransmitter whose release is stimulated by cocaine); the excess dopamine results in increased anxiety, higher blood pressure, restlessness and other unpleasant symptoms. Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to the harmless acetic acid. Disulfiram blocks this reaction at the intermediate stage by blocking the enzyme acetaldehyde dehydrogenase. After alcohol intake under the influence of disulfiram, the concentration of acetaldehyde in the blood may be 5 to 10 times higher than that found during metabolism of the same amount of alcohol alone. As acetaldehyde is one of the major causes of the symptoms of a “hangover” this produces immediate and severe negative reaction to alcohol intake. Some 5–10 minutes after alcohol intake, the patient may experience the effects of a severe hangover for a period of 30 minutes up to several hours. Symptoms include flushing of the skin, accelerated heart rate, shortness of breath, nausea, vomiting, throbbing headache, visual disturbance, mental confusion, postural fainting, and circulatory collapse. Disulfiram should not be taken if alcohol has been consumed in the last 12 hours. There is no tolerance to disulfiram: the longer it is taken, the stronger its effects. As disulfiram is absorbed slowly through the digestive tract and eliminated slowly by the body the effects may last for up to two weeks after the initial intake; consequently, medical ethics dictate that patients must be fully informed about the disulfiram-alcohol reaction.[4] A recent nine-year study found that incorporation of supervised disulfiram and a related compound calcium carbimide into a comprehensive treatment program resulted in an abstinence rate of over 50%.

Naltrexone is an opioid receptor antagonist used primarily in the management of alcohol dependence and opioid dependence. It is marketed in generic form as its hydrochloride salt, naltrexone hydrochloride, and marketed under the trade names Revia and Depade. In some countries including the United States, an extended-release formulation is marketed under the trade name Vivitrol. Also in the US, Methylnaltrexone Bromide, a closely related drug, is marketed as Relistor, for the treatment of opioid induced constipation. Naltrxone should not be confused with naloxone (which is used in emergency cases of overdose rather than for longer-term dependence control) nor nalorphine. Both nalorphine and naloxone are full antagonists and will treat an opioid overdose, but naltrexone is longer-acting than naloxone (although neither is an irreversible antagonist like naloxazone), making naloxone a better emergency antidote. Its use in alcohol (ethanol) dependence has been studied and has been shown to be effective [1]. Its mechanism of action in this indication is not fully understood, but as an opioid-receptor antagonist it’s likely to be due[citation needed] to the modulation of the dopaminergic mesolimbic pathway which is hypothesised to be a major center of the reward associated with addiction (being one of the primary centers for risk-reward analysis in the brain, and a tertiary “pleasure center”) that all major drugs of abuse are believed to activate. The standard regimen is one 50 mg tablet per day. Initial problems of nausea usually disappear after a few days, and other side effects (e.g., heightened liver enzymes) are rare. Drug interactions are not significant, besides the obvious antagonism of opioid analgesics. Naltrexone has two effects on alcohol consumption.[8] The first is to reduce craving while naltrexone is being taken. The second, referred to as the Sinclair Method, occurs when naltrexone is taken in conjunction with normal drinking, and this reduces craving over time. The first effect persists only while the naltrexone is being taken, but the second persists as long as the alcoholic does not drink without first taking naltrexone. In alcohol dependence, naltrexone is considered a safe medication. Control of liver values prior to initiation of treatment is recommended. There has been some controversy regarding the use of opioid-receptor antagonists, such as naltrexone, in the long-term management of opioid dependence due to the effect of these agents in sensitising the opioid receptors. That is, after therapy, the opioid receptors continue to have increased sensitivity for a period during which the patient is at increased risk of opioid overdose. This effect reinforces the necessity of monitoring of therapy and provision of patient support measures by medical practitioners. Naltrexone can induce early morning erections in patients who suffer from psychogenic erectile dysfunction. The exact pathway of this effect is unknown. Priapism has been reported in two individuals receiving Vivitrol. Naltrexone has been shown to be effective in the reversal of sexual satiety and exhaustion in male rats.[22]The Chicago Stop Smoking Research Project at the University of Chicago studied whether naltrexone could be used as an aid to quit smoking. The researchers discovered that Naltrexone improved smoking cessation rates in women by fifty percent, but showed no improvement for men.[23] Some studies suggest that self-injurious behaviors present in developmentally disabled and autistic people can sometimes be remedied with naltrexone.[25] In these cases, it is believed that the self-injury is being done to release beta-endorphin, which binds to the same receptors as heroin and morphine.[26] By removing the “rush” generated by self-injury, the behavior may stop. Naltrexone helps patients overcome urges to abuse opiates by blocking the drugs’ euphoric effects. While some patients do well with the oral formulation, there is a drawback in that it must be taken daily, and a patient whose craving becomes overwhelming can obtain opiate euphoria simply by skipping a dose before resuming abuse. There are indications that naltrexone might be beneficial in the treatment of impulse control disorders such as kleptomania (compulsive stealing), trichotillomania, or pathological gambling.[28] Clinical trials are ongoing regarding the use of naltrexone in combination with another drug, bupropion, as a weight loss therapy.[29]

Alcohol Dependence and Anti-Depressants

In 2002, Dr. Fulton T. Crews, Bowles Center director, and Bowles Center research associate Dr. Kim Nixon were the first to report that alcohol, during intoxication, has a detrimental effect on the formation of new neurons in the adult rat hippocampus. This brain region is important for learning and memory – in animals and humans – and is linked to psychiatric disorders, particularly depression.

“When used in excess, alcohol damages brain structure and function. Alcoholics have impairments in the ability to reason, plan or remember,” said Crews, also professor of pharmacology and psychiatry in UNC’s School of Medicine. “A variety of psychological tests show alcoholics have a difficulty in ability to understand negative consequences.”

In the new study, senior co-author Crews and co-author Nixon found inhibition of neurogenesis, or brain cell development, during alcohol dependency, followed by a pronounced increase in new neuron formation in the hippocampus within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence.

“And when they stop drinking, you can show in a period of weeks, months, years, the brain grows back, there’s a return of metabolic activity, and cognitive tests show a return of function,” Crews said.

“Pharmacological agents such as antidepressants and behaviors such as running, increased physical activity and learning experiences apparently help regulate the process of neurogenesis,” he added. “Our research suggests they could be considered in the treatment of chronic alcohol dependency.”

 

 

 

 

 

 

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