December's mystery drug has a story that is just beginning to be written. Although the drug has been in widespread use and distribution in the U.S. and abroad, the drug is not all that well known or understood by patients and healthcare professionals. It is a prescription drug. It is mainly used to treat a specific drug dependency. It is a medication that has had some run-ins with the FDA in what were documented as serious side effects in some patients. These events first occurred in 2007. In 2009, the FDA required the drug to include in its packaging a "black box warning" to alert patients to the potential for the drug to trigger or exacerbate suicidal ideations and erratic behaviors. Making matters worse for this drug were reports in 2011 that the drug had now been associated with certain types of cardiovascular events in individuals who had underlying cardiovascular disease. But some very recent news from a large study in Denmark failed to link this month's drug (or bupropion) with any special risk for cardiovascular events[1]. It has been a bumpy start for this medication's career. But after peeling away the various reports, special warnings, and the media hype that envelops it, there is a very interesting drug with the potential to be a form of drug therapy that can be applied to many situations where people are addicted or dependent on a drug of abuse.

This month's drug faces some competition in the marketplace. Bupropion is one of those competitors. Brand name Wellbutrin, bupropion is an antidepressant that exerts action by way of blocking the reuptake of norepinephrine and dopamine in specialized receptors in the brain. Bupropion's method of action is very different from that of this month's drug. In fact, this December mystery represents a novel pharmacologic approach in treating the type of drug dependency described here. Its precise designation is a partial giveaway towards the drug's final identity. Readers probably will not have to think twice about it. But here goes. This drug is a partial agonist of a subtype of the nicotinic acetylcholine receptor in the brain. With an official IUPAC designation of 7,8,9,10-tetrahydro- 6,10-methano- 6H-pyrazino (2,3-h)(3) benzazepine, this drug is unique. It has no similarly acting alternative drug for competition.

As a drug that targets and activates the nicotinic acetylcholine receptor complex, it interacts with areas in the brain where nicotine itself exerts action. Nicotine is the active stimulant in tobacco. It is the chemical that conveys the pleasurable effects of smoking and chewing of smokeless tobacco. It is at this microscopic transmitter juncture where nicotine triggers adaptations by the receptor complex to accept and ultimately institute a preference for nicotine. As long as a smoker keeps minimal levels of nicotine available for the nicotinic-acetylcholine receptor complex, things go swimmingly. When nicotine levels are low or are somehow disrupted, the receptors exert a chemical message back to the smoker that results in craving for a cigarette. For the nicotine-dependent person, tobacco cravings are a form of drug withdrawal. Cravings can be quite powerful, even overwhelming for some smokers. The poor success rate for smokers who quit "cold turkey" is due in large part to the potency of cravings.

This month's drug, by partially activating receptors incorporated in the nicotinic acetylcholine complex, serves to reduce the level of cravings of an abstinent smoker. The drug also limits the levels of pleasurable effects that a smoker experiences. In these ways, this month's drug serves to help motivated smokers to quit smoking.

Perhaps more interesting is the roll that this month's drug may play in limiting another potentially harmful vice. As it turns out, this drug increases the negative effects of alcohol. It may be entirely possible that this smoking cessation aid reduces the degree of "liking" the drinker's experience when consuming alcohol. Early studies suggest that when taken several hours before consumption of alcoholic beverages, the amounts of alcohol consumed are fewer and the pleasurable effects are dimmer. Incidentally, some smokers who had been prescribed the drug to stop smoking also reported to physicians that they had reduced their level of alcohol consumption as well.

At the moment, a wide-ranging clinical trial of this drug is progressing. An agency of the National Institutes of Health has launched a study of alcohol-dependent smokers to determine the effects of the drugs in a multivariate set of environments. If some of the earlier, smaller, scattered studies are indeed accurate, it is likely that the drug will prove to be helpful to alcoholics as part of their recoveries.

And last stay tuned for more news about this month's drug and treatment of cocaine dependency. All evidence available at this preliminary point in time suggests that the drug reduces the euphoria of a cocaine high and that it may also blunt cocaine-caused cravings. Very interesting indeed.

Click Here for this month's mystery drug.

For those who are unable to open the link, email info@darstraining.com for the answer.

A recently published report for the U.S. Preventive Services Task Force in the Annals of Internal Medicine revealed the state of the evidence associated with adolescent smoking, smoking cessation, and smoking prevention[1]. The authors scoured a number of older studies and reviews to summarize the broad outlines of the problems associated with teenage smoking and the roll that the healthcare system has affected it. The state of the research suggests the problems of teenager smoking as being a very difficult one. With a focus on the roll of the primary care physician and primary health workers, there seemed to be very little that can be successfully employed to either prevent kids from starting to smoke or to engage cessation efforts in those who have already started to smoke.

The authors did report that roughly 10% of middle school students and nearly 25% of those in high school use tobacco products. Tobacco, of course, contains nicotine. Nicotine is arguably one of the most addictive drugs known to man. Early lifetime nicotine dependency, whether with cigarettes or smokeless products, can be a precursor to the development of other drug dependencies. A 2011 National Institute of Health report on the impact of nicotine on the brains of mice demonstrated a biological priming mechanism towards the use of cocaine. Epidemiological studies have shown that nicotine and alcohol are the first drugs that most people take before entering into patterns of hard, illicit drug use. Working hard at preventing and arresting tobacco use in kids may be a smart and effective way to reduce toxic drug use as adults.

A glimmer of hope was found in the analysis of all this data though. Researchers did find that behavior-based interventions undertaken to prevent kids from smoking had a small but positive effect on statistics. Nothing seemed successful though with efforts to get current adolescent smokers to quit. Neither behavior-based efforts nor drug-based (bupropion, varenicline, etc.) efforts were successful. But secondary interventions that isolate kids from secondhand smoke and the smoke generated by parents who use tobacco have not been clearly evaluated. It may be that isolation from those confined and congested smoking locations and their social situations may be an effective prevention strategy, especially when employed alongside documented, effective behavior-based therapies in the primary care setting.

Over the course of the last 12 months, the DARS Journal has reported on several reports related to research focusing on cannabis abuse. These reports have put forth a collection of signs and symptoms associated with abuse of the drug. At this juncture, it is worthwhile to summarize these effects and focus attention on the most prominent impacts that result from abuse of the drug (organic marijuana).

The wide-ranging effects of cannabis effects can be summarized as follows:

Altered mood. Marijuana can instigate effects that range from calmness and social relaxation to stimulation and profound dysphoria. Long-term use can result in depression that is difficult to treat and is resistant to medication. In persistent patterns of abuse, marijuana can trigger paranoia and disrupt natural patterns for sleep and relaxation.

Slowed reaction time and degraded motor coordination. Especially in higher concentrations, tetrahydrocannabinol (THC) results in motor deficits that are similar to comparable doses of ethyl alcohol and benzodiazepines (diazepam, lorazepam, etc.). Not a good drug to ingest before one takes a practical driving exam.

Degraded judgment and decision making. Marijuana abuse can trigger higher risk sexual behavior that could lead to the transmission of sexually transmitted diseases and AIDS.

Elevated vital signs and processes. Users experience dilated pupils, increased heart rates, and elevated blood pressure. In many cases, blood pressure may be elevated well beyond the hypertension alarm of 140/90 mm/hg.

Drug dependency. Chronic marijuana users can easily become dependent on the drug. This means that any interruption in the drug's use or drop in average daily plasma level will result in a very unpleasant withdrawal syndrome. Withdrawal may include insomnia, agitation, paranoia, anxiety, and social withdrawal. Withdrawal signs and symptoms may persist for weeks or months following last use.

Poorer educational achievement and outcomes. Chronic marijuana users present with noticeably lower levels of educational and work achievement. Users also report lower levels of job satisfaction; they have a difficult time finding and maintaining work.

Cognitive impairment. Early onset of cannabis abuse may result in measureable declines in IQ that may extend well beyond last periods (years) of ingestion and intoxication.

Respiratory problems. Smoking marijuana conveys tars and chemicals inherently found in the marijuana plant. Further, pesticides and fertilizers used to grow the plant bind to the final products that are smoked and inhaled into the lungs. Chronic cough and bronchitis are frequent consequences of persistent marijuana abuse.

This list of marijuana symptoms and effects is not all-inclusive. But addiction professionals should understand that marijuana use and abuse is a serious addictive disease. Marijuana dependency necessitates a commitment to therapy and intensive outpatient treatment. Despite what the marijuana legalization lobbies say, it is not a drug that should be taken lightly in any sense of intervention and treatment.

One of America's greatest drug problems involves the hundreds of thousands of people who abuse the narcotic analgesic medication that contains hydrocodone and acetaminophen. In brand form, the drug is known as Vicodin. There are a variety of pharmaceutical firms that manufacture generic formulas of this drug. This drug combination is produced in several sizes and forms that include 5, 7.5 or 10 mg of hydrocodone along with 500 mg of acetaminophen. The intent of this special blend is to take advantage of the pain relieving synergy that is created by the partnering of a narcotic (hydrocodone) with a non-narcotic analgesic drug (acetaminophen). Acetaminophen is an over-the-counter drug and was made famous as the central ingredient in Tylenol preparations. Acetaminophen is combined with other narcotic analgesics, such as codeine and oxycodone that provide physicians with a variety of therapeutic options to treat moderate to moderately severe pain.

In a recent bulletin posted by the FDA, it was announced that drug manufacturer Qualitest, a subsidiary of Endo Health Solutions, had issued a voluntary nationwide recall for over 100 lots of 10/500 mg hydrocodone and acetaminophen tablets (sometimes referred to as "extra strength" tablets). As it turns out, some of the tablets in these lots may contain excessive or heavy doses of one or both of the ingredients. Under these conditions, it is possible that a patien  t prescribed these drugs could unwittingly ingest more narcotic than intended. Depending on an affected patient's level of tolerance to opioids, a little extra hydrocodone in a tablet like this could have onerous effects. Similarly, a patient may unknowingly ingest more acetaminophen than intended. Both drugs pose notable liabilities. First and foremost, hydrocodone carries with it the potential for over sedation if a patient were to take a "heavy" dose. On the streets, narcotic abusers (heroin, oxycodone etc.) refer to more concentrated or rarefied narcotic products as "hot shots" or in some locales they are called a "load." Were a patient to get one of these off-kilter tablets, an additional threat exists with an extra dosage of acetaminophen. That drug is a particular challenge for the liver, especially if an affected patient is in the habit of drinking three or more alcoholic beverages each day.

The DARS Journal has reported on a variety of novel drug therapies that have emerged in the last few years as pharmacotherapy for substance abuse and drug dependency disorders. And now with mistletoe and New Year's toasts afoot comes news that the human love hormone called oxytocin has demonstrated real promise as an effective therapy to mitigate onerous withdrawals associated with alcohol withdrawal. Oxytocin is best known as a hormone central to child birthing and the child-mother bonding processes that initiates immediately after the birth of a child.

What's not as well known about oxytocin is the role the hormone plays in maintaining healthy interpersonal relationships and its effects for sexual orgasm in both men and women. The hormone is currently under investigation for a number of effects that it may have in conditions such as depression and mood disorder. But of more interest perhaps is the potential that oxytocin may have in attenuating the withdrawals that alcohol-dependent men and women experience during and after drug detoxification. In past experimentation and research in rodents, oxytocin had demonstrated influence in blocking tolerance to alcohol. Oxytocin also reduced some of the more discomforting pains associated with alcohol withdrawal.

Recently announced in the Journal of Alcohol Clinical Research were the results of a small pilot study of 11 actively drinking and alcohol-dependent men who had documented histories of alcohol withdrawals. The participants were screened to ensure that they were not susceptible to seizures or delirium tremors in withdrawal. The patients were placed in an inpatient center where alcohol detoxification was initiated. The group was split into two cohorts. One group was administered intranasal (spray) oxytocin twice daily for three days; the other group received a matching intranasal placebo. Both groups were treated with lorazepam (Ativan) as needed based upon the severity of alcohol withdrawal symptoms. Amazingly, oxytocin-treated patients required almost five times less lorazepam than those participants who received the placebo. The oxytocin-treated patients also reported less severe withdrawals and self-report of anxiety and tension.

Although a small preliminary study, there is some very hopeful news here. In treating alcohol-dependent patients, healthcare professionals nearly always come to rely on benzodiazepines (Ativan and Librium) to mitigate withdrawals. For many addiction specialists, the utilization of benzodiazepines in withdrawal is a risky proposition and often becomes a pharmacological crutch for those patients who take it. For some, withdrawal from alcohol dependency can be a direct route to relapse. Alcohol withdrawals can be deadly too. Seizures during alcohol withdrawal can cause serious damage to the brain and central nervous system. In prior human experimentation, oxytocin has shown itself to be a safe hormone to use. Its demonstrated effects in stimulating interpersonal trust and social intelligence are added benefits to the effects oxytocin may have in treating alcohol withdrawal. Should oxytocin live up to the potential that is suggested in this study, addiction professionals may have a potential therapy that reduces the complications of alcohol withdrawal, reduce problem drinking, and perhaps act as pharmacotherapy to treat other non-alcohol related anxiety disorders.

It is obvious that oxytocin is not yet ready for primetime utilization in addiction medicine. But it will be exciting to watch the hormone's progress through the labyrinth of research and clinical experimentation that is sure to follow.

Cannabis use by adolescents is a concern at any level and with any child. But attention has been focusing on the roll that persistent marijuana use in adolescence plays in cognitive decline in adulthood. For some time now, the marijuana legalization lobby has asserted that the smoking of marijuana represents a more benign alternative to the use of alcohol. This argument has been a reliable underpinning of recent political campaigns to legalize the use of marijuana in the states of Washington and Colorado. The truth in this matter is something altogether contrary to these claims.

To examine the relationship between adolescent onset and "persistent" cannabis use and resultant cognitive changes in adulthood, researchers analyzed data provided by 1037 participants in the Dunedin Longitudinal Study. This ongoing research endeavor involves 1037 babies born in Dunedin, New Zealand between April 1972 and March 1973 at Queen Mary Maternity Hospital. Nearly 1100 studies have been spawned by the data offered up by the Dunedin Study. In the study referenced here, data included interviews of participants at ages 18, 21, 26, 32, and 38; IQ testing in childhood and again at age 38[1].

Compared with respondents who reported adult-onset cannabis use, adolescent-onset users reported an average of an eight-point decline in IQ by the age of 38. Adolescent cannabis users in this study reported on average at least three marijuana dependence diagnoses as evidence of their abuse. Those respondents who reported adolescent onset (as opposed to adult onset) showed significant impairments across multiple forms of cognitive functioning. The data in these analyses were controlled for a variety of confounding factors, such as mental illness, alcohol abuse, and other types of substance use disorders. Causing more alarm in this study was that respondents who had quit use of cannabis one year before cognitive testing displayed little neuropsychological improvement on test outcomes.

Paradoxically, onerous research results tied to early onset cannabis use has emerged just as a number of American states have chosen to significantly liberalize their statutes related to use and abuse of marijuana. Further muddying this situation is the rapid expansion of states that allow the use of medical marijuana. In most of these venues, the medicalization of marijuana has been nothing other than a thin veil for those groups devoted to complete marijuana legalization. In fact, for those states with medical marijuana statutes in place, there have been few who have advanced superseding initiatives to legalize the drug. They don't need to; medical marijuana status has become tantamount to outright legalization.

To date, research related to chronic cannabis use, especially early (adolescent) abuse has been tied to a variety of cognitive and neuropsychiatric conditions in adulthood. There has not been any research to indicate that cannabis is a more benign depressant. In fact, the accumulated data suggests that marijuana use matches the potential for disaster that alcohol does. Making this point more poignant is the emergence of synthetic cannabinoids as "legal" alternatives to organic marijuana. Unfortunately, the public's contemporary infatuation with marijuana leaves little hope that cannabis abuse will decline anytime soon.

---

[1] Meier MH et al. Persistent cannabis users show neuropsychological decline from childhood to midlife. Proceedings of the National Academy of Sciences USA 2012 August 27; [e-pub ahead of print]. (http://dz.doi.org/10.1073/pnas.1206820109)

Thank you subscribers. We appreciate your dedicated readership. At DARSYS we are committed to providing clients with the service and solutions you need to run successful drug awareness programs. Our Journal is just one way that we show that commitment. We always encourage feedback from our Journal readers. Please send your thoughts to info@darstraining.com.

Sincerely,

DARSYS Journal