Современные лекарственные стратегии лечения алкоголизма

γ-Hydroxybutyrate (GHB), anticonvulsants, and α2-agonists have been studied as stand-alone or adjunctive agents in the treatment of alcohol withdrawal syndrome. Although these medications are promising for mild to moderate alcohol withdrawal syndrome, there is a dearth of information about their ability to prevent or treat complicated alcohol withdrawal.

Alcohol Disorders: Practical Tips From New Research

Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence

налтрексон

While naltrexone has yet to become the huge treatment breakthrough for alcoholism that addiction researchers hoped for it, naltrexone did, in the end, prove to be the first anti-craving medication widely available for alcoholics. Using an opiate antagonist as an aid to the prevention of alcoholic relapse would have been unthinkable without the underpinnings of a neurophysiological model of addiction. Various investigators have also speculated that naltrexone, the drug used as an adjunct of heroin withdrawal therapy, may find use against symptoms of marijuana withdrawal in people prone to marijuana dependence

Naltrexone has something of a mixed reputation, however, in part due to its use in the highly controversial practice of “rapid detox.” Naltrexone, like methadone and buprenorphine, blocks the heroin high in a relatively neutral manner. It does so by knocking the opiate molecule off its receptors and replacing it with “dead weight,” so to speak. Naltrexone would seem to be the perfect drug for heroin addicts—but it is not. It does little to reduce cravings. Like acamprosate for alcohol, another blocking approach, its record of accomplishment is mixed, and the dropout rate is high. There is not even a mild drug-like effect to provide cross-tolerance and dampen the effects of withdrawal, as with methadone. Recently, naltrexone for heroin addiction has been offered as a form of rapid detoxification.

Naltrexone combined with buprenorphine is marketed as Subutex, and represents another treatment modality for opiate addiction. In addition, a University of Minnesota study of kleptomania—the compulsion to steal—showed that naltrexone drastically reduced stealing among a group of 25 shoplifters.

Unfortunately, naltrexone is a potential problem for people with liver disease or hepatitis. At high doses, naltrexone has been implicated in liver damage. More common adverse effects include dizziness, lethargy, and headache.

Addiction Inbox

Булимия, блуждающий нерв, опиоидные и серотониновые рецепторы

The first major breakthrough in the treatment of bulimia came with the era of SSRI antidepressant medications. The initial motivation was a perceived link between bulimia and depression, which commonly exist as co-morbid disorders. Serotonin was clearly involved in some way in the mechanisms of active bulimia. In 1997, Prozac became the first drug ever licensed by the FDA for the treatment of bulimia nervosa. The drug’s formal approval was based on clinical studies showing median reductions in binging of as much as 67 per cent for Prozac, compared with 33 per cent for placebo. Vomiting was reduced by 56 per cent, compared to 5 per cent for female placebo users. (About 10 per cent of diagnosed bulimics are males.) While cure is too strong a word, the benefits were quite dramatic in some cases.

What about the roughly 50% of bulimics who do not respond to serotonin-boosting medications? Recent research covered by the science blog Neurotopia points the finger at a long nerve running through the cranium. The tenth cranial nerve, better known as the vagus nerve, branches through the neck, thorax and abdomen, and is involved in breathing, tasting, swallowing, and digestion. Most of the signal traffic carried by the vagus nerve is one way: from the body to the brain. Suspicion fell on the vagus nerve because of its direct involvement with one of bulimia’s most salient traits — the inability to feel normal levels of fullness, or satiety.

Bulimics must eat more at a sitting than non-bulimics in order to feel satisfied. There is evidence of vagus nerve involvement in meal satiation, portion size, and, notably, control of vomiting. Researchers have suggested that bulimics have a relatively insensitive vagus nerve, made even less sensitive by the debilitating cycle of overeating and vomiting. Hence, bulimia patients need greater vagus nerve stimulation in order to stop eating. Interestingly, studies have also shown that people suffering from bulimia have high pain thresholds, compared to non-bulimics.

This dysregulation of the vagus nerve responds to the drug ondansetron, according to recent research published in Physiology & Behavior by Patricia L. Faris and colleagues. The antiemetic effects of ondansetron, which reduce vagus nerve activity by acting on the 5-HT3 serotonin receptor, seem to decrease vomiting while increasing the number of normal meals eaten.

Finally, a third path toward treatment has been sparked by research on opioid receptors. Decreased endogenous opioid activity may also underpin bulimia. A small 2005 study by Johns Hopkins University School of Medicine analyzed the results of brain MRIs on eight bulimic women and eight controls. Bulimics showed decreased opioid receptor binding in the insula, another area of the brain implicated in MRI studies of addiction. The insula has been called the brain’s “gustatory cortex,” and it may be that the repeating cycle of binge and purge activates the opioid system. Opioid receptors are involved in the processing of the reward value of food. This suggests that a drug like naltrexone, which blocks opiate receptors, might also have a role to play in the treatment of bulimia.

Drugs for Bulimia

Сертралин+налтрексон

More depressed alcohol-dependent patients receiving the sertraline plus naltrexone combination achieved abstinence from alcohol, had delayed relapse to heavy drinking, reported fewer serious adverse events, and tended to not be depressed by the end of treatment.

A Double-Blind, Placebo-Controlled Trial Combining Sertraline and Naltrexone for Treating Co-Occurring Depression and Alcohol Dependence

психотропные лекарственные средства и вес (таблица)

Клептомания

Additionally, there is some suggestion that selective serotonin reuptake inhibitors, the treatment of choice for obsessive compulsive disorder,may lack efficacy for kleptomania. Instead, other medications (lithium, anti-epileptics, and opioid antagonists) have shown early promise
in treating kleptomania. Evidence suggests that theremay be subtypes of kleptomania that aremore likeOCD, whereas others have more similarities to addictive and mood disorders.
Understanding and Treating Kleptomania:NewModels and New Treatments

терапия деперсонализации

For example, a number of studies suggest that opioid receptor antagonists such as naltrexone and naloxone are useful in at least a subgroup of patients. In spite of initial expectations, the use of lamotrigine as a sole medication has not been found useful. However, open-label trials suggest that its use as an add-on treatment with selective serotonin reuptake inhibitors (SSRIs) is beneficial in a substantial number of patients. Similarly, the use of clonazepam, particularly in conjunction with SSRI antidepressants, appears to be beneficial in patients with high levels of background anxiety.
Depersonalization disorder: pharmacological approaches

Two recent controlled medication trials, one with lamotrigine and one with fluoxetine, failed to show efficacy. There is some evidence for dysregulation of endogenous opioid systems in depersonalization, and a few studies have suggested that opioid antagonists may have efficacy in the treatment of dissociation and depersonalization symptoms. In this prospective open treatment trial, 14 subjects were recruited and treated with naltrexone for 6 weeks to a maximum dose of 100 mg/d (first 7 subjects) or 10 weeks to a maximum dose of 250 mg/d (next 7 subjects). Mean naltrexone dose was 120 mg/d. There was an average 30% reduction of symptoms with treatment, as measured by 3 validated dissociation scales. Three patients were very much improved, and 1 patient was much improved with naltrexone treatment.
An open trial of naltrexone in the treatment of depersonalization disorder