A number of U.S. adolescent drug use experts have proposed a different approach towards reducing the harms of adolescent alcohol abuse. This technique would give parents an opportunity to teach their kids to drink alcohol responsibly. Given a reality that kids are exposed to alcohol at a relatively early age by way of advertising and society-wide consumption, this proposal would increase parental shaping of values and behaviors with the initiation of parentally supervised alcohol consumption by kids as early as the eighth grade. This harm-minimization hypothesis was put to the test in a recently published study that compared the experiences of teenagers in Washington to a similarly constituted population of students "down under" in Victoria, Australia.[1] The kids in Washington were subjected to a zero-tolerance abstinence-based program of policies and laws. The Australian cohort operated in a system where responsible drinking was taught and allowed as part of a larger harm minimization program.

The instant study involved an in-school survey for students starting in the seventh grade and continued through completion of the ninth grade. In the seventh grade, family factors involved with alcohol consumption, such as familial substance abuse and parental attitudes towards alcohol abuse, were evaluated. In the eighth grade, the incidence of alcohol use with adult supervision was assessed. And in the ninth grade, alcohol use and harmful consequences of drinking (engaging in violence, being unable to stop drinking alcohol, and having regrettable sexual encounters) that occurred in the past year were documented and evaluated.

For seventh graders, lifetime alcohol use was significantly greater in the Australian cohort (59% vs. 39%). When considering ninth graders the spread was even greater (71% vs. 45%). In the eighth grade, Australian students revealed significantly greater incidence of parent supervised alcohol consumption (66% vs. 35%). For ninth graders, Australian participants reported alcohol-related harms more frequently as well (36 vs. 21%). When data was controlled for both family factors and alcohol use in seventh grade, the survey showed that greater opportunity to use alcohol under adult supervision was linked to drinking more often and the reporting of more alcohol-related harms for students in both countries.

These results bolster other smaller studies where parental supervision as a harm-minimization strategy seems to be ineffective in reducing alcohol use and the problems that result from teenage drinking. Alcohol use by teenagers is a troublesome social problem. Supervised parental supervision is not a wise answer to this challenge

Smoking has devastating consequences for those addicted to it. Smoking is nothing more than a slick delivery system for nicotine into the blood stream. It is fast, efficient, and deadly. And smoking is a widely accepted habit for many drug treatment and rehabilitation programs in America. It is especially evident in many mental health programs which are treating people with serious mental illness. Smokers have an increased risk for cancer, lung disease, and cardiovascular disease. And on average, they die many years sooner than those who do not smoke.

In the drug treatment setting there is broad sentiment that smoking is a stimulus that calms and soothes people at a time where environmental and emotional stressors are apt to trigger a relapse. In other words, it is an anti-drug drug. Mentally ill patients and recovery populations commonly smoke. The connection appears to be tightly interwoven. Twenty years ago, the Joint Commission on the Accreditation of Healthcare Organizations (JACHO), now called the Joint Commission, advanced a nationwide ban on tobacco use in hospitals. Quite a battle ensued. Advocacy groups for the mentally ill argued that the banning of cigarettes would result in mass insurrection in treatment institutions. These protests caused JACHO to back down and exempt psychiatric hospitals from the rule. For those hospitals that voluntarily complied with the ban, there was little or no disturbance in patient behaviors.

In the drug treatment community, smoking is still widely accepted. And only recently have institutions begun to offer quit-smoking assistance to those who want it. The first obstacle in this initiative is to admit people in recovery actually do want to quit. There is little to doubt this population has the same desire to quit smoking as the general population. Typically, between 20-25% of smokers state that they intend to quit in the next 30 days. That number gets higher the further the time frame is pushed out. But efforts to assist patients with smoking cessation are weak. And smoking is an expensive habit. With a pack of cigarettes costing more than a gallon of gas, many people in recovery from substance abuse disorders are saddled with the additional financial burden of smoking.

Drug treatment programs should be encouraged to engage with patients and discuss smoking habits. They should provide resources and information needed to act on a tobacco dependency. Barriers to lifestyle changes are already down in the treatment setting, thus the opportunity to introduce smoking cessation initiatives are greatest at that time. But smokers have to be ready to quit, and building a foundation towards that willingness can take time, patience and resources. But with the tools and assistance available in the treatment setting, there are abundant reasons for making the effort to stop smoking. The fact that the recovering addict is more likely to die from smoking than he or she is to die from the addiction is a sobering fact. The time has come to provide effective smoking cessation resources to all who are seeking treatment for substance abuse disorders.

This month's drug is a nasal spray that is potentially addictive. A very important clue towards the identity of this month's drug is that it is commonly encountered in the form of a prescription nasal mist. And no, it is not a new delivery system for cannabis, although cannabis aficionados have dabbled with marijuana-laced nose spray. This month's drug is something of an enigma. This substance was once thought to be a breakthrough formula for the treatment of moderate to moderately severe pain. When approved by the FDA for release to market, the drug's pharmacological characteristics were unique. Utilized mostly in hospital settings, the drug was believed to be a safer, less addictive alternative to powerful opiate analgesics such as Dilaudid, Demerol, and morphine. In many respects, the drug was less prone to abuse, diversion, and addiction. As you may surmise now, this month's drug is an opiate, or more specifically, a synthetic opiate. It is a drug that is still reasonably popular in the worldwide analgesic market today. And although it poses a reduced risk as a drug of abuse, this month's drug can be abused recreationally. To the dismay of its advocates, this drug has hooked many patients who have been prescribed the medication. Abusers of this drug are members of a sect of opiate addicts who are attracted to the highs triggered by other opiate drugs such as pentazocine (Talwin) and buprenorphine (Suboxone). Another important clue to the drug's identity is that like Talwin and Suboxone, this month's drug is a mixed property opiate. It attracts opiate abusers who prefer a mix of traditional sedating opiate effects as well as some edgy, stimulating sensations. This drug will deliver such an experience.

This month's drug is widely distributed as a veterinary medicine, especially in the treatment of equine pain. The drug is not the animal tranquilizer ketamine, although ketamine is currently used to treat a variety of painful conditions in humans. In fact, ketamine is the go-to therapy in the treatment of pain for opiate-addicted humans. But that's another story for another day.

As seen in the treatment of horses with this drug, symptoms of use in humans rarely look like those of opiate abusers. This drug exhibits mixed agonist and antagonist activity at the mu opiate receptor; it is this ligand that is most responsible for triggering the powerful analgesic and euphoric effects of drugs such as heroin and oxycodone. The drug exerts little action over the delta opiate receptor. But at the remaining kappa receptor, the drug is a powerful agonist. And because of this activity, the symptoms associated with the use of this drug can run contrary to the expected pattern of effects generated by other opioids. Signs of intoxication associated with this month's drug include, but are not limited to, the following:

• Constricted pupils with a slow reaction to direct light
• Dry oral cavity
• Slow (not slurred) speech
• Droopy eyelids
• Lethargy
• Slow, deliberate mannerisms
• Over-expressed gestures
• Romberg internal clock: range of normal
• Pulse: range of normal to "up"
• Blood pressure: range of normal to "elevated"

This drug is scheduled and regulated under the terms of DEA Schedule IV. Physicians may dispense this drug in person or by calling a pharmacy. Automatic refills can be authorized for the drug if a physician feels it necessary. This drug is available in two administrative forms: intravenous and intranasal. In the form of the latter, the drug is diverted and abused on the street. This drug is used routinely in hospital settings where it is viewed as having fewer risks in creating dependency. It is also appreciated that unlike other traditional opiates, it achieves analgesia without broadly depressing the central nervous system. Over the years, the drug has been used as therapy in the treatment of migraine headaches. And despite the emergence of the Triptan class of migraine medications, this month's drug has hung on as frontline therapy in treating these very painful headaches. Whereas the Triptan class is used to prevent the fulmination of a migraine headache, this month's drug is an analgesic that reduces the pain and pressure brought on as a consequence of the headache. Evidence suggests that the sooner the drug is administered to early symptoms of onset, the more effective it will be in alleviating the pain. Considering that migraine headaches strike women in greater numbers than men, this drug is more often prescribed to women. But curiously, the drug seems to be overall more efficacious in relieving pain experienced by women than it does in men.

Frequent or chronic use of this drug can result in a classic opiate dependency. Drug withdrawal will occur at about the 12^th hour following the passage of symptoms of intoxication. Withdrawal intensity peaks approximately 72-96 hours following onset. Those who abuse this drug have few choices in how to use it...it is a nasal spray. The I.V. form of the drug is carefully regulated and hard to find outside a hospital. The nasal spray is easy to use. It is quickly absorbed and the onset of its effects is rapid. For a drug user, the characteristics augur well for a predictable and reliable high. Chronic use as a consequence of dependency to this month's drug can cause intranasal bleeding, mucosal swelling, and an overall sense of sinus congestion. Frequent nosebleeds are hallmarks of a chronic user or abuser.

This month's drug is a member of the morphinan class of opioids. It very closely resembles levorphanol, another potent member of the opioids analgesic community. This month's drug became a major analgesic player under the brand name of Stadol. But the company that originally produced this drug and held the patent stopped manufacturing it.

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To be sure, double shot espresso drinks are electric chemical jolts to the human central nervous system. Over the course of time, some of those who might be considered frequent consumers of these drinks have complained of psychotic-like effects, experiences not unlike those that result from chronic use of amphetamines. It has been well established that persistent use of methamphetamine can cause users to experience auditory hallucinations. But not every chronic methamphetamine (or amphetamine) abuser develops a psychosis; there is a growing belief in the rehabilitation world that methamphetamine abuse triggers a latent or underlying psychological disorder that leads to the development of hallucinations. To assess whether typical consumption levels of caffeine can instigate auditory hallucinations, researchers studied 92 recruited individuals who were free of psychosis or other neurological problems and who had not been prescribed psychotropic medications.[1] Participants were evaluated for the combined effects of stress and caffeine consumption on the incidence of auditory hallucinations.

Participants in this study were grouped according to their self-ratings of life stress and their stated levels of caffeine consumption. Participants in this study were required to listen to the song "White Christmas." The music was piped into the laboratory over stereo speakers. Next, the participants donned headphones where they then listened to three minutes of white noise. The participants were asked to document the number of times, if any, they heard "embedded song fragments." These alleged insertions of music were faked; none were actually played over the course of the three minutes of white noise. Compared to individuals with lower levels of stress and low levels of caffeine intake, those with high stress and high levels of caffeine consumption displayed noticeably greater incidence of auditory hallucinations, occasions where "embedded song fragments" were detected in the white noise. These effects occurred most often with those participants who consumed more than five highly caffeinated (defined as more than 200 mg of caffeine per drink) beverages per day.

The importance of this study relates to the impact of concentrated caffeine beverages and the rate of consumption by those people who are under notable environmental stress and who may be prone to psychosis. And because caffeine consumption may increase during times of stress, it may be that environmental factors trigger hallucinatory symptoms that are exacerbated by excessive caffeine consumption.

There was no evidence here that connected low to moderate consumption of caffeinated beverages to hallucinatory events. Perhaps the next step in caffeine research should focus on the potential for energy drinks to trigger these experiences. 

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

Nicotine is arguably one of the most addictive substances known to man. The drug prompts and modulates a variety of central nervous system effects that impact mood, motivation, and relaxation. A recently published study in the Journal of Experimental Biology suggests that we might be able to add neuro-protection from Alzheimer's disease to the list of things that nicotine is capable of doing. Nicotine seemingly protects nerve cells from destruction in rodents who were genetically manipulated to produce defective dopamine neurons. Dopamine and dopamine-producing cells are key players in the development of the dementia that flows from the onset of Alzheimer's disease. Research swirls around the role of dopamine and central nervous system pathways where the transmitter plays a major signaling roll.

Of course the results of this research produced a variety of biological and pharmacological caveats. Not every type of mouse brain experienced the same neuronal protections of these genetically modified mice. Nicotine elevates the levels of dopamine in the brain, a very consequential effect that helps explain why it is addictive. The drug's effects are complicated. And any drug that must be consumed by smoking is a drug whose strategic importance is dubious. Healthcare professionals certainly will not argue for Alzheimer's patients to run out and buy a pack of cigarettes. But the evidence was significant and it has been published in peer-reviewed journals. It looks like the hunt is on to determine the precise mechanism involved with nicotine's neuro-protective effects; sometimes good things come out of the investigation into how bad drugs work.