https://webmail.hhs.gov/exchweb/bin/redir.asp?URL=http://www.cdc.gov/nchs/products/pubs/pubd/hestats/methadone1999-04/methadone1999-04.htm
Increases in Methadone-Related Deaths: 1999-2004 by Lois A. Fingerhut, Office of Analysis and Epidemiology
Introduction
Poisoning deaths include those resulting from accidental overdoses of a drug, being given the wrong drug, taking the wrong drug in error, or taking a drug inadvertently. Poisoning also includes deaths that are unintentional, intentional, or of undetermined intent from ingestion of other solid or liquid substances, or exposure to or inhalation of gases or vapors (1). Such deaths can be defined either by their International Classification of Diseases and Related Health Problems (ICD)-10th revision external cause of injury codes or by their ICD-10 diagnosis codes. The external cause codes have two dimensions that indicate: 1) the broad categories of substances involved such as drugs, alcohol, or other solid or liquid biological substances, gases or vapors, or other substances such as pesticides or unspecified chemicals; and 2) the intentionality of the death, reflecting whether the death was certified as unintentional, a suicide, homicide or legal intervention, or of undetermined intent. The ICD-10 external cause codes used to define poisoning as an underlying cause of death include X40-X49, X60-X69, X85-X90, Y10-Y19, Y35.2 or *U01(.6-.7). These are the codes that have been adopted internationally to define poisoning in the external cause of injury matrix for ICD-10.
Poisoning diagnosis codes are used in conjunction with external cause codes to identify the specific substance(s) or agent(s) responsible. A poisoning death can have one or multiple substances listed on the death certificate; the ICD-10 codes range from T36.0-T65.9. While these codes help to describe a poisoning-related underlying cause, they are not used for underlying cause of death coding (2). Rather, the corresponding external cause code will be designated as the underlying cause.
Methadone is classified separately from other opiates and related narcotics in ICD-10, which has been in use in the United States since 1999, but was not classified separately in ICD-9. Vital statistics data from the period 1999-2004, therefore, provide the first opportunity to examine a 6-year trend in methadone-related deaths in this country. The ICD-10 code for methadone is T40.3. This drug is listed within the overall category, ICD-10 T40, for “Poisoning by narcotics and psychodysleptics (hallucinogens).”
Since 1999, between 73 and 79 percent of poisoning deaths mentioning methadone have been classified as unintentional (3,202 such deaths in 2004), with an additional 11-13 percent being of undetermined intent, 5-7 percent as suicides, less than 1 percent as homicides, and about 1 percent were injuries other than poisoning. Over this same period, only 4-6 percent of deaths where methadone was mentioned were not coded as injury deaths (Table 1).
Trends
The number of all poisoning deaths increased 54 percent to 30,308 over the 1999-2004 period, while the number of poisoning deaths mentioning methadone increased 390 percent to 3,849 (Figure 1). Poisoning deaths mentioning methadone increased from 4 percent of all poisoning deaths to 13 percent of all poisoning deaths. Most recently, all poisoning deaths increased 6 percent from 2003-04, while those mentioning methadone increased 29 percent.
Of all narcotics (ICD-10 T40.0-T40.9) mentioned in poisoning deaths, methadone had the largest relative increases. The absolute number of poisoning deaths mentioning methadone was less, however, than the number of deaths mentioning cocaine (ICD-10 T40.5) or other opioids (T40.2). Other opioids include pain relief drugs such as oxycodone and hydrocodone among others (Table 2). The relative increase in methadone-related poisoning deaths from 1999 to 2004 was greater than for any individual substance in the T36-T65 range of codes (data available upon request).
Age
Age specific rates of methadone death are higher for persons age 35-44 and 45-54 years than for those younger or older. This pattern has been true for most of the 1999-2004 period (Figure 2). Admittedly, the rates are quite low relative to all poisoning, but the patterns are similar in that the rates are high for those in middle-age groups. Among those age 55-64 years, the rate in 2004 was seven times the rate in 1999; for those in each of the 10-year age groups covering the span 25-54 years, the rates in 2004 were 3-5 times the rates in 1999. The largest increase, however, is noted for young persons 15-24 years; the rate in 2004 was 11 times that in 1999.
Table 3 shows data for all deaths for which the underlying cause was unintentional poisoning with a mention of methadone. The number of these deaths increased 414 percent to 3,202 over the 1999-2004 period; that is, the number of deaths in 2004 was five times the number in 1999. State specific comparisons should be interpreted with caution as many of the State-specific data are based on very small numbers. Therefore rather than provide a state-by-state ranking, Table 2 subdivides the states into groups based on ratio ranges (ratio of deaths in 2004 to those in 1999) and then orders the states within the groups alphabetically.
Following are examples of 1999-2004 ratios in states with “large” numbers of methadone–related deaths (greater than 50 for at least 3 of the 6 years): West Virginia (25:1), Kentucky (15:1), Florida and Oregon (14:1), North Carolina and Texas (7:1), Virginia (6:1) and Washington (5:1). New York showed no overall change during the 6 years (1:1).
References
1. World Health Organization. International Statistical Classification of Diseases and Related Health Problems (Tenth revision), volume 1. Geneva, World Health Organization. 1992.
2. MiniƱo AM, Anderson RN, Fingerhut LA, Boudreault MA, Warner M. Deaths: Injuries, 2002. National vital statistics reports; vol 54 no 10. Hyattsville, Maryland: National Center for Health Statistics. 2006.
latest gateway theory paper
https://webmail.hhs.gov/exchweb/bin/redir.asp?URL=http://ajp.psychiatryonline.org/cgi/content/full/163/12/2134
Am J Psychiatry 163:2134-2140, December 2006
Predictors of Marijuana Use in Adolescents Before and After Licit Drug Use: Examination of the Gateway Hypothesis
Ralph E. Tarter, Ph.D., Michael Vanyukov, Ph.D., Levent Kirisci, Ph.D., Maureen Reynolds, Ph.D. and Duncan B. Clark, M.D., Ph.D.
ABSTRACT:
OBJECTIVE: The authors investigated whether the transition from licit drug use to marijuana use is determined by particular risk factors, as specified by the gateway hypothesis. They also evaluated the accuracy of the "gateway sequence" (illicit drug use following licit drugs) for predicting a diagnosis of substance use disorder.
METHOD: Boys who consumed licit drugs only (N=99), boys who consumed licit drugs and then transitioned to marijuana use (gateway sequence) (N=97), and boys who used marijuana before using licit substances (alternative sequence) (N=28) were prospectively studied from ages 10–12 years through 22 years to determine whether specific factors were associated with each drug use pattern. The groups were compared on 35 variables measuring psychological, family, peer, school, and neighborhood characteristics. In addition, the utility of the gateway and alternative sequences in predicting substance use disorder was compared to assess their clinical informativeness.
RESULTS: Twenty-eight (22.4%) of the participants who used marijuana did not exhibit the gateway sequence, thereby demonstrating that this pattern is not invariant in drug-using youths. Among youths who did exhibit the gateway pattern, only delinquency was more strongly related to marijuana use than licit drug use. Specific risk factors associated with transition from licit to illicit drugs were not revealed. The alternative sequence had the same accuracy for predicting substance use disorder as the gateway sequence.
CONCLUSIONS: Proneness to deviancy and drug availability in the neighborhood promote marijuana use. These findings support the common liability model of substance use behavior and substance use disorder.
-----
INTRODUCTION SECTION:
The gateway hypothesis holds that consumption of abusable drugs progresses in orderly fashion through several discrete stages (1, 2). The entire sequence, which is exhibited by only a small minority of drug users, begins with beer or wine and moves progressively through hard liquor or tobacco, marijuana, and finally hard drugs (3). Each stage is thus a component of both a temporal sequence and a hierarchy.
Kandel and Yamaguchi (3) asserted that a causal linkage drives the sequence: "One licit drug is required to make the progression to marijuana use" (p. 71). This claim has not been empirically supported, however. Young et al. (4) observed that marijuana was the first drug used by 42% of a sample of delinquent youths. Other researchers have reported that marijuana use is not a requirement for progression to hard drugs. Golub and Johnson (5) found that 75% of inner-city heavy drug users began using cocaine before using marijuana. These authors also report that 1%–4% of hard drug users skipped both the alcohol/tobacco and marijuana stages (6). Mackesy-Amiti et al. (7) reported that 39% of their sample started using marijuana after they had used hard drugs. Blaze-Temple and Lo (8) reported that 29% of their sample began using marijuana after having used heroin, stimulants, or LSD.
The high rate of nonconformance with the "gateway sequence" notwithstanding, it is nevertheless the most common pattern, although the reasons remain obscure. One possible reason is that specific factors connect each successive stage of drug use comprising the overall sequence. According to Kandel and Yamaguchi (3), "the identification of drug-specific risk factors for progression is technically related to the demonstration of causal linkages between stages" (p. 64). Alternatively, abuse of illicit drugs, whether or not preceded by use of licit compounds, may be more parsimoniously explained by their availability in the social environment and the level of the individual’s liability that is common to all abusable substances. For example, conduct problems in childhood presage consumption of all classes of abusable drugs. Genetic (9–12), neurophysiological (13, 14), neurochemical (15, 16), and behavioral (17, 18) investigations have shown that the same factors are associated with consumption of licit and illicit drugs. Indeed, 100% of the genetic variance in the risk for diagnosis of substance use disorder is common across all illicit substances (10).
Thus, two competing explanatory frameworks have been advanced to explain the transition from licit to illicit drug use. The gateway hypothesis (3) holds that factors specific to the use of each drug determine the transition from one compound to the next in a meaningful causal sequence. The common liability model (19), by contrast, specifies that the level of liability that is common to all abusable compounds accounts for the propensity to transition to illegal drugs.
This unresolved controversy has important policy and practical ramifications. For example, the presumption that specific risk factors are associated with the use of illicit drugs remains the cornerstone of U.S. drug policy (see, for example, Congressional Record, July 1999, pp. H6640–H6642). Similarly, the focus on illicit drugs by the White House Office of National Drug Control Policy tacitly assumes that the predisposing characteristics and the correlates of illegal drug use are different from those of licit drug use. Each perspective also has important implications for prevention of illicit drug use. Interventions framed conceptually within the gateway hypothesis emphasize breaking the pattern of drug use transitions by ameliorating the risk factors that cause use of the next drug in the sequence. The common liability model instead focuses on early childhood development, particularly socialization of normative attitudes and behavior, in which avoidance of illegal behavior, including marijuana use, is established.
In this prospective study, we sought to ascertain whether specific risk factors are associated with the transition from licit to illicit drug use. We used a panel of 35 variables encompassing individual, family, school, peer, and neighborhood characteristics to determine whether youths whose illicit drug use exhibited the gateway sequence are distinguishable from those whose use exhibited a reverse sequence (licit drug use following illicit drug use). We also sought to determine whether the gateway sequence has a superior (or at least different) capacity to predict substance use disorder and its rate of development between late childhood and young adulthood. Contrasting the gateway and reverse sequences provides an opportunity to evaluate the prognostic utility of the gateway pattern. On the basis of mounting evidence of common mechanisms that predispose individuals to consumption of abusable substances (19), we hypothesized that 1) the first two stages constituting the gateway sequence—that is, use of licit drugs (alcohol and/or tobacco) and then use of illicit drugs (marijuana)—do not feature distinct characteristics; 2) in keeping with the common liability model, the propensity to progress to illicit drugs is due to general behavioral deviancy; and 3) there are no differences between youths who exhibit the gateway sequence (with licit drug use preceding marijuana use) and those who exhibit the reverse gateway sequence (with marijuana use preceding licit drug use).
-----------
DISCUSSION SECTION:
The gateway hypothesis holds that abusable drugs occupy distinct ranks in a hierarchy as well as definite positions in a temporal sequence. Accordingly, substance use is theorized to progress through a sequence of stages, beginning with legal, socially acceptable compounds that are low in the hierarchy, followed by use of illegal "soft" and later "hard" drugs ranked higher in the hierarchy. One of the main findings of this study is that there is a high rate of nonconformance with this temporal order. In a neighborhood where there is high drug availability, youths who have low parental supervision are likely to regularly consume marijuana before alcohol and/or tobacco. Consumption of marijuana prior to use of licit drugs thus appears to be related to contextual factors rather than to any unique characteristics of the individual. Moreover, this reverse pattern is not rare; it was observed in over 20% of our sample.
An adjustment style featured by delinquency, affiliation with deviant peers, and low connectedness to school is associated with the transition from licit to illicit drug use. Kandel and Yamaguchi (28) similarly concluded that deviancy and affiliation with nonnormative peers are associated with marijuana use. In effect, the greater the deviancy, the more likely an individual is to use an illegal drug. These findings underscore the need to prevent conduct problems in early childhood to diminish the risk of later illicit drug use.
The main task in prevention of substance use and substance use disorder thus involves promoting normative socialization such that during adolescence, when exposure to abusable substances sharply increases, the values and attitudes required for avoidance of illegal behavior, including marijuana use, will have been established. Toward this goal, fostering the caregiver’s emotional bonding to the child establishes the motivation for long-term investment in child supervision. Periodic home visits by nurses to counsel high-risk pregnant women have been shown to have a positive long-term impact on social adjustment in the women’s children (29). It is also noteworthy that a difficult temperament amplifies the risk of conduct disorder (30). Because parental reaction to children with difficult temperaments commonly features avoidance or harsh punishment, consolidating positive parent-child interactions by potentiating parenting skills facilitates the child’s normative development. Children with difficult temperaments disengage from the parental influence earlier in life than "normal" children (31). Given our finding in this study that low parental involvement predisposed to marijuana use before licit drug use, it would appear to be important to implement interventions directed at improving the quality of parent-child interactions by taking into account the child’s temperament. Attention deficit hyperactivity disorder (ADHD) also frequently presages conduct disorder. Evidence suggests that pharmacotherapy of childhood ADHD reduces the risk of substance abuse (32). Thus, rather than focus on putative drug-specific risk factors, the common liability model emphasizes an ontogenetic framework wherein prevention of early conduct problems reduces the likelihood of illegal behavior, including marijuana use.
The results of this study reinforce the need for conceptual clarity in research on the etiology of substance use and substance use disorder. Our key findings were that 1) there are no unique factors distinguishing the gateway sequence and the reverse sequence—that is, the sequence is opportunistic; 2) the gateway sequence and the reverse sequence have the same prognostic accuracy; and 3) a sizable proportion of substance users begin regular consumption with an illicit drug. These results, considered in the aggregate, indicate that the gateway sequence is not an invariant pathway and, when manifest, is not related to specific risk factors and does not have prognostic utility. The results of this study as well as other studies (4–8) demonstrate that abusable drugs occupy neither a specific place in a hierarchy nor a discrete position in a temporal sequence. These latter presumptions of the gateway hypothesis constitute what Whitehead (33) referred to as the "fallacy of misplaced connectedness," namely, asserting "assumptions about categories that do not correspond with the empirical world."
In contrast to the gateway hypothesis, the alternative common liability model has heuristic potential for quantifying a child’s risk for substance use disorder. Vanyukov and colleagues (19, 27) have described the rationale and method for quantifying the common liability for substance use disorder. They also describe a provisional scale that quantifies liability severity and has discriminative and predictive validity. With further validation of this scale, the empirical foundation will be established to tailor the intensiveness of prevention of substance use disorder to severity of the child’s risk.
Several limitations of this study should be noted. First, the sample was confined to males; inasmuch as there are gender differences in the pattern of initiation and progression of substance use (28), the results may not generalize to females. Second, only the first two stages of the gateway sequence were evaluated, and all licit drugs (beer, wine, liquor, tobacco) were combined into one stage to provide the best opportunity for confirmation of the gateway hypothesis. In early formulations of the gateway hypothesis, beer and wine were theorized to precede tobacco and hard liquor; however, the sequence was subsequently collapsed to combine tobacco and alcohol into one stage. Finally, it was not possible to rule out entirely the absence of unique associations between individual and environmental characteristics and use of a specific type of drug. Although 35 variables were examined, it is conceivable that other factors have a specific association.
The results of this study suggest that general behavioral deviancy and not specific risk factors accounts for illicit drug use. When illicit drug use occurs first, it is very likely due to the opportunity afforded by the neighborhood environment in context of low parental supervision. The probability and rate of development of a diagnosis of marijuana use disorder and alcohol use disorder were the same whether or not there was conformance with the gateway sequence. Evidence supporting "causal linkages between stages," as specified by the gateway hypothesis (3, p. 64), was not obtained. Nor were specific risk factors identified that were related to consumption of each drug. Our results indicate that efforts to prevent marijuana use should utilize strategies directed at averting the development of the characteristics prodromal to the manifestation of behavior problems.
Chronicle article on psychedelic research
Researchers Explore New Visions for Hallucinogens The Chronicle of Higher Education, 6.12.8
https://webmail.hhs.gov/exchweb/bin/redir.asp?URL=http://chronicle.com/weekly/v53/i16/16a01201.htm
After a long hiatus, medical investigators return to studying the benefits of once-banned compounds
By SUSAN BROWN
Recently, 36 people who had never taken hallucinogens before gave them a try. The pill they took launched a daylong psychedelic journey, sometimes fantastic, sometimes frightening. When it was over, a few who took the drug said it was the most meaningful experience of their lives, as momentous as the birth of a first child or the death of a parent. Others wished never to repeat it.
The drug they took was psilocybin, the hallucinogenic molecule found in "magic" mushrooms.
Their tales do not come from an all-night desert trance or a radical festival like Burning Man but from Baltimore, where they participated in an experiment at the Johns Hopkins University Bayview Medical Center.
The study, which began in 2001, explored the drug's ability to induce a mystical state. Published in the journal Psychopharmacology this summer, it was the first federally approved research on psilocybin in humans to be reported in four decades and leads a vanguard of studies that mark a quiet revival of research on psychedelic drugs.
When scientists in the United States and Europe first learned of the mushrooms' strange effects in the 1950s, along with those of related hallucinogens like LSD, research on the topic exploded. More than a hundred published reports cataloged the effects of the drugs, some rigorously, others not so.
Most notorious of the researchers was Timothy Leary, a psychologist at Harvard University who abandoned standard research conventions from the start and relied instead on testimonials, encouraging his subjects to record their experiences in whatever way they felt appropriate. He also took the drug along with his student subjects and conducted his "research" in his home, where participants listened to music and looked at art. Harvard took a dim view of this and, in 1963, declined to renew his contract.
By then, hallucinogens had escaped from the laboratory, and Mr. Leary and others began promoting their use as paths toward spiritual enlightenment. Legislators swiftly made the drugs illegal following alarming reports of bad trips and people arriving at emergency rooms convinced they had gone mad. Public opinion turned against the work, making psychedelic research a bad career move for scientists and a public-relations minefield for research institutions.
"It was a crazy period where these compounds were irresponsibly promoted for recreational use, and their use was widespread," says Roland R. Griffiths, a psychiatrist who led the study at Hopkins. "We got into what appears to me to be a little bit of cultural hysteria about their risks. They were swept out of the research domain."
Dr. Griffiths agrees that the compounds should have been made illegal. "That was a wise and prudent thing to do, given what happened," he says. "But to eliminate them as research tools just doesn't make any sense to me from a scientific point of view, from understanding the nature of consciousness and cognitive and perceptual experience."
Now the inquiry is quietly resuming. Federal agencies have granted a handful of investigators the licenses they need to do the work. And ethics-review boards at universities are approving the studies, after careful (and sometimes lengthy) consideration. Four studies of psilocybin in humans are either in progress or have recently been completed.
The researchers want to learn how to safely induce transcendent states that could help patients make positive changes in their lives or, with lower doses, end intractable pain or halt intrusive thoughts. Advocates hope this is the beginning of a new era of carefully considered exploration of the possible benefits of psychedelic drugs.
Wall Street to Haight Ashbury
Nearly 50 years ago, a Wall Street banker and fungi enthusiast named R. Gordon Wasson first brought hallucinogenic mushrooms to widespread attention in the United States and Europe.
When he heard that traditional Mexican healers used mushrooms to summon their visions, he traveled to Oaxaca to try them himself and emerged from the experience awestruck. "I was seeing the archetypes, the Platonic ideas, that underlie the imperfect images of everyday life," Mr. Wasson later wrote. His article, published in Life in May 1957, gave the fungi their popular name: magic mushrooms.
Within a year, a Swiss chemist had isolated the active chemicals in the mushrooms by sampling the extracts himself to determine which altered his perceptions. He named the compounds psilocybin and psilocin, and his employer, Sandoz Pharmaceuticals, quickly patented the drugs.
In contrast to Mr. Wasson's vigil in a cave guided by a traditional healer, Mr. Leary's first experience with mushrooms was poolside at a Cuernavaca resort. He too was enchanted. Upon returning to Massachusetts, Mr. Leary joined a growing number of researchers who, intrigued by anecdotal accounts of the effects caused by the curious chemicals, began to study their mind-altering properties.
Some thought psychedelic drugs might help the troubled by making them more responsive to psychotherapy. Others hoped a spiritual experience might help alcoholics abstain from drink or convicts renounce crime. Still others thought psychedelics might open a window into the human mind, providing a telling glimpse of how our brains assemble the experience we call consciousness, or explaining how that shatters in mental illnesses like schizophrenia.
In one famous experiment, Walter Pahnke, a physician and minister working on a Ph.D. with Mr. Leary, assembled 20 theology graduate students in the basement of Marsh Chapel at Boston University for a worship service on Good Friday in 1962. The idea was simple: Would psilocybin enhance their spiritual experience, even induce a mystical state? Half were given psilocybin and half nothing at all.
The result was chaos. One participant had a psychotic reaction and needed to be restrained, and those who were disappointed not to receive the drug became bored and disruptive. Still, those who received psilocybin were reportedly transformed by the experience.
But the promise of mind-opening experience also led to widespread misuse, and the researchers' hopes were dashed in 1970 when Congress outlawed hallucinogenic drugs. Federal money and support for the work vanished and commercial supplies were recalled, making further research, even responsible studies, nearly impossible.
As memories of the excesses of that time have faded, a more tolerant public climate has emerged. In 1989 the Food and Drug Administration reorganized its division in charge of drug testing, and the officials in charge of psychedelics signaled they would approve well-designed studies that met established criteria for good clinical research. That shift made it possible for researchers to once again consider studying hallucinogenic compounds.
Among the first to venture forward was Dr. Griffiths of Hopkins. He wanted to see if psilocybin could induce a mystical experience, like those reported by some participants in Dr. Pahnke's Good Friday experiment, but in a safe environment, with careful experimental controls. It took him two years to get the approval of the FDA, a license from the Drug Enforcement Administration, and the permission of the university committee that oversees human research.
The committee at Johns Hopkins reviewed Dr. Griffiths's proposal with unusual caution. "The concern that went into the approval process was unlike anything I've ever experienced in my 30-plus years of doing human research," he says.
The review board wondered if people given psilocybin during the study might go on to abuse the drug. But people have been taking psilocybin for decades, and that history has shown that it is not addictive. Reviewers also worried that a vulnerable subject could be tipped into psychosis by taking psilocybin. Dr. Griffiths and his colleagues ruled out potential participants who had previous mental troubles or even a family member with psychiatric illness.
That screening left them with 36 adult participants who had never used hallucinogens before. All the participants followed some sort of spiritual practice, whether it was participation in organized worship or individual meditation. Curiosity led them to join the experiment: They wished to try psilocybin in a context of self-reflection.
Transcendence and Fear
Each subject took the drug in one of two sessions. During the other, they were given methylphenidate, commonly known as Ritalin, which changed their physiology -- their heart rate, for example -- in a way similar to psilocybin but possessed no hallucinogenic
properties.
Participants spent each daylong session in a room furnished with an Oriental carpet, pictures, and a sofa on which they were encouraged to lie down. Their monitors gave them eye masks and earphones with a playlist of classical music and encouraged them to focus inward. At the end of each session, after the drug wore off, they answered questionnaires designed to assess their spiritual and perceptual experiences.
After taking psilocybin, participants reported intense emotions -- grief, joy, anxiety -- and feelings of transcendence, a reprieve from the normal constraints of space and time. Colors brightened, and some people reported a confusion of senses called synesthesia -- musical tones that take on hues, for example. In contrast, the methylphenidate improved self-control and concentration.
But nearly a third of the participants felt fearful after taking psilocybin, and four of the 36 spent their entire session in unpleasant psychological struggles. Two compared the experience to being in a war, and three said they would never wish to repeat the experience, the research team reports.
"It really underscores the risks of using these kinds of compounds in a nonsupervised, nonresearch setting," Dr. Griffiths says. "It's really not difficult at all to imagine that under uncontrolled conditions these kinds of things could escalate into panic and
engaging in risk-taking behaviors."
Yet two months later, none of the subjects, not even those who reported an unpleasant encounter with the drug, said that the experience had decreased their sense of well-being or satisfaction with life.
Rachel Yehuda, a psychologist who specializes in post-traumatic stress at Mount Sinai School of Medicine and the Bronx Veterans Affairs Medical Center and who was not involved in the study, says she is not concerned by the anxiety experienced by some of the participants in the experiment. "What people don't realize about trauma is that it often ends up being a meaningful experience," she says. "It's a watershed event."
Other researchers hope Dr. Griffiths's article will stand as a benchmark for a new era of psychedelic research. "It sailed through the review process because it was a well-done study by a very recognized researcher," says Harriet de Wit, a behavioral pharmacologist at the University of Chicago who, as a principal editor of Psychopharmacology, shepherded the paper through review.
Dr. Griffiths hopes his work with healthy, well-functioning adults might eventually help those who struggle with addiction. The most effective interventions in use now are 12-step programs. But they rely heavily on a belief in a "higher power," and people who lack
faith have trouble embracing them.
"It's possible that if you could occasion a single primary transcendent experience of the type that was seen in our study," he says, "that that single experience alone would allow somebody subsequently to engage in a 12-step process with renewed interest, vigor, and excitement in a way that they couldn't otherwise."
Charles S. Grob, a psychiatrist at Harbor-UCLA Medical Center, agrees that this line of inquiry is worth pursuing again. Some of the most impressive work in the 1960s was done with alcoholics, he says. More support comes from Dr. Grob's own work 10 years ago with a native church in Brazil. He found that former alcoholics who drank a hallucinogenic herbal brew twice a month as part of a religious ceremony stayed sober.
Dr. Grob is in the midst of a study that asks whether psilocybin might ease the anxiety of people who are dying. In an experiment similar in design to Dr. Griffiths's, he is giving the drug to patients with end-stage cancer. So far, seven patients have received psilocybin, and Dr. Grob has approval to treat five more.
The Harbor-UCLA study follows up on research done by Stanislav Grof and Dr. Pahnke, who worked at the Maryland Psychiatric Research Center, in Baltimore, in the late 1960s, the very end of the psychedelic era. They gave the more powerful hallucinogen LSD to patients with terminal cancer. About two-thirds of their subjects got by with less pain medication as a result. They feared death less or not at all, and their anxiety abated, which is known to help ease pain.
"Their outcomes were best with people who had what they described as a mystical experience, or a full-on, spiritual, transpersonal epiphany," Dr. Grob says.
Because the review board at his institution required a lower dose of psilocybin than he had wanted to use, about half of that used in the Hopkins experiment, his patients' experiences are not as intense. "We're hoping to get approval, when we're done with this group, for a higher dose," says Dr. Grob.
A Target in the Brain
Advances in neuroscience over the past four decades have helped pave the path toward acceptance of this revived line of research. "At one time, when people were just exploring consciousness, it was hard to justify," says John H. Krystal, a psychiatrist at Yale University School of Medicine who was an editor of Psychopharmacology when Dr. Griffiths's paper was submitted.
But once researchers had worked out the molecular basis of the drugs, he says, "then a whole new opportunity to study important aspects of the neurobiology of consciousness opened up."
David E. Nichols, a medicinal chemist at Purdue University who synthesized the psilocybin used in two of the recent studies, agrees. "We know quite a bit more about the brain now than we did then, and human experimental methods are certainly much better," he wrote in a commentary that appeared in the same issue of Psychopharmacology as Dr. Griffiths's paper.
Psilocybin closely resembles serotonin, a neural signaling molecule or neurotransmitter. Calm, happy states coincide with the release of serotonin in the brain. Psilocybin fits serotonin receptors that are especially abundant in a kind of cell in the cerebral cortex that gathers and sorts signals coming in from other parts of the brain.
Psilocybin's effect is to make these "computational" cells more likely to register an incoming signal, Mr. Nichols explains, "potentially amplifying processes that are normally running, but which are not generally apparent in everyday awareness."
Psilocybin could have medical uses if the way it latches onto brain cells remedies an imbalance or malfunction in the serotonin system. In fact, a few patients have found relief from their maladies in magic mushrooms, and those reports of self-medication have led to two recent clinical reports.
The first was spurred by an online discussion group on cluster headaches. The pain from such headaches repeats in regularly timed bouts that typically continue for two to four months, and it strikes quickly, without warning, and rapidly becomes excruciating. Some of the people posting on the site reported relief from LSD or magic mushrooms.
That those drugs would help is not particularly surprising: LSD was initially created as a potential treatment for migraine, and psilocybin is chemically related to sumatriptan, the most commonly prescribed drug for heading off cluster headaches.
One member of the group, a 34-year-old man, had suffered cluster headaches since he was 16, except for a period of two years in early adulthood when he was experimenting with LSD. Later he found he could prevent his attacks altogether if he drank mushroom tea every three months. When that patient contacted a group of psychiatrists at Harvard University's McLean Hospital, R. Andrew Sewell, then a postdoctoral fellow, and John H. Halpern, an assistant professor of psychiatry, decided to follow up.
The team found 53 people who had been treating their headaches with psilocybin or LSD and were willing to release their medical records. When they questioned their subjects by telephone or e-mail about their drug use, they found that for many, the drugs could end the paroxysms of pain in the midst of a headache and extend the pain-free period between attacks, something no other treatment could do.
"Research on the effects of psilocybin and LSD on cluster headache may be warranted," the researchers conclude in their case reports, which were published in the journal Neurology this summer.
No serious opposition to this new work has yet emerged. The Chronicle contacted more than a dozen psychiatrists and psychologists -- including specialists on anxiety and post-traumatic stress -- and none expressed concern about this round of research, in part because the experimenters closely supervised each subject.
Mindful of the past, though, all of the scientists said they did not advocate illegal or indiscriminate use of mushrooms or other hallucinogens. And most said further work should be pursued if the initial results of carefully designed studies showed promise, particularly if they helped patients for whom standard treatments failed.
Quieting Intrusive Thoughts
That is exactly the kind of patient that Francisco A. Moreno hoped to help. Last month Dr. Moreno, a psychiatrist at the University of Arizona, reported success in treating particularly difficult cases of obsessive-compulsive disorder with psilocybin.
Dr. Moreno was inspired to try the drug when a patient reported that the only time his symptoms had ever abated was when he was using magic mushrooms as a young adult. Prozac and similar drugs, which extend the working period of serotonin, sometimes help people with OCD. Others find no relief. Dr. Moreno thought psilocybin might help patients for whom approved drugs and psychotherapy had failed. He gave the drug to nine patients with OCD.
The patients he treats are seriously impaired. They have intrusive thoughts of harming themselves or others, he says, such as "the urge to pinch or bite little babies." But they are not suicidal or homicidal. "They are horrified by their thoughts," he says.
In this small and preliminary study, psilocybin ended the obsessive thoughts and compulsive actions -- such as hand washing -- of some patients completely, and for the first time in their adult lives, for at least the brief follow-up period of 24 hours. The symptoms of all nine subjects markedly improved.
That the drug worked so soon was surprising: Other medications can take weeks to kick in. "Nothing works as quickly and as drastically as these hallucinogens do," Dr. Moreno says.
Despite his promising results, Dr. Moreno is not an advocate for the drug. He published his report quietly in the Journal of Clinical Psychiatry last month. Neither the journal nor the university has alerted the media as they usually do when a promising new treatment is found.
Dr. Moreno hopes his work might lead to the discovery of a safer drug that treats OCD more effectively. He does plan, however, to continue his work with psilocybin, following his patients for longer periods next time, he says. "If this, if any drug, could help people with OCD, with mental illness," he says, "then we should explore it."
Ethics in drug abuse research
https://webmail.hhs.gov/exchweb/bin/redir.asp?URL=http://www.sciencedirect.com/science?_ob=ArticleURL%26_udi=B6T63-4KPP48G-7%26_coverDate=01%252F12%252F2007%26_alid=499852109%26_rdoc=1%26_fmt=%26_orig=search%26_qd=1%26_cdi=5019%26_sort=d%26view=c%26_acct=C000046147%26_version=1%26_urlVersion=0%26_userid=861681%26md5=c24c15a1d8a77e06013026f5f773e972
Drug and Alcohol Dependence Volume 86, Issues 2-3 , 12 January 2007, Pages 95-105
Review
The need for evidence-based research ethics: A review of the substance abuse literature
Emily E. Anderson and James M. DuBois
Abstract
Participants in substance abuse research may be vulnerable for multiple reasons.
International research ethics guidelines and policy statements require that researchers provide extra protections when conducting research with vulnerable subjects, but it is uncertain which measures best protect vulnerable individuals.
Concerns about vulnerability have been translated into only the vaguest regulatory requirements, and very little empirical data exist to guide researchers and ethics review committee members who want to protect participants.
This article reviews two bodies of substance abuse research ethics literature.
First, “normative” articles, that is, articles that discuss ethical issues that may arise in substance abuse research, are discussed.
The resulting taxonomy of ethical issues then guides a review of empirical studies on issues like the informed consent process and the use of financial incentives in substance abuse research.
While the ethical issues in substance abuse research are numerous and well-documented, the evidentiary base for addressing these issues is inadequate.
If any one major theme emerged from the existing studies, it is that many well-intentioned, protectionist concerns – about recruitment incentives, consent comprehension, and drug administration studies – are not supported by empirical data.
While these findings are at best tentative, they suggest how research on research ethics might ultimately benefit participants.
retraction of '02 Ricaurte MDMA paper
Even back in 2003, there was speculation and perhaps knowledge that a second paper woule be retracted. This paper, however, but was a rat study comparing "MDMA" to p-chlorophenylalanine, a serotonin synthesis inhibitor. Methamphetamine, disguised as MDMA, reduced serotonin uptake site density in rats given 20 mg/kg twice daily for four consecutive days.
Pubmed reference: Ricaurte GA. MDMA- and p-chlorophenylalanine-induced reduction in 5-HT concentrations: effects on serotonin transporter densities. Brendon P. Boot, Annis O. Mechan, Una D. McCann, George A. Ricaurte [Eur. J. Pharmacol. 453 (2002) 239-244].
Eur J Pharmacol. 2004 Apr 5;489(1-2):1. No abstract available. PMID: 15063148 [PubMed - indexed for MEDLINE]
MAPS Biblio link to retraction: http://www.maps.org/sys/w3pb.pl?mode=search%26c_pkey=22643%26displayformat=allinfo%26type=citation
MAPS link to 2002 paper https://webmail.hhs.gov/exchweb/bin/redir.asp?URL=http://www.maps.org/sys/w3pb.pl?mode=search%26c_pkey=5478%26displayformat=allinfo%26type=citation
retraction of '02 Ricaurte MDMA paper
> http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1J-%3e%204KRNR3N-1&_coverDate=12/28/2006&_alid=498960439&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=4892&_sort=d&view=c&_acct=C000046147&_version=1&_urlVersion=0&_userid=861681&md5=5035b05ff3717a4ddaf > 4KRNR3N-1&_coverDate=12%2F28%2F2006&_alid=498960439&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=4892&_sort=d&view=c&_acct=C000046147&_version=1&_urlVersion=0&_userid=861681&md5=5035b05ff3717a4ddaf1875f9a3eb71d
> > > European Journal of Pharmacology > Volume 553, Issues 1-3 , 28 December 2006, Page 304 > > Retraction notice to > > “MDMA- and p-chlorophenylalanine-induced reduction in 5-HT > concentrations: Effects on serotonin transporter densities” > > [Eur. J. Pharmacol. 453 (2002) 239–244] > > Brendon P. Boot, Annis O. Mechan, Una D. McCann and George A. > Ricaurte > > > Refers to: > > RETRACTED: > > MDMA- and p-chlorophenylalanine-induced reduction in 5-HT > concentrations: effects on serotonin transporter densities, > > European Journal of Pharmacology, > Volume 453, Issues 2-3, > 25 October 2002, > Pages 239-244 >
anti-drug ads
Viewing anti-mj ads seems to have led to LESS negative views about mj....
--------
http://www.sciencedirect.com/science?_ob=ArticleURL%26_udi=B6VC9-4JW15NF-5%26_coverDate=01%252F31%252F2007%26_alid=498970364%26_rdoc=1%26_fmt=%26_orig=search%26_qd=1%26_cdi=5949%26_sort=d%26view=c%26_acct=C000046147%26_version=1%26_urlVersion=0%26_userid=861681%26md5=fba246a284ea1b78c98ee4a7aedacd25
Addictive Behaviors Volume 32, Issue 1 , January 2007, Pages 114-127
Explicit and implicit effects of anti-marijuana and anti-tobacco TV advertisements
Maria Czyzewsk and Harvey J. Ginsburg
Abstract
Effects of anti-tobacco and anti-marijuana TV advertisements on explicit (i.e., semantic differential ratings) and implicit (i.e. Implicit Association Test, IAT) attitudes toward tobacco and marijuana were compared.
Two hundred twenty nine, 18- to 19-year-old U.S. college students were randomly assigned to anti-tobacco or anti-marijuana PSA viewing conditions. Participants completed a short survey on attitudes to tobacco and marijuana. Afterwards they watched 15 PSAs embedded in a 15-min science program. At the end, all participants completed IAT for marijuana, IAT for tobacco and the assessment of explicit attitudes.
Results of ANCOVA revealed a significant interaction between type of TV PSAs watched and implicit attitudes, F(1,223) = 7.12, p <>
At this point, without further research we can only speculate what might be the behavioral consequence of the dissociation pattern in attitudes to marijuana produced in response to anti-marijuana ads.
Clearly more research is needed [is there ever a case when more research *isn't* needed??] to better understand the interaction between implicit and explicit attitudes in general and more specifically, in the content areas relevant for prevention (e.g., substance use).
Nevertheless, findings from research on smoking behavior seem to provide enough evidence to be concerned about our results suggesting that anti-marijuana advertising might produce unintended change in positive direction in explicit attitudes to marijuana among college students.
That Darned Khat
http://villagevoice.com/news/0647,gardiner,75103,2.html
That Darned Khat In search of New York's most elusive drug
by Sean Gardiner November 21st, 2006 Village Voice
Hamada Alsaedi, a slight 19-year-old, flashes me a distrusting stare as I enter the Eexus Deli & Discount store in Harlem, where he is jammed in a claustrophobically narrow space behind a Plexiglas partition. When I ask another worker about where to get khat, referring to it as a drug, Alsaedi interjects, "It's not drugs. . . . Even the children in my country use it." Alsaedi says he has been in the U.S. since he was seven, but regularly returns home, where he chews khat, the leaf of a shrub/tree called Catha edulis. Highly if not completely Americanized, Alsaedi explains to me how we might decide to use khat, if we—Hamada and Sean—were hanging together in Yemen. "I'd be like, 'Sean, where we gonna chill today?' [Me] 'Let's go over there to the special place' or whatever. 'OK, I'm gonna get some khat.' 'OK.' And we chill."
Khat is used the same way as the leafy version of chewing tobacco, balled into a side of a cheek. But the chewing lasts for hours and hours (usually some liquid— water, tea, or soda—is needed to ward off dry mouth) and the juice is swallowed, not spit out. Although he's been chewing it since boyhood, Alsaedi says the effect is "hard to explain." You become very relaxed while at the same time very energized. You talk a lot but also listen better. It's great for helping you focus. After the initial khat rush, a contemplative state can take over (some have described it as a mild mushroom trip).
Some people claim khat is an aphrodisiac; others say it's the opposite. Apparently it also quells hunger. It's especially helpful on long drives and has become a staple for truckers and taxi drivers and students, he explained. It's also big at weddings, celebrations, and some religious ceremonies.
Alsaedi said he hasn't been able to find khat in the U.S. for years. Although it's apparently dried up here, it's obvious to him why the government is still interested in it.
"The thing is, the U.S. is so protective now, like when you have a little child. They're saying these motherfuckers are all Al Qaeda. But you can't just judge someone for someone else's mistakes. Every village has good people and bad people."
Good point. But I'm not here just to theorize about khat. I want to try some. Time to keep looking.
My search for khat began late in September after the Queens district attorney sent out a press release detailing an arrest for khat possession. In 15 years covering crime, I had never heard of the substance. Apparently, after picking up a 13-pound box of khat, workers at a Queens UPS warehouse tipped off police. As the cops moved in for the pinch, the suspects were still sitting in their car outside UPS contentedly munching mouthfuls of the leaves. The press release went on to surprise me with the news that khat "is in the same legal category as heroin or cocaine."
A computer search quickly revealed references to Black Hawk Down, the 2001 Ridley Scott movie about the U.S.'s botched military raid in Mogadishu. Khat was the substance that supposedly juiced up the Somali warlords' gun-wielding militias. Later, I find that over the past year khat (pronounced "kot") was second only to marijuana in total pounds seized by U.S. Customs agents nationwide—more than double that of cocaine, and 28 times more than methamphetamine.
Just this past summer, authorities busted the first substantial khat-trafficking ring in the U.S. "Operation Somali Express" resulted in 44 men and women arrested in connection with importing of 25 tons of khat the previous 18 months, with an estimated street value of $10 million. The head of New York's FBI office then expressed concern that khat profits were being used to fund terrorists associated with Al Qaeda. On Nightline, a Drug Enforcement Administration official said he feared khat was being "marketed . . . in all cross-sections of our country." And the newscaster ended on this ominous note—"Today's raid is the nation's first attempt to stop this new drug before it's able to take hold. The question is, will it work?"
An interesting question, but I still wanted to know the answer to mine: Where can I find some?
--------------------------------------------------------------------------------
There was a time, not so long ago, when instead of being labeled a Schedule I controlled substance alongside heroin, LSD, and magic mushrooms, khat, which has been cultivated for over 600 years, was considered a cultural custom—a curiosity, not a crime.
In 1924, Dr. Louis Lewin, a pharmacologist, described a traveling friend's first encounter with khat, or kat—it has dozens of different spellings and names—in his Phantastica: A Classic Survey on the Use and Abuse of Mind-Altering Plants.
"When during my travels in Yemen I saw the high, many-storied houses of the mountain villages late at night brilliantly illuminated, and their windows shining in the darkness, I enquired what the inhabitants did at that time of the night. I was told that 'friends and acquaintances meet and sit for hours round the brazier drinking their coffee prepared from the husks and chew their indispensable kat, which keeps them awake and promotes friendly intercourse.' "
Friendly intercourse . . . sounds innocent enough.
The question of whether khat should be recognized internationally as an illegal drug began percolating in 1957, when the United Nations Commission on Narcotic Drugs was asked to take up the question. Fifty years later there still isn't a clear-cut answer.
Over the years, the U.N. commissioned several studies on khat, including a 1975 report that determined cathinone was the chemical that really gives fresh khat its kick. Previously, cathine, which is basically ephedrine, the low-level speed used in diet pills, was believed to be the main active ingredient. Cathinone is many times more powerful, close to amphetamine in its makeup.
Finally, in 1986 the United Nations added cathinone, but not the khat plant, to its list of substances that should be regulated.
While England and most of Europe did not follow suit and still haven't, the Drug Enforcement Administration placed cathinone on its temporary list of controlled substances in 1987. It was permanently made illegal in 1993 after, as the law requires, the Food and Drug Administration did a study on the effects of cathinone. Despite various myths, such as one that khat helped to prevent an outbreak of the plague, the FDA found that too much cathinone is not good for you. The side effects, its study found, included rapid heart rate, increased blood pressure, hyperthermia, headaches, insomnia, anorexia, constipation, gingivitis, and in the case of one longtime user, cerebral hemorrhaging and death.
The FDA reported that a staggering 75 to 90 percent of the men in Somalia and Yemen used khat daily, numbers that have held steady over the intervening years.
On the other hand, the study also says cathinone isn't physically addictive. Dr. Scott Lukas, director of the Behavioral Psychopharmacology Research Laboratory at McLean Hospital in Boston, added that it's important to differentiate between pure cathinone and khat, especially the stuff that arrives in the U.S., which is much less potent than the fresh-picked plant.
Chewed in moderation, Lukas says, "the chances are the person will not get into difficulties with it." In fact, he adds, because it takes hours of chewing to slowly draw the chemicals into the blood system, the khat here is milder on your system than Red Bull or some of these other trendy energy drinks.
Now I really wanted to try some.
--------------------------------------------------------------------------------
Days later, as I enter the office of John Gilbride, head of New York's Drug Enforcement Administration, I remain undecided about the real dangers of khat. Gilbride, soft- spoken and more affable than the average drug enforcer, says it's not his job to sort out the cultural and historical issues around khat. He's just supposed to stop it from getting into the country. Without bravado, Gilbride says Operation Somali Express has "struck a severe blow" to khat's presence in the United States because there isn't another organization of its kind here.
But as Gilbride lays out what's known about khat, my skepticism grows. There's no real related spin-off crime (burglaries, robberies, shootings); it's traded and consumed in private, not out on the street; and there's no proof it has spread beyond the small Somali and Yemeni communities scattered throughout the United States.
So, I ask Gilbride, what's the big deal?
Unlike other drug dealers, Gilbride explains, none of the khat traffickers who have been caught had anything to show for it. No boats, no Escalades, no second homes, no offshore bank accounts, no bling whatsoever. Finally it sinks in—the notion of drug runners from an openly hostile Muslim country taking in millions, with nothing, ostensibly, to show for it. I guess I can see how that might be a concern for someone like Gilbride.
"We know the money from khat sales is not staying in the U.S., it's leaving," he says. "Our task now is to find out where the money is going."
In a way, Alsaedi is right. We do think all these motherfuckers are Al Qaeda.
--------------------------------------------------------------------------------
Like a reformed drunk reminiscing about his days off the wagon, Ammar Sulaiman can almost taste the bitter juice slipping down his throat as we talk inside his father's Hadra-mout Restaurant in Cobble Hill, Brooklyn.
"When I first chewed it, I didn't feel anything. I was like, what's the big deal?" says Sulaiman. "But the more you do it, the better it gets. When you think about something, you really think. When you read a book, you're really into it. When you're listening to a story, you're really imagining it."
Growing up, khat use was so ingrained in everyday life, it was difficult not to chew it, he says. Yemen has a caste system, and if someone from an upper rung offers you some, you have to chew, even if you're against it like Sulaiman's father. There's also a great deal of khat peer pressure. "You can't be the one person who doesn't do it, you'd look like an idiot," he says.
But mostly the reason to chew it is that "there is nothing else to do," he explains, pointing out that in his desperately poor hometown electricity doesn't come on until 6 p.m.
Sulaiman, stocky with short dark hair, carries himself like a man much older than his 25 years. He says his khat consumption is limited to trips home to Yaffa for several reasons. For starters, his father is a strict Muslim who's dead set against it. Also, the khat in the U.S. is excessively expensive (at least $40 and as high as $80 a "bundle," the amount usually chewed in one session, compared to $5 back home for a pile three times as big). And since it arrives five or six days after picking, it doesn't pack the punch of the stuff back home.
But the real reason neither Sulaiman nor any of his Yemeni friends here use khat is they simply can't find it.
Looking around to make sure his father's out of earshot, Sulaiman tells me of the time a few years back when he and some friends decided to get some khat. It used to be sold and used openly in the Yemeni restaurants and stores in Cobble Hill, so they didn't think it'd be a problem. After a day spent independently searching, they all came back empty-handed.
"Since the crackdown on it, " Sulaiman says, "I think everybody's in hiding."
The crackdown he speaks of is twofold: Six years ago, there was a routine bust of three restaurants in the neighborhood, in which nine Yemeni men were arrested and 200 pounds of khat seized. That raid put the community on notice; police weren't tolerating the previously open khat trade anymore. The other part of the crackdown, Sulaiman says, has been the extra law enforcement scrutiny of his community since September 11. Get a Muslim for any infraction and try to flip them for information about terrorism. To that end, there have been visits to Sulaiman's restaurant from snooping cops and several customers suspected of being undercovers or informants inquiring about khat.
But Sulaiman doesn't see the khat- terrorism connection. Al Qaeda are the most fervently religious Muslims and believe khat violates the Koran. As he puts it, "Whoever sells it [khat] would have to be not one of those religious guys."
--------------------------------------------------------------------------------
After weeks of coming up empty, I need to physically see some khat. I'd almost given up on an energy boost, but at this point I could use a morale boost. So I go to the one place where I know they have a lot of it—John F. Kennedy International Airport.
Last year, Customs seized 52,239 pounds of khat, about half a ton each week, at JFK alone. In 2004, over 90,000 pounds of the stuff was seized there. New York is the nation's khat hub.
The U.S. Customs building is located in a huge, nondescript hangar on the ass end of JFK. As I drive out there, I daydream of possible scenes I might be privy to: fired-up Customs agents with drug-sniffing dogs taking down outlaw khat couriers. Or maybe a seizure of a shipment of khat hidden in some ingeniously devious way.
Upon arrival, I'm steered into a conference room to meet agents from Customs, which does the seizing, and Immigration and Customs Enforcement, which does the investigations.
Customs agent Laura Rios starts out by telling me traffickers usually list the khat shipments as being magazines, coffee, or tea, items that would be of a similar weight. Most seizures come from Yemen or Kenya or England, where khat is still legal. Khat used to be shipped in banana leaves to keep it moist, but nowadays most times it's wrapped in newspaper that is wetted before mailing. Because the khat is so odoriferous and the boxes are usually soggy, detecting it is pretty easy, Rios says.
As I press on I notice that, before answering, the agents seem to be first glancing at a Customs supervisor who's sitting in on the session. His job, apparently, is to make my interview as uninteresting as possible.
When I ask Rios where the khat is taken after it's seized, he butts in, "Let's just say to another facility." In the city, out of the city, where? "Let's just say another facility." OK . . . how is it destroyed? "Let's just say it gets destroyed."
After 20 or so minutes of this, we move into the hangar—a gigantic mail room. Despite the fact they tell me 1.3 million pieces of mail move through JFK a day, there are no workers in sight.
Can I see some seizures in action? No, the supervisor says. Instead, I'm led to a desolate corner of the hangar. There, sitting on a hand truck, are five or six boxes of varying sizes. Behind them is a nearly empty fenced-in area with the sign "Khat Cage" on it. My photographer is told not to take pictures of the mail room, and an agent asks me if I could keep my description of the generic-looking boxes of khat generic. They don't want the bad guys "knowing that we know," she tells me. I look at the boxes again to see if I'm missing something.
The unveiling of the khat is, in a word, disappointing. A date on the English newspaper it came wrapped in marks the shipment as 10 days old. The stems and leaves are covered in a thick, white mold. Just a clump of rotting, smelly vegetation.
I later learn that the majority of khat seizures, weight-wise, come from passengers carrying suitcases, usually each filled with 40 or 50 pounds of it. The couriers—usually poor white people from the United Kingdom— are supplied with an airplane ticket, a paid hotel room, and some spending money. Some know it's illegal; others don't. Over 1,000 couriers have been caught smuggling khat into New York over the past five years.
None have been arrested or prosecuted.
Instead, the khat is seized, the couriers deported and placed on a return-restricted list and, in some cases, fined $500. It turns out prosecuting these cases is too difficult because, three days after the khat's picked, the cathinone breaks down and disappears.
Apparently it's hard to hold couriers on suspected possession of twigs.
--------------------------------------------------------------------------------
Cathinone's propensity to disappear has turned 67-year-old Sidney L. Moore into the Perry Mason of the khat world.
Moore knows the chemistry of the plant and its more than 40 alkaloids and the testing procedures as well as anyone alive—certainly far more than cops and prosecutors, from both small and big towns, who are usually involved in their first khat cases. He throws numbers at the jury, like telling them you'd have to chew 650 pounds of khat to squeeze one gram of cathinone out of it. Or chipping an aspirin into a smidgen to show how much actual cathinone another huge shipment contains. He says the defendants don't know from cathinone; they chew it because they've always chewed it. It's just a habit. The juries get it. Sending a man away for such a piddling amount of drugs doesn't fly, "even in the reddest of red states," he says.
Speaking to me on the phone from his Atlanta office, his words come out unhurried and in a Southern drawl. Moore estimates he has handled, from Maine to Texas, about 70 cases, which probably constitutes a majority of the khat prosecutions nationwide. About 10 of them are still pending, 51 or 52 ended in acquittal, and the other eight or nine he lost.
Most of the prosecutions have occurred over the past five years, with many thrown out because of unconstitutional searches.
"We've had so many funny, funny cases," says Moore, set to be the lead prosecutor in the Operation Somali Express case next summer in New York. "It's been like Keystone Kops ever since 9-11. . . . For some reason when these local police forces encounter anyone named Mohamed they're going to consider him a terrorist until proven otherwise." His comment brings to mind the case against the tall, lanky, bearded Somali wedding singer who looked so much like Osama bin Laden, his musician friends took to calling him that. A hotel clerk heard "Osama" and saw the resemblance. You can imagine the rest.
After a string of losses, prosecutors recently changed strategies, forgoing possession cases in favor of conspiracy and money-laundering charges. "By using the conspiracy theory they seek to avoid having to prove there was any cathinone," Moore says. "They just have to prove there was an attempt to obtain cathinone."
Last November, Brooklyn federal prosecutors made such charges stick to Abdirashid Hassan. Despite a heartfelt plea for mercy, "Please, I beg, let me go with my family. Let me raise my kids. I have a beautiful family waiting for me. . . . I would never touch it again," Hassan got banged.
For importing plants (even if it was 20,000 kilos' worth) that at best contained only trace amounts of the illegal substance cathinone, Hassan was sentenced to a minimum seven and a quarter years in prison, the second-longest khat sentence ever handed down in the U.S.
--------------------------------------------------------------------------------
In reading some of Hassan's court documents, I found a reference to khat business being conducted at the Yemen and Somalia Restaurant on West 116th Street. Can this be my salvation at last?
I find the spot on the northern side of the street between Seventh and Eighth avenues, on a block dominated with African shops. Much to my chagrin, the Yemen and Somalia Restaurant has disappeared.
I head down the block and spot an awning for the Masjid Salam mosque. The second-floor mosque is open, but there's no one around to talk to. So I duck into the Addis CafƩ & Deli in the storefront beneath. Sitting at a table with a laptop and a folded copy of The New York Times, owner Mekonnen Tadesse is tapping away at his computer as I approach.
When I tell him what I'm doing, he offers, "The feds think it is a drug so it's hard to get it now."
Tadesse obviously doesn't agree. "It's like drinking a coffee . . . like an espresso."
Tadesse, 46, grew up in the Ethiopian town of Addis Ababa and has lived in the United States for 18 years. He knows a lot of those swept up in Operation Somali Express and says they're all "quality people," not criminals. Most are in or nearing middle age and are hardworking. Their one vice was chewing khat and bullshitting about their homeland.
From his usual table in his deli he has a clear view of the comings and goings of the mosque next door. Since the khat supply has dried up in the past couple years, it seems more people are attending services. He doesn't think it's just a coincidence, nor does Tadesse, who's Christian, think it necessarily a good thing.
"We're going to force these people to become radicalized, like the Taliban. [Without khat] they don't have any alternative but to turn to Islam."
When I ask about the Yemen and Somalia Restaurant, he says several years ago khat was openly used there, but different owners run the place that's there now, the Dibiterie Cheikh Restaurant.
I stop in anyway, hoping to find a holdover from the old days. I meet the manager, Gracya Fall, a pretty, smiling moonfaced woman with a swath of gold cloth in her hair matching her dress, and ask if West Africans also use khat. I puff out my cheek and started making a chewing motion as a visual aid. Fall looks perplexed for a moment and then starts listing foods, "Lamb, beef, chicken." Suddenly I realize she thinks I'm asking if they serve cat.
--------------------------------------------------------------------------------
I'm feeling about as useless as 10-day-old khat—not that I wouldn't settle for some—when a call to Minnesota, which has the largest Somali community in the U.S., bucks me up.
Lieutenant Gregory Reinhardt of the Minneapolis Police Department, supposing, correctly, that I'm not Somali, informs me: "Oh, you and I can never go out and get it. [I'd] buy crack cocaine and marijuana when I was an undercover agent. I'd never be able to buy khat."
Sorry, Greg. I'm not giving up yet.
I hear from a friend that he knows a guy who says he bought khat a couple years back from a bodega at Canal and Essex streets. The outskirts of Chinatown seem an unlikely place for khat, but I'm desperate.
The bodega on that corner is T & Tai Hung Food Market Inc. I figure, even if they are selling it there, it's a long shot they'd sell it to me—a beefy, white guy with short hair who has occasionally been mistaken for a cop.
But I've got nothing to lose. I stick my notebook in my pocket and ask the store clerk, a small bespectacled Asian man with a wispy mustache, if they sell khat. He smiles but doesn't seem to know what I'm talking about. I tell him, "Khat, the plant from East Africa. I was told you guys sell it here."
"Africa? Ah, no, no," he says, smiling.
He seems to be telling the truth. Just to make sure, I walk across the street and watch to see if any Somali- or Yemeni-looking people enter the store. I'm khat profiling.
As I watch a steady procession of Asian customers enter, buy lottery tickets, and leave, I hear a woman with an African-sound ing accent next to me ask for what I think is khat. She's talking to an Asian man who works in the ABA Super Gift store. Maybe I have the wrong place. Maybe the khat dealers are on this side of the street.
The man grunts and continues arranging bags of luggage for sale outside the store, ignoring her. The woman, who is carrying three large garbage bags, demands, "Do you have it or not?" The man grunts yes, and as he shuffles into the store, she says, "I need strong. A strong one."
This is it, I think, finally. I start thinking of how I should approach the guy. Maybe I should stake it out. Or should I enlist the help of someone who looks less like a narc, maybe Hamada or Ammar, to help me buy it? Or should I . . . just give up and leave khat to the small community of ƩmigrƩs who go through even more trouble than I have to get it?
Because, instead of khat, the Asian man emerges from the store holding several carts, the fold-up kind people carry groceries home in.
"Fifteen dollars," he says to the lady.
My search continues.
Methadone advisory
http://www.fda.gov/medwatch/safety/2006/safety06.htm%23Methadone
Dolophine (methadone hydrochloride)
Audience: Pain management specialists, pharmacists, and other healthcare professionals
Indication: Treatment of moderate to severe pain not responsive to non-narcotic analgesics; detoxification of opioid addiction; and maintenance treatment of opioid addiction
FDA notified healthcare professionals of reports of death and life-threatening adverse events such as respiratory depression and cardiac arrhythmias in patients receiving methadone.
These adverse events are the possible result of unintentional methadone overdoses, drug interactions, and methadone's cardiac toxicities (QT prolongation and Torsades de Pointes). The reports underscore the importance of knowing methadone's toxicities and unique pharmacologic properties, including dosing and monitoring recommendations.
-----
http://www.fda.gov/cder/drug/advisory/methadone.htm
FDA Public Health Advisory Methadone Use for Pain Control May Result in Death and Life-Threatening Changes in Breathing and Heart Beat
FDA has received reports of death and life-threatening side effects in patients taking methadone. These deaths and life-threatening side effects have occurred in patients newly starting methadone for pain control and in patients who have switched to methadone after being treated for pain with other strong narcotic pain relievers. Methadone can cause slow or shallow breathing and dangerous changes in heart beat that may not be felt by the patient.
Prescribing methadone is complex. Methadone should only be prescribed for patients with moderate to severe pain when their pain is not improved with other non-narcotic pain relievers. Pain relief from a dose of methadone lasts about 4 to 8 hours. However methadone stays in the body much longer—from 8 to 59 hours after it is taken. As a result, patients may feel the need for more pain relief before methadone is gone from the body. Methadone may build up in the body to a toxic level if it is taken too often, if the amount taken is too high, or if it is taken with certain other medicines or supplements.
To prevent serious complications from methadone, health care professionals who prescribe methadone should read and carefully follow the methadone (Dolophine) prescribing information
FDA is issuing this public health advisory to alert patients and their caregivers and health care professionals to the following important safety information:
Patients should take methadone exactly as prescribed. Taking more methadone than prescribed can cause breathing to slow or stop and can cause death. A patient who does not experience good pain relief with the prescribed dose of methadone, should talk to his or her doctor.
Patients taking methadone should not start or stop taking other medicines or dietary supplements without talking to their health care provider. Taking other medicines or dietary supplements may cause less pain relief. They may also cause a toxic buildup of methadone in the body leading to dangerous changes in breathing or heart beat that may cause death.
Health care professionals and patients should be aware of the signs of methadone overdose. Signs of methadone overdose include trouble breathing or shallow breathing; extreme tiredness or sleepiness; blurred vision; inability to think, talk or walk normally; and feeling faint, dizzy or confused. If these signs occur, patients should get medical attention right away.
FDA recently approved new prescribing information for methadone products approved for pain control. The information in the new prescribing information is based on a review of the scientific literature completed by FDA. A Medication Guide for patients is planned.
LA Times on psilocybin
http://www.latimes.com/news/printedition/la-sci-mushroom19nov19,1,6831099.story?page=1%26ctrack=1%26cset=true
Mushrooms take a trip back to the lab Banned hallucinogens may have medical benefits, but results are unpredictable. By Denise Gellene LA Times Staff Writer
November 19, 2006 Resting on a hospital bed beneath a tie-dyed wall hanging, Pamela Sakuda felt a tingling sensation. Then bright colors started shimmering in her head.
She had been depressed since being diagnosed with colon cancer two years earlier, but as the experimental drug took hold, she felt the sadness sweep away from her, leaving in its wake an overpowering sense of connection to loved ones, followed by an inner calm.
"It was like an epiphany," said Sakuda, 59, recalling the 2005 drug treatment.
Sakuda, a Long Beach software developer, was under the influence of the hallucinogen psilocybin, which she took during a UCLA study exploring the therapeutic effects of the active compound in "magic" mushrooms. Although illegal for general use, the drug has been approved for medical experiments such as this one.
Scientists suspect the hallucinogen, whose use dates back to ancient Mexico, may have properties that could improve treatments for some psychological conditions and forms of physical pain.
Long dismissed as medically useless, the banned mushrooms — a staple of the psychedelic 1960s — are taking a long, strange trip back to the lab.
The medical journal Neurology in June reported on more than 20 cases in which mushroom ingestion prevented or stopped cluster headaches, a rare neurological disorder, more reliably than prescription pharmaceuticals.
In July, researchers at Johns Hopkins University in Baltimore reported that mushrooms could instill a sense of spirituality and connection, a finding that scientists said could lead to treatments for patients suffering from mental anguish or addiction.
The research has been driven in part by the success of mood-altering pharmaceuticals, such as the antidepressant Prozac, which work on the same brain chemicals and pathways.
Nothing scientists have learned so far indicates that recreational use of mushrooms is safe. The psychological effects remain unpredictable. Deaths have been linked to mushroom intoxication. A Ventura County teen was killed by a car two years ago as she wandered naked across the 101 Freeway after eating mushrooms.
Even under the tightly controlled conditions of a clinical trial, some patients have had terrifying experiences marked by anxiety and paranoia; two people in the Johns Hopkins study likened the experience to being in a war.
The drug "takes your thoughts through a prism and turns them around," Sakuda said.
Her drug trip left her with a sense of peace — a serenity she hadn't felt since her diagnosis.
"It was like rebooting a computer," she said.
Drugs' medical history
Forty years ago, the study of hallucinogens in therapy was a mainstream endeavor. The Swiss drug company Sandoz provided pharmaceutical-grade tablets of psilocybin and various researchers explored its use as a treatment for depression and other psychological problems.
Used for centuries during spiritual ceremonies by the Mazatec Indians in southern Mexico, mushrooms helped fuel the counterculture of the 1960s. Author Carlos Castaneda, while a graduate student at UCLA, wrote of his "magical time" with a Mexican shaman who introduced him to mushrooms and other hallucinogens.
In 1970, Congress made it illegal to posses hallucinogens, including psilocybin and LSD, by classifying them as Schedule I, meaning they had no legitimate medical use.
"All research was shut down," said UCLA psychiatrist Dr. Charles S. Grob.
In the late 1990s, regulators began approving experiments again, sparked by discoveries in neuroscience that illuminated the biochemical basis of mood and consciousness. The advances focused on the complex role of the brain chemical serotonin — a neurotransmitter that passes signals between cells.
Spread throughout the brain are a variety of receptors that respond to serotonin. In some instances, a flow of serotonin can alter moods, such as depression, euphoria, anxiety and aggression. The chemical is also believed to be involved with nausea, body temperature and appetite control.
Many hallucinogens, including psilocybin, mimic the action of serotonin on various receptors. When the drugs circulate in the brain, they can amplify, distort and cross signals. Sounds have colors, and motions become out-of-body experiences.
The drugs can trigger emotionally charged states and potentially dangerous behavior. Even the most optimistic psychedelic researchers acknowledge that at best psilocybin will become a special-purpose drug administered under tight supervision because reactions vary.
In addition to the sensory effects, hallucinogens create mental states in which patients become unusually open to suggestion, Grob said.
He wanted to test whether that ability could be used to alleviate the suffering of terminal cancer patients overcome with a sense of hopelessness.
Grob modeled his study after one conducted at Spring Grove Medical Center, a psychiatric hospital near Baltimore.
The Spring Grove patients took LSD. Grob is using psilocybin, which is shorter-acting and considered somewhat less risky. The drug is produced in small quantities under special Drug Enforcement Administration permits.
Grob has given the drug to seven terminally ill cancer patients.
In Sakuda's case, weeks of counseling planted a desire to overcome her fears and sense of isolation. Since her diagnosis, she had avoided friends and kept her feelings bottled up.
The experiment took place in a comfortable hospital room, under the close watch of a medical team. She wore eyeshades and headphones with soft music playing.
Sakuda recalled sensing her husband's sadness over her illness and feeling a burden lifted from her.
"It is not logical. It comes to you like that," she said.
Sakuda died Nov. 10. Her husband, Norbert Litzinger, feels that the drug made a difference. "There was a rebirth around her and it didn't stop."
The power of the drug extends beyond psychological effects. Dr. John Halpern and colleagues at McLean Hospital in Boston have been looking at the ability of magic mushrooms to treat cluster headaches, which affect about 1 million Americans, mostly men.
The pain can be so severe that they are known as "suicide" headaches, occurring like clockwork at the same time each day, or the same month each year. No treatment has been shown to extend remissions from pain.
Halpern examined medical records of 48 patients who had taken hallucinogenic mushrooms and reported in Neurology that the majority of them found partial or complete relief from cluster attacks.
He speculated that the drug acts on the thalamus, a brain region populated with serotonin receptors. A clinical trial is needed to establish whether the mushrooms really work, Halpern said.
"These are not people you'd expect from the drug culture," he said. "They are lawyers, teachers, business owners. They have a painful and debilitating condition, and found meaningful relief."
Clandestine self-treatment
Those who have used hallucinegenic mushrooms in the U.S. to ease their headaches are all lawbreakers.
They have become part of a new mushroom underground. Many of its denizens are like Bob Wold — a 53-year-old maintenance worker and Little League coach who had never taken hallucinogenic drugs before. He knew they could be dangerous.
Wold, who lives near Chicago, said his headaches felt like an ice pick being jammed through his eye. Once, they made him drive his fist through a plaster wall at home. Another time he pounded his head against the shower tiles so hard some of them cracked.
Seeking help, Wold stumbled across a website for cluster headache sufferers touting hallucinogenic mushrooms.
A man he met on the Internet mailed Wold 20 dried brown mushrooms. The recipe called for a very light tea, not strong enough to cause hallucinations.
After that, Wold started growing his own mushrooms.
Wold has formed an organization to fund research aimed at developing a pharmaceutical version of psilocybin.
But at home, he must make sure his crop is well hidden from his young grandchildren.
Former Washington lobbyist Stuart Miller, 49, described his secret life as a mushroom user as "bizarre."
Miller had frequent cluster headaches and carried capsules containing ground mushrooms everywhere. As he passed through security daily on Capitol Hill, or made his way through an airport, Miller worried that a search would uncover the capsules "and my career would be gone."
He was never caught. He has moved to Mexico to care for an aging parent.
Magic mushrooms grow wild in a nearby field.
