Tracking Synthetic Highs

UN office monitors designer drug trade.

Produced by the United Nations Office on Drugs and Crime (UNODC), the Global SMART Update  (PDF) for October provides interim reports of emerging trends in synthetic drug use. The report does not concern itself with cocaine, heroin, marijuana, alcohol, or tobacco. “Unlike plant-based drugs,” says the report, “synthetic drugs are quickly evolving with new designer drugs appearing on the market each year.” The update deals primarily with amphetamine-type stimulants, but also includes newer designer drugs such as mephedrone, atypical synthetics like ketamine, synthetic opioids like fentanyl, and old standbys like LSD.

I have summarized some of the findings below:

The first methamphetamine lab in 15 years has been discovered in Japan. Japanese law enforcement seized a suspected residential methamphetamine laboratory outside of Tokyo, the first such seizure since 1995. Two Iranian nationals were arrested. Given the continuously high price of imported crystalline methamphetamine in Japan, there is an increased likelihood that more domestic manufacturers could emerge.

Record ketamine seizures and use has been reported by Taiwan province of China. The FDA reports that ketamine seizures in the first five months of 2010 alone totaled 1465 KG, nearly 300 KG more than last year. Concurrent increases in use were also noted.

The first methamphetamine laboratory in Turkey was discovered. Local media reported the seizure of the lab, in the southern part of the country. The facility reportedly planned to manufacture 100,000 tablets for retail sale at USD 13.40 apiece. In 2009, Turkey reported its first seizures of methamphetamine totaling 103 KG at Istanbul’s airport, which has become a transit point for methamphetamine traffic from Iran to markets in East Asia.

Law enforcement faces unique challenges when dealing with synthetic drug analogs. Customs officers at Prague’s Ruzyne airport reported arresting a Polish national for transporting a substance initially testing positive for ephedrone, a controlled synthetic stimulant. Confirmatory tests, however, revealed the substance to be mephedrone, an analogue not under international control. The event illustrates the challenges law enforcement face when encountering new synthetic substances not under national or international control.

Amphetamine breathalyzer tests may soon be possible, say Swedish researchers. The June issue of the Journal of Analytical Toxicology report reported that the first breath test for methamphetamine and amphetamine detection was successfully conducted in Sweden. Drugs in the exhaled breath are captured in a filter and analyzed using a combination of liquid chromatography and mass spectrometry. Experimental trials on amphetamine-dependent patients admitted to hospital urgency rooms for overdose provided the same results as traditional drug tests.

The U.S. is expanding controls on precursor chemicals for fentanyl and LSD. The Drug Enforcement Administration (DEA) has designated a compound called ANPP as a precursor chemical for fentanyl, an extremely potent synthetic analgesic. Earlier this year, the DEA proposed new controls over ergocristine, a chemical precursor sometimes used in the manufacture of LSD. Clandestine laboratories in the United States employ it as a substitute for ergotamine and ergometrine, both of which are already under international control.

The U.S. indicts 15 people in one of the largest MDMA busts ever. The U.S. Department of Justice announced that a federal grand jury indicted 15 men linked to one of the country's largest ecstasy manufacturing and trafficking rings. Two storage facilities were also seized during the investigation, yielding about 710,000 MDMA tablets. Law enforcement authorities seized more than 1.1 million tablets in all. Authorities believe that the group had been responsible for the distribution of hundreds of thousands of MDMA tablets each month.

Belize stops large shipments of methamphetamine precursors bound for Mexico. Customs authorities in Belize reportedly stopped two large shipments of phenylacetic acid (PAA), or roughly 46 metric tons. Phenylacetic acid can be used in the manufacture of methamphetamine. Reports suggest the chemical came from China and was ultimately destined for Mexico.

Graphics Credit: http://www.unodc.org/

Anandamide Hits the “Hedonic Hot Spot.”

Marijuana and the munchies.

It’s no secret that marijuana very reliably increases appetite. Recently, research published in Nature has teased out an apparent mechanism by which internal cannabinoids are involved with gut microbiota. This affects inflammation, the metabolism of adipose tissue, and other factors implicated in obesity.

In addition, research published in the Proceedings of the National Academy of Sciences, and blogged about by Neuroskeptic, showed that CB1 cannabinoid receptors on the tongue selectively boost our pleasurable responses to sweet-tasting food. Conversely, drugs that block cannabinoid receptors have been actively pursued as appetite suppressants. One such drug, trade name rimonabant, was disallowed by the FDA on the grounds that it worked so well in the guise of anandamide’s opposite number that it frequently caused debilitating depression in users. But it did appear to reduce appetites.

Neuroskeptic suggests that a CB1 antagonist that only affects specific sites, like taste buds, might be able to lessen the sweet-tooth effect with fewer complications. “Who knows,” he writes, “in a few years you might even be able to buy CB1 antagonist chewing gum to help you stick to your diet.”

We know that cannabinoids make rats and humans eat more. But how, exactly, does that happen? One reasonable hypothesis is that anandamide, other endocannabinoids, and cannabinoid drugs—anything that tickles the CB1 receptors--must increase sensations of palatability, if eaters are to eat more. A group of University of Michigan researchers chose to investigate the theory that “endogenous cannabinoid neurotransmission in limbic structures such as nucleus accumbens mediates the hedonic impact of natural rewards like sweetness.” They went looking for the precise brain location—the “hedonic hotspot for sensory pleasure”—where endocannabinoids do their work. 

 Writing in Neuropsychopharmacology in 2007, the investigators sought to discover “if anandamide microinjection into medial nucleus accumbens shell enhances these affective reactions to sweet and bitter tastes in rats.” And it did. Anandamide “doubled the number of positive ‘liking’ reactions elicited by intraoral sucrose, without altering negative ‘disliking’ reactions to bitter quinine.” Anandamide reliably increased the number of “positive hedonic reactions” the rats showed to sucrose, and never caused any aversive reactions, or increases in water drinking or other behaviors. In addition, the process worked in reverse: “Food-related manipulations, such as deprivation and satiety, or access to a palatable diet produce changes in CB1 receptor density,” leading to higher levels of endogenous anandamide. 

One location in particular, when dosed with endocannabinoids, increased “liking” responses in the rats threefold. A tiny spot, 1.6 millimeters cubed, but the hottest spot of all: the dorsal half of the medial shell of the nucleus accumbens. At that site, cannabinoid receptors and opioid receptors appear to coexist and interact. If this form of colocalization occurs regularly in rats and humans, it would constitute strong support for the idea that “endocannabinoid and opioid neurochemical signals in the nucleus accumbens might interact to enhance ‘liking’ reactions to the sensory pleasure of sucrose.”

As the authors sum it up, “magnifying the pleasurable impact of food reward” appears to be the baseline effect of endocannabinoids on “appetite or incentive motivation.” Because all of this takes place along the brain’s primary reward pathways in the limbic system, the authors conclude that it would be of interest to know “whether other types of sensory pleasure besides sweetness can be enhanced by the endocannabinoid hedonic hotspot described here.”

Mahler, S., Smith, K., & Berridge, K. (2007). Endocannabinoid Hedonic Hotspot for Sensory Pleasure: Anandamide in Nucleus Accumbens Shell Enhances ‘Liking’ of a Sweet Reward Neuropsychopharmacology, 32 (11), 2267-2278 DOI: 10.1038/sj.npp.1301376

Graphics Credit: NIDA

A New/Old Treatment for Opiate Addiction

 

Gov makes naltrexone legit for heroin.

Last week, the government officially sanctioned the use of naltrexone, trade name Vivitrol, for use in the treatment of heroin addiction. Approved years ago by the FDA for use in the treatment of alcoholism, naltrexone is a long-acting opiate receptor antagonist that has been widely used for heroin detoxification, withdrawal, and maintenance for some time. In that light, the official approval was a bit of an anticlimax, and of less scientific interest than naltrexone’s earlier approval for alcohol dependence. 

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. The addict is anesthetized and placed on a respirator, then injected with naltrexone. The result: complete detoxification in a matter of hours, as the naltrexone molecules knock the opium molecules off their receptors. It can be lethal if not carefully controlled and supervised. The problem, as always, is that the detoxified addict is just as vulnerable to heroin addiction as before. Rapid detox does nothing to combat subsequent cravings, and relapse is frequent.

 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.

Naltrexone will be offered as a monthly injection, an approach that has not been widely tested on opiate addicts, but is potentially an advantage over frequent visits to methadone clinics or daily ingestion of other treatment drugs. 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.

 Graphics Credit: http://www.cancercenter.ph/

Does Ketamine Cause Bladder Damage?

Special K and Cystitis.

Normally, Addiction Inbox steers clear of alarmist stories about drug use. A lifetime of wildly overstated verbiage about “false drugs,” as the Firesign Theatre comedy group once delightfully phrased it, has left me wary of drug scare stories. Even obvious cases, like Fetal Alcohol Spectrum Disorder and crack babies, are more nuanced problems than most coverage has alleged.

For years now, rumors about bladder problems in recreational users of ketamine have periodically surfaced. These stories go all the way back to the adventures of Dr. John Lilly, famous for dolphin research, as well as sensory deprivation experiments with LSD, ketamine, and other drugs (wildly overdramatized in the movie, “Altered States”). According to hipster lore, Lilly went through a long period of hourly ketamine ingestion in the 1970s, and ended his days in adult diapers, having lost control of his bladder due to ketamine damage.

To the best of my knowledge, this story has never been officially confirmed. But in the last two years, research has surfaced that tends to bolster the Lilly anecdote. What is disturbing is that today, unlike 40 years ago, ketamine has become a fairly common party drug among young users. The drug technically produces a state of “dissociative anesthesia.”  Treated like a hallucinogen, ketamine was originally a tranquilizer used in veterinary medicine. In 1970, the FDA approved the use of ketamine for humans for the maintenance of anesthesia.

The journey from horse tranquilizer to party drug has eluded drug researchers until quite recently. However, in early 2008, researchers sat up and took notice of a report published in BJU International, a urology journal. “The destruction of the lower urinary tract by ketamine abuse: a new syndrome?”

The report details the discovery by physicians in Hong Kong of 59 ketamine abusers who had been admitted to urology units in local hospitals from 2000 to 2007. Interstitial cystitis, also known as painful bladder syndrome, can vary from mild to severe, and its cause is often not known.  Symptoms include painful, frequent, or urgent urination. The researchers found that 71 % of the patients “showed various degrees of epithelial inflammation similar to that seen in chronic interstitial cystitis. All of 12 available bladder biopsies had histological features resembling those of interstitial cystitis.”

The authors conclude that “secondary renal damage can occur in severe cases, which might be irreversible, rendering patients dependent on dialysis.”

Scary stuff. If this were the only study available, it would be tempting to question the results. As it turns out, the Hong Kong study was neither the first nor the last. What is believed to be the first official report of the problem appeared in 2007 in Urology, documenting the case of nine Canadian ketamine users with bladder complications. The authors, affiliated with the University of Toronto, conclude: “As illicit ketamine becomes more easily available, ulcerative cystitis and potential long-term bladder sequelae related to its use may be a more prevalent problem confronting urologists.”

This year, similar reports from Bristol in the UK were published in Clinical Radiology. Researchers with the National Health Service and the Bristol Royal Infirmary discovered “a series of 23 patients, all with a history of ketamine abuse, who presented with severe lower urinary tract symptoms.”  Various imaging techniques revealed smaller bladder volume, bladder wall thickening, inflammation, urethral strictures, and other bladder pathologies. The patients all reported symptoms similar to those reported by the earlier Hong Kong ketamine users.

The report concludes that “many users are well aware, but are often not forthcoming with this information.” They also maintain that “the key to the effective management of ketamine-induced bladder pathology is early diagnosis.”

 Frequent recreational use of ketamine appears ill advised until more research can confirm the true scope of the problem.

Chu, P., Ma, W., Wong, S., Chu, R., Cheng, C., Wong, S., Tse, J., Lau, F., Yiu, M., & Man, C. (2008). The destruction of the lower urinary tract by ketamine abuse: a new syndrome? BJU International, 102 (11), 1616-1622 DOI: 10.1111/j.1464-410X.2008.07920.x

Mason K, Cottrell AM, Corrigan AG, Gillatt DA, & Mitchelmore AE (2010). Ketamine-associated lower urinary tract destruction: a new radiological challenge. Clinical radiology, 65 (10), 795-800 PMID: 20797465

Graphics Credit: http://theintelhub.com/

Strong Pot: What Do Schizophrenics Think?

Small study asks patients for their opinions.

The theory, fiercely debated in the research community, that strong cannabis can actually cause schizophrenia—or is associated with relapse in schizophrenics who smoke it—is the subject of a small study from Switzerland on outpatient schizophrenics, some of whom were pot smokers.

 A study of this kind, with only 10 subjects, verges on the anecdotal. Nonetheless, it is worth a look, just to see if any verification of the theory lurks therein.

In their paper for the open access Harm Reduction Journal—“Do patients think cannabis causes schizophrenia? A qualitative study on the causal beliefs of cannabis using patients with schizophrenia”—psychiatric workers with the Research Group on Substance Use Disorders interviewed patients who attended an outpatient clinic at the Psychiatric University Hospital in Zurich. The researchers did it because, as the paper states, “patients’ beliefs on the role of cannabis in the pathogenesis of schizophrenia have—to our knowledge—not been studied so far…”

“None of the patients described a causal link between the use of cannabis and their schizophrenia,” the researchers determined. However, several of the schizophrenics did have their own version of a disease model to account for their illness. Five of the patients attributed their schizophrenia to “upbringing under difficult circumstances,” and three placed the blame on “substances other than cannabis (e.g. hallucinogens).” The remaining two patients gave “other reasons.”

Interestingly, four of the patients “considered cannabis a therapeutic aid and reported that positive effects (reduction of anxiety and tension) prevailed over its possible disadvantages (exacerbation of positive symptoms).” The authors conclude that excluding schizophrenic patients from treatment settings because of marijuana use “may cause additional harm to this already heavily burdened patient group.”

Graphics Credit: http://www.salem-news.com

Codeine Blues: End of the Line for an Opiate with Issues

Canada, UK consider phasing out the drug.

Among the many memorable anecdotes that have been uttered at the opening of an AA or NA meeting, surely one of the great ones is this: “I’m an addict, and a heroin junky. I went to the dentist today, and he sent me home with a prescription for Tylenol 3. And I thought: Do I really want to endanger my sobriety over a shitty buzz like codeine?”

Canada and the United Kingdom are ready to phase it out entirely. The U.S. Food and Drug Administration (FDA) issued a warning about it for nursing mothers as far back as 2007. Codeine, widely popular for its low euphoriant effects, and subsequent (if theoretical) decreased potential for abuse, may not be as strong as morphine and dilaudid, but it is perhaps the most commonly prescribed opiate in the world—and it comes with a major flaw. Unlike other opiates, codeine is very unpredictable in its interactions with an enzyme called CYP2D6. This enzyme is a primary workhorse in the body’s process of breaking down and excreting many different drugs. Poor metabolizers produce less of this crucial enzyme, which means that drugs are broken down and excreted at a much slower pace (See my earlier post ).

 Specifically, as two physicians recently wrote in the Canadian Medical Association Journal (PDF),

“polymorphisms occur in the cytochrome P450 isoenzyme CYP2D6 that enhance codeine metabolism to morphine.” In 2007, following the death of an infant nursed by a codeine-using mother, the FDA “warned nursing mothers that if they took codeine after childbirth, their newborns might be at risk for a morphine overdose,” according to a New York Times report.

Alternatively, other metabolizers may have little or no reaction to codeine-based medications. Drugs of abuse severely complicate these enzymatic issues, since addicts and alcoholics are not known for volunteering information about their condition to medical or hospital personnel.

Testing for the enzyme is possible, but not likely to catch on with cash-strapped medical and dental centers. Dr. Noni MacDonald at the University of Halifax and Dr. Stuart MacLeod at the University of British Columbia argue in the CMAJ that these genetic variations “can have potentially serious clinical consequences. The wrong combination can result in toxic levels of morphine, even at conventional doses of codeine.” The younger the user, the more susceptible he or she will be to these effects, “possibly because of age-related maturation differences in the blood-brain barrier.” The authors warned that serious side effects “including life-threatening respiratory depression,” have also been reported in adults.

The ultrafast metabolizing variant of CYP2D6 is not evenly distributed throughout the world’s population. The number of people in danger of experiencing high morphine levels after codeine use range from 40% in North Africa to 3% in Europe, the authors say. Rates in the U.S. are 8%, meaning roughly one in ten Americans risk an adverse reaction when taking codeine.

Since the groups at highest risk are infants and children, nations have taken various steps to mitigate the risk. “Switzerland sets the minimum age for codeine-based treatment at 1- years, the Netherlands at 1 year, the United States at 3 years and Canada at 2 years.”

Despite these controls, the authors strongly argue for “a more direct approach,” calling for doctors to “stop using the prodrug codeine altogether and instead use its active metabolite, morphine. Not only is the metabolism of morphine more predictable that that of codeine, but also it’s cheaper.” So codeine is just not consistently good at what it does. Problem is, an opiate doesn’t have to be good to be great, as innumerable codeine addicts can attest.

The argument in Canada made sense to Britain’s watchdog agency for medicines, the Medicines and Healthcare products Regulatory Agency (MHRA). According to a report in The Independent by science editor Steve Connor, the MHRA “wrote to medical authorities in the UK warning that its experts have advised that all over-the-counter liquid cough medicines containing codeine should no longer be used in children under the age of 18,” and that “the risks of [over-the-counter] cough medicines for children containing codeine outweigh the possible benefits.”

Codeine is typically offered in paired form, with either acetaminophen or aspirin, as protection against opiate abuse. In theory, a drug abuser would be likely to trigger a Tylenol overdose before reaching an opiate overdose on codeine pills. However, it is perfectly possible to maintain an active opiate addiction on prescription Tylenol 3s, Fiorinal, or Phenergan cough syrup, among other drugs.

And finally, I would not be revealing any great secrets by suggesting that the extraction of codeine from a codeine-acetaminophen tablet through basic solubility and filtration procedures may not be something one needs to be a chemistry major to pull off. 

The OTC medicine industry in the UK views all of this as a tired argument. A spokesperson for Britain’s Proprietary Association, which represents over-the-counter manufacturers, said: "There has already been a long-drawn-out discussion of codeine. If its value as a pain reliever had not outweighed the risks then it would have been withdrawn and the point is that codeine still has a value as a pain reliever.”

photo credit: http://www.buzzle.com/

Who Controls Addiction Research?

The ongoing merger wars at the NIH.

As researchers await the National Institute of Health director’s decision on the matter of merging the nation’s two major addiction research agencies, interested parties to the dispute continued to wonder whether the alcoholic beverage industry will weigh in on the matter—with cash.

The National Institute on Drug Abuse (NIDA) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) exist within the large institutional framework of the National Institutes of Health (NIH), and operate under mandates that overlap enough to make them prime candidates for a cost-saving consolidation. Advocates of the merger, most of them advocates for NIDA, also suggest that the research itself will improve as a result of a decrease in “overlapping missions.” (See my earlier post.)

Recently, Nature News suggested the possibility of efforts against the merger from another interested party: “Although the alcohol industry is unlikely to relish its legal product being lumped in for study with street drugs such as cocaine and heroin, it has so far remained silent. US Trade groups including the Beer Institute, the Wine Institute, the American Beverage Institute and the Distilled Spirits Council of the United States all declined to comment for this article.”

DrugMonkey, an anonymous NIH-funded researcher, has noted on his blog: “I’m still betting [the beverage industry’s] entire strategy (if they actually care about this, which I suspect they do) is going to be by trying to get a pet Congress Critter or two to oppose the plan. Spirited opposition can probably block the whole plan.”

 DrugMonkey even notes that by one common yardstick—recent success rates for grant applicants—NIAAA has actually put up better numbers than its larger cousin, NIDA, “something that NIAAA people have been quietly bragging about for the past several years.”

There have been other rumblings. Behind the scenes, some NIAAA proponents have criticized NIDA’s Nora Volkow for what they see as a heavy-handed attempt on her part to steamroll any opposition to the merger.  The battle lines were clearly drawn earlier this year when Volkow testified before the Scientific Management Review Board. Quoted in the NIH Record, a National Institutes of Health publication, Volkow said that “all psychiatric disorders have similar roots involving combinations of genes and environment…. it is a serious problem, a devastating problem, whether you are talking about alcohol or drugs.”  The NIDA director also said she was “impatient” with progress on the matter, arguing that the separation of resources had already resulted in missed research opportunities. “Why put roadblocks in the way of treatment and prevention?”

At the same meeting, acting NIAAA director Dr. Kenneth Warren offered up what has come to be seen as the basic counter-argument: “The best way forward is a structure that increases collaboration all across NIH… nothing is gained by structural merger.” Warren said he favored “a separate, but equal” pair of agencies. “Alcoholism is a much broader issue than simply addiction.”

Here is where it starts to get tricky. The assertion that alcoholism is not simply an addiction distills the disagreement down to its essence, which can be found not so much within the arena of science as within the arenas of morality, ethics, and the law. NIH Director Francis Collins told Science (sub. required): “Alcohol is after all a legal substance and 90% of us at some point in our lives are comfortable with taking it in while the drug abuse institute is largely focused on drugs that are not legal.”

As Maia Szalavitz wrote at TIME Healthland:

There's another, somewhat moralistic argument for keeping the institutes separate. As Dr. Deborah Hasin argued at a February national advisory meeting on the question, “[There is] a need for a public health message more nuanced for alcohol than for drugs, including nicotine. In contrast with drugs, light drinking is not “bad.'’ It was a curious statement from a scientist who is supposedly charged with studying the effects of psychoactive substances objectively.

Does the NIAAA really have any solid, science-based arguments against the creation of a combined research agency?

Just ask them. Officially, the NIAAA has a very long list of reasons why they are just saying no to the merger—which looks, from the NIAAA point of view, more like an acquisition, anyway. Here are some of acting director Warren’s arguments, taken from an appendix to the minutes of the February 3-4 meeting of the National Advisory Council to the NIAAA, over which Warren presided:

--Alcohol use disorders are different than drug addiction. "The genetics of alcoholism differs from the genetics of drug addiction. Prospective studies have shown that the sons of alcoholics are at greater risk for alcoholism than for drug dependence.”

--The existence of certain commonalities in the brain pathways that mediate the rewarding effects of alcohol and other drugs of abuse does not justify the merger of NIAAA and NIDA. "The fact that dopamine is an important neurotransmitter in signaling reward associated with motivational stimuli does not provide a strong rationale for merging institutes.”

 --Most people with AUDs (alcohol use disorders) do not abuse other drugs.  “The large size of the population with AUDs who don’t abuse other drugs and the enormous public health burden of their illness justify NIAAA’s focused approach to research on AUDs, separate from drug dependence.”

--Alcohol differs from other drugs of abuse in the degree to which heavy use damages the brain and other organs. "Alcohol damages multiple organ systems through common mechanisms of toxicity, including oxidative stress, the disruption of critical cell signaling systems, and the generation of toxic metabolites, cytokines, and chemokines. The coordinated study of these multiple organ toxicities is best suited to a single alcohol Institute.”

--The systems approach is essential to the study of alcohol beneficial and adverse effects. "The merger of NIAAA with NIDA to form a new Institute focused on addiction would orphan and dissociate critical programs focused on alcohol and cardiovascular health, liver disease, pancreatitis, fetal alcohol spectrum disorders, immune disorders, myopathy, neuropathy, and brain disorders.”

Almost all of these contentions are open to debate. I believe some of them are just plain wrong. Nonetheless, the notion that a merger of two or more sprawling federal agencies will automatically streamline and strengthen government operations is equally open to question (See Department of Homeland Security). 

But the greater weight of logic, it seems, continues to tip the argument in the direction of a merger. Legal or illegal should have very little to do with it. David Rosenbloom, director of Join Together, said in an excellent article by Bob Curley that a single NIH addiction institute could “yield important science and public health benefits.”

Rosenbloom added that “many individuals with addiction use alcohol and tobacco and drugs at the same time. A broad addiction institute may be better able to design and sponsor clinical, basic, and health services research that matches this real-world reality instead of focusing on just one substance at a time.”