Dirk Hanson

46 posts · 24,994 views

Dirk Hanson is a freelance science reporter and novelist. He is the author of "The Chemical Carousel: What Science Tells Us About Beating Addiction." He has written two previous books—"The New Alchemists: Silicon Valley and the Microlectronics Revolution," and "The Seventh Level: A Novel." He runs the Addiction Inbox blog.

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  • April 6, 2010
  • 03:36 PM
  • 924 views

Impulsivity and Addiction

by Dirk Hanson in Addiction Inbox


The perils of a hypersensitive dopamine system.

The brooding, antisocial loner, the one with impulse control problems, a penchant for risk-taking, and a cigarette dangling from his lip, is a recognizable archetype in popular culture. From Marlon Brando to Bruce Lee, these flawed heroes are perhaps the ones with restless brain chemicals; the ones who never felt good and never knew why (“What are you rebelling against?” “What’ve you got?”).

A recent study at Vanderbilt University, published in Nature Neuroscience, used PET scans and fMRI imaging to suggest that impulsivity and other “antisocial” traits “predicted nucleus accumbens dopamine release and reward anticipation-related activity in response to pharmacological and monetary reinforcers, respectively.”

In other words, the Vanderbilt researchers maintained that so-called “psychopathic traits” like impulsivity and risk taking are linked to addiction and gambling by means of an overly active dopamine system. PET scans of dopamine responses to a low dose of amphetamine showed that “individuals who scored high on a personality assessment that teases out traits like egocentricity, manipulating others, and risk taking had a hypersensitive dopamine response system,” according to a press release from the National Institute on Drug Abuse (NIDA), which funded the study.

Putting a different spin on the matter, NIDA director Nora Volkow said: “By linking traits that suggest impulsivity and the potential for antisocial behavior to an overreactive dopamine system, this study helps explain why aggression may be as rewarding for some people as drugs are for others.”

Lead author Joshua Buckholtz of Vanderbilt said that “the amount of dopamine released was up to four times higher in people with high levels of these traits, compared to those who scored lower on the personality profile.  Buckholtz suggested that a pattern of exaggerated dopamine responses “could develop into psychopathic personality disorder.”

Dr. Robert Cloninger, a prominent addiction researcher, has asserted in the past that children who show a high propensity for risk-taking, along with impulsivity, or “novelty-seeking,” are more likely to develop alcoholism and other addictions later in life.

And, in interviews with the late psychologist Henri Begleiter for my book on addiction science, Begleiter insisted that addicts were stuck with a package of symptoms he called behavioral dysregulation. “Disinhibition, impulsivity, trouble fitting into society—you have certain behavioral disorders in kids who later develop into alcoholics and drug addicts,” he said. The behavior itself doesn’t cause the addiction. The dysregulated behavior is a symptom of the addiction.”

“When you talk to these people, as I have,” Begleiter said, “you see that the one thing they pretty much all report is that, under the influence of the drug, they feel much more normal. It normalizes their central nervous systems. Initially, what they have is a need to experience a normal life.”

So, it wasn’t ducktails, pool halls, tattoos, casual sex, or lack of parental involvement that caused addiction to alcohol and cigarettes and pot, and maybe cocaine and speed and heroin. It wasn’t just the “bad kids.” Irrational anger, impulsive decisions, certain compulsive behaviors like gambling—these behaviors were symptoms of the same group of related disorders that included drug and alcohol addiction, and which involved specific chemicals and areas of the brain related to reward, motivation, and memory.

The trait of impulsivity is a possible marker for addiction that may help explain why it is usually impossible to persuade addicts to give up their drugs by sheer force of logic—by arguing that the drugs will eventually ruin their health or kill them. “They tell me it’ll kill me,” sang Dave Van Ronk, “but they don’t say when.”

Consider the always-instructive case of cigarette smoking. In 1964, the Surgeon General’s Report on Smoking and Health laid out the case for the long-term ill effects of nicotine quite effectively—and millions of people quit smoking. A stubborn minority did not, and many of them still have not. Are they simply being hedonistic and irresponsible? Or are the long-term negative consequences, so dramatically clear to others, simply not capable of influencing their thinking to the same degree? Biochemical abnormalities similar to those predisposing certain people to addiction may also prevent them from comprehending the long-term results of their behavior.

Buckholtz, J., Treadway, M., Cowan, R., Woodward, N., Benning, S., Li, R., Ansari, M., Baldwin, R., Schwartzman, A., Shelby, E., Smith, C., Cole, D., Kessler, R., & Zald, D. (2010). Mesolimbic dopamine reward system hypersensitivity in individuals with psychopathic traits Nature Neuroscience, 13 (4), 419-421 DOI: 10.1038/nn.2510

Graphics Credit: http://www.nature.com/neuro/journal/


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Buckholtz, J., Treadway, M., Cowan, R., Woodward, N., Benning, S., Li, R., Ansari, M., Baldwin, R., Schwartzman, A., Shelby, E.... (2010) Mesolimbic dopamine reward system hypersensitivity in individuals with psychopathic traits. Nature Neuroscience, 13(4), 419-421. DOI: 10.1038/nn.2510  

  • February 24, 2011
  • 03:34 PM
  • 886 views

Smoking and Adolescent Attention Deficit

by Dirk Hanson in Addiction Inbox


Are young smokers risking cognitive impairment as adults?

 Call it “nicolescence.” It’s that time of life when certain 18-and-unders discover cigarettes. Most adult smokers begin their habit before the age of 19, and a majority of adolescents have tried cigarettes at least once. But for some of them—those who were “born to smoke,” in a sense—early exposure to nicotine may influence adolescent cognitive performance in ways that adult exposure to nicotine does not. Furthermore, early exposure may result in “cognitive impairments in later life.”

These provocative notions are raised by a group of researchers at VU University, Amsterdam, The Netherlands, in a paper for Nature Neuroscience. And while the specifics of glutamate activity they have documented are fascinating, the leaps back and forth between adolescent humans and adolescent lab mice are dizzying. Nonetheless, the bold claims made in the paper prompted the scientists “to reconsider our views on the etiology of attention deficits.”

That may be more than many addiction researchers are willing to countenance, but the study makes an intriguing case for long-term effects on attentional processing. The Dutch researchers exposed adolescent rats to nicotine, assessed visuospatial attention and other markers associated with synaptic activity in the prefrontal cortex, and found impaired measures of attention and signs of increased impulsivity in adulthood after five weeks of abstinence. Adult rats exposed to nicotine for the first time did not show similar long-term consequences.

The molecular underpinnings for this phenomenon appear to be reduced glutamate receptor protein levels in the prefrontal cortex. Glutamate is a neurotransmitter involved in attention, among other cortical tasks. Glutamate levels were “altered specifically by adolescent and not adult nicotine exposure” in the lab animals, the researchers found.

The glutamate receptor mGluR2 is the likely culprit.  The researchers report that “a lasting downregulation of mGluR2 on presynaptic terminals of glutamatergic synapses in the prefrontal cortex persists into adulthood causing disturbances in attention…. Restoring mGluR2 activity in vivo in the prefrontal cortex of adult rats exposed to nicotine during adolescence remediated the attention deficit.”

The study concludes: “Not only from a behavioral, but also from a molecular point of view, the adolescent brain is more susceptible to consequences of nicotinic receptor activation.” In other words, there is at least some evidence that the neurotoxic effects of nicotine are potentially more severe in the early developmental stage called adolescence.

The Dutch study is not the only one of its kind. In 2005, Biological Psychiatry published a report on cognition in which adolescent smokers “were found to have impairments in accuracy of working memory performance irrespective of recency of smoking. Performance decrements were more severe with earlier age of onset of smoking.”

And a 2007 study published in Neuropsychopharmocology, based on testing and fMRI scans of 181 male and female adolescent smokers, concluded that “in humans, prenatal and adolescent exposure to nicotine exerts gender-specific deleterious effects on auditory and visual attention…” Boys were more sensitive than girls to attention deficits involving auditory processing, while girls tended to show equal deficits in both auditory and visual attention tasks. 

Counotte, D., Goriounova, N., Li, K., Loos, M., van der Schors, R., Schetters, D., Schoffelmeer, A., Smit, A., Mansvelder, H., Pattij, T., & Spijker, S. (2011). Lasting synaptic changes underlie attention deficits caused by nicotine exposure during adolescence Nature Neuroscience DOI: 10.1038/nn.2770

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Counotte, D., Goriounova, N., Li, K., Loos, M., van der Schors, R., Schetters, D., Schoffelmeer, A., Smit, A., Mansvelder, H., Pattij, T.... (2011) Lasting synaptic changes underlie attention deficits caused by nicotine exposure during adolescence. Nature Neuroscience. DOI: 10.1038/nn.2770  

  • May 24, 2010
  • 06:11 PM
  • 802 views

X-ed Out.

by Dirk Hanson in Addiction Inbox


Another look at MDMA and serotonin.
A study by Canada’s Centre for Addiction and Mental Health (CAMH) has confirmed earlier findings that chronic users of ecstasy (MDMA) have abnormally low levels of serotonin transporter molecules in the cerebral cortex.
While a decade of research on the effects of ecstasy on brain serotonin has been controversial and largely inconclusive, the latest study used drug hair analysis to confirm levels of MDMA in 49 users and 50 controls. An additional division was made between chronic X users who also tested positive for methamphetamine, and those who did not. Regular usage of MDMA was defined as two tablets twice a month.
The Canadian study, funded by the U.S. National Institute on Drug Abuse (NIDA) and published in the journal Brain, suggests that the serotonin surge responsible for ecstasy’s effects results in a net depletion in regular X users. That is not a new finding--but the Canadian study goes further, suggesting that the serotonin depletion is localized in one area of the brain.
“We were surprised to discover that SERT was decreased only in the cerebral cortex and not throughout the brain,” said study leader Stephen Kish in a press release, “perhaps because serotonin nerves to the cortex are longer and more susceptible to changes.”
Low SERT levels in the cerebral cortex were found in all X users, with or without amphetamine. Dr. Kish noted that the CAMH findings replicate what Kish referred to as “newer data” from Johns Hopkins University. In 1999, a controversial serotonin study of ecstasy users at Johns Hopkins laboratory was criticized for overestimating the level of danger posed by ecstasy-induced serotonin impairments.
Okay, the finding is becoming more robust. But what does it mean? According to co-author Isabelle Boileau, a low SERT level does “not necessarily” indicate structural brain damage. “There is no way to prove whether low SERT is explained by physical loss of the entire serotonin nerve cell, or by a loss of SERT protein within an intact nerve cell.”
For his part, Dr. Kish indicated that his concerns centered on the connection between lower serotonin measurements and MDMA tolerance levels. “Most of the ecstasy users of our study complained that the first dose is always the best, but then the effects begin to decline and higher doses are needed,” he said. “The need for higher doses, possibly caused by low SERT, could well increase the risk of harm caused by this stimulant drug.” The published study concluded that “behavioural problems in some ecstasy users during abstinence might be related to serotonin transporter changes limited to cortical regions.”
However, in addition to the confounding variable of methamphetamine (see my post, “How Pure is Ecstasy?”), it remains unclear whether the SERT alterations detected in the study are transient or permanent. Moreover, the nature of the link that “might” exist between lower SERT levels and cognitive impairment in the brains of regular ecstasy users remains a subject of dispute in the drug research community, as in this earlier post.  (And just to emphasize that drugs are complicated things, a spate of promising recent research has suggested that ecstasy might be an effective option for treating people with post-traumatic stress disorder).
The CAMH, affiliated with the University of Toronto, is Canada’s largest mental health and addiction teaching hospital.

Kish, S., Lerch, J., Furukawa, Y., Tong, J., McCluskey, T., Wilkins, D., Houle, S., Meyer, J., Mundo, E., Wilson, A., Rusjan, P., Saint-Cyr, J., Guttman, M., Collins, D., Shapiro, C., Warsh, J., & Boileau, I. (2010). Decreased cerebral cortical serotonin transporter binding in ecstasy users: a positron emission tomography/[11C]DASB and structural brain imaging study Brain DOI: 10.1093/brain/awq103
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  • June 3, 2011
  • 08:45 PM
  • 785 views

For Smokers, Nowhere to Run and Nowhere to Hide

by Dirk Hanson in Addiction Inbox


(With love and apologies to Martha and the Vandellas.)

That wonderful song goes on to declare:

'Cause I know
You're no good for me
But you’ve become
A part of me.

The song is not about cigarette addiction, but it could be. Full Disclosure: I smoked cigarettes myself for almost 25 years. And then, after several failed attempts, I quit. I out myself on this subject because a paper from the May 25 issue of the New England Journal of Medicine (NEJM) decries what the authors call the “denormalization” of smoking—and I find myself agreeing with them, smokeless though I may be. I recently visited New York, coincidentally on the day that smoking outdoors in New York City became illegal. Okay, that’s not quite fair to say—it became illegal to smoke in Central Park, or at Brighton Beach, or along the newly pedestrian mallways of Times Square. There is no smoking along the High Line. There is no smoking at any park, beach, or pedestrian mall. As both the tobacco industry and anti-smoking activists well know, this was an iconic victory that has the potential to change smoking laws in virtually every other American city.

It’s a fascinating progression, starting in the 70s when the Civil Aeronautics Board decreed non-smoking sections on domestic airline flights, to the recent New York City Council Decision to ban smoking en plein air, so to speak. Thomas Farley, New York City Health Commissioner, summed it up as follows in a public hearing: “I think in the future, we will look back on this time and say ‘How could we have ever tolerated smoking in a park?’”

I’m not so sure on that, myself. James Colgrove, Ronald Bayer, and Kathleen Bachynski of the Mailman School of Public Health at Columbia University wrote the paper, entitled “Nowhere Left to Hide? The Banishment of Smoking from Public Spaces,” in the NEJM. The authors note that more than 500 towns and cities in 43 different states have already enacted laws banning smoking “in outdoor recreation areas.” At first, as the authors summarize the history, it all seems like a sensible compromise, built on common courtesy. First airplanes and buses, then restaurants and bars, began setting aside seats for non-smokers. By the early 90s, the first data on secondhand smoke was rolling in. Schools, convention centers, and finally even private workplaces either banned smoking or created smoke-free areas. But even then, the primary motivator, according to the researchers, was that secondhand smoke was “unpleasant and annoying,” not deadly. Smokers weren’t being asked to refrain from public smoking for the good of their own health, but as a courtesy to others.

The solid scientific evidence kept accumulating, however—even though tobacco cigarettes were, and still are, completely legal products for adult Americans to purchase and consume if they so choose. Now the arguments shifted to the innocent bystanders, those within the six-foot ring, the immediate smoke zone surrounding a smoker, and the elevated risk of lung cancer, heart disease, and asthma that smokers were subjecting them to. In 1993, the Environmental Protection Agency (EPA) classified secondhand smoke as a Class A carcinogen, and more school, stadiums and offices proscribed smoking.

So far so good, really, from a public health standpoint. But now comes the bend in the road. Suddenly, parks and beaches were being added to the no-smoking roster. “As the zones of prohibition are extended from indoor to outdoor spaces, however, the evidence of physical harm to bystanders grows more tenuous.” In 2008, the authors report, “The editor of the journal Tobacco Control dismissed as ‘flimsy’ the evidence that secondhand smoke poses a threat to the health of nonsmokers in most outdoor settings.”

This confusion was much in evidence at public hearings last fall on the proposed outdoor smoking bans. While Health commissioner Farley argued that 57% of New Yorkers showed nicotine by-products in their blood, he also argued that exposing young children to adults in the carnal act of smoking was detrimental to the public health and welfare. “Families,” he said, “should be able to bring their children to parks and beaches knowing that they won’t see others smoking.” This is really quite an astonishing assertion, given the range of bad habits youngsters are exposed to as they go about a normal day in the adult world. The authors are particularly concerned about this push to stigmatize smokers. “Given the addictive nature of nicotine and the difficultly of quitting smoking, strategies of denormalization raise both pragmatic and ethical concerns.” Furthermore:

The decline in U.S. smoking rates since the 1960s has coincided with the development of a sharp gradient along the lines of socioeconomic status. Whereas about one fifth of all Americans are smokers, about one third of those with incomes below the federal poverty level smoke. These data are especially pertinent to the question of bans in parks. Since smokers are more likely to be poor and therefore dependent on free public spaces for enjoyment and recreation, refusing to allow them to smoke in those places poses potential problems of fairness.

The anti-tobacco movement, frustrated by the slow pace of gains over several years of active efforts, with rates of smoking remaining essentially unchanged, has to face the fact that an outright ban on cigarettes is a ticket to black market, crime syndicate hell. But a de facto ban is something altogether different, and “steadily winnowing the spaces in which smoking is legally allowed may be leading to a kind of de facto prohibition.” More and more employers prohibit smoking in doorways, within ten feet of doorways, anywhere on university campuses, and so on. No one has voted to make cigarette smoking illegal. But the public space in which this legal activity can be pursued is disappearing. And here is where the tough questions start: “In the absence of direct health risks to others, bans on smoking in parks and beaches raise questions about the acceptable limits for government to impose on conduct,” the authors conclude. Not to mention issues of personal autonomy, individual choice, and the stigma attached to addictive behavior. Perhaps the ACLU will soon take an interest in the civil rights of outdoor smokers, where the only health being hazarded is the smokers’ own.

Colgrove J, Bayer R, & Bachynski KE (2011). Nowhere Left to Hide? The Banishment of Smoking from Public Spaces. The New England journal of medicine PMID: 21612464

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Colgrove J, Bayer R, & Bachynski KE. (2011) Nowhere Left to Hide? The Banishment of Smoking from Public Spaces. The New England journal of medicine. PMID: 21612464  

  • March 23, 2010
  • 04:35 PM
  • 763 views

Meth Babies—Fact or Fiction?

by Dirk Hanson in Addiction Inbox


Research team finds brain abnormalities.

When it came to babies born to crack-addicted mothers, the media went overboard, creating a crisis in the form of an epidemic that never quite was. By contrast, when it came to babies born to alcoholic mothers, Fetal Alcohol Syndrome went unrecognized in the science and medical community until 1968.


Now comes a study on prenatal methamphetamine exposure in The Journal of Neuroscience, headed up by Elizabeth Sowell of the University of California, Los Angeles, with support from both the National Institute on Drug Abuse (NIDA) and the National Institute of Alcoholism and Alcohol Abuse (NIAAA.) The report garnered considerable media attention. “We know that alcohol exposure is toxic to the developing fetus and can result in lifelong brain, cognitive and behavioral problems,” Sowell said in a press release. “In this study, we show that the effects of prenatal meth exposure, or the combination of meth and alcohol exposure, may actually be worse.”

It makes sense that meth might effect the health of unborn children.  There is a modest body of research to support the notion. The Sowell study points a finger at the caudate nucleus, a brain region involved with learning and memory.  The study showed that the caudate nucleus of the meth-using group was reduced in size. “Identifying vulnerable brain structures may help predict particular learning and behavioral problems in meth-exposed children,” the press release optimistically states. And the potential problem is real enough: More than 16 million Americans have used meth, according to government numbers. An estimated 19,000 of these users are pregnant women.

But is this particular study a definitive one? The icing on the cake? To begin with, the press release from The Journal of Neuroscience admits to a major problem right up front: “About half of women who say they used meth during pregnancy also used alcohol, so isolating the effects of meth on the developing brain is difficult.”  Even in cases of meth exposure only, there are a host of negative behavioral factors that often accompany meth addiction (bad nutrition, minimal health care, poor health) that can significantly effect fetal development.

The study team compared the MRI brain scans of 61 children: “21 with prenatal MA (methamphetamine) exposure, 18 with concomitant prenatal alcohol exposure (the MAA group), 13 with heavy prenatal alcohol but not MA exposure (ALC group), and 27 unexposed controls. While finding “striatal volume reductions,” as well as increases in the size of certain limbic structures in both groups with meth and/or alcohol exposure, the researchers conclude that striatal and limbic structures “may be more vulnerable to prenatal MA exposure than alcohol exposure.” However, that conclusion was apparently reached despite the fact that only 3 of the 61 children under study were born to mothers who did meth, and meth only, during pregnancy.

Furthermore, there is significant controversy over brain scan studies that measure gross anatomical changes in the size of specific brain regions, rather than brain region activity based on blood flow.

Is there other evidence for the danger of meth use during pregnancy? There is, but as is frequently the case, some of the best evidence comes from animal studies. A 2008 guinea pig study by Sanika Chirwa
showed neural damage to the hippocampus, another region involved in memory, in newborn animals with prenatal meth exposure. Furthermore, the newborn animals showed an impaired ability to distinguish novel objects from familiar ones.

In 2006, a study at Brown Medical School, published in Pediatrics , found that newborns exposed to meth during pregnancy were born “small for gestational age,” meaning they were born full-term, but smaller than babies not exposed to meth in utero.  According to study author Barry Lester, “Children who are born underweight tend to have behavior problems, such as hyperactivity or short attention span, as well as learning difficulties.”

However, Lester added an important caveat in a Brown University press release : “I hope that the ‘crack baby’ hysteria does not get repeated. While these children may have some serious health and developmental challenges, there is no automatic need to label them as damaged and remove them from their biological mothers.”

Similar caution was urged by the authors of a 2009 report in the Journal of Developmental and Behavioral Pediatrics: “Efforts to understand specific effects of prenatal methamphetamine exposure on cognitive processing are hampered by high rates of concomitant alcohol use during pregnancy.”

In 2005, an open letter from the Center for Substance Abuse Research at the University of Maryland warned about the dangers of hyperbole, calling upon the media and public officials to “stop perpetuating ‘meth baby’ myths.” The Center argued that “The terms ‘ice babies’ and ‘meth babies’ lack medical and scientific validity and should not be used,” and requested that “policies addressing prenatal exposure to methamphetamines and media coverage of this issue be based on science, not presumption or prejudice.”


Sowell, E., Leow, A., Bookheimer, S., Smith, L., O'Connor, M., Kan, E., Rosso, C., Houston, S., Dinov, I., & Thompson, P. (2010). Differentiating Prenatal Exposure to Methamphetamine and Alcohol versus Alcohol and Not Methamphetamine using Tensor-Based Brain Morphometry and Discriminant Analysis Journal of Neuroscience, 30 (11), 3876-3885 DOI: 10.1523/JNEUROSCI.4967-09.2010


Smith, L., LaGasse, L., Derauf, C., Grant, P., Shah, R., Arria, A., Huestis, M., Haning, W., Strauss, ... Read more »

  • July 9, 2011
  • 09:11 PM
  • 760 views

Teachable Moments in the Life of a Cigarette Smoker

by Dirk Hanson in Addiction Inbox


Child surgery makes smoking parents more likely to try quitting.

Here’s a strange one: Doctors at Mayo Clinic wanted to find out whether children undergoing surgery had any effect on the smoking behavior of their parents. And it did—but the effect appears to be short-lived.

The Mayo researchers began from the already well-tested proposition that smokers who have surgery are more likely to quit smoking. In fact, they quit at twice the rate of smokers who haven’t had surgery. Not hard to understand, intimations of mortality and all that. They pass through a teachable moment, the scientists write in Anesthesiology, defined as “an event that prompts behavioral change.” As for smokers with kids, doctors have always had recourse to two tactics for creating teachable moments for cigarette cessation. First, they could point to increased illness and asthma in the innocent children of smokers. And when that didn’t work, they could throw in the cold fact that children exposed to secondhand smoke have a higher risk of respiratory complications during and after surgical anesthesia. And in a further queasy irony, “the increased frequency of conditions such as middle ear diseases caused by secondhand smoke may also make it more likely that children will require surgery.”

For documentation, the investigators turned to the massive National Health Interview Survey (NHIS), a questionnaire served up annually to 35,000 households by personal interview. About 12% of children in the NHIS survey in 2005 were exposed to secondhand smoke. Of the thousands of children undergoing surgery, there was an increased likelihood that a parent of one of them would inaugurate a no-smoking attempt. But these quitters were no more likely to succeed in their attempt than any other quitters.

However, “parents having surgery within the previous 12 months was associated with more quit attempts, more successful attempts, and a greater intent to quit among those still smoking.” What happened to the indestructable bond between parent and child? It appears that concerns about one’s own health trump concerns about the health of offspring when it comes to quitting cigarettes. “We can only speculate about why surgery was a significant factor associated with sustained abstinence when experienced by the smoker but not the smoker’s child.”

There are plenty of limitations to these kinds of self-reported surveys, but it is hard not to speculate, along with the researchers. One obvious implication: the chances of a smoker quitting are at their maximum when parent and child both have surgeries.

“Our current findings suggest that having a child undergo surgery can serve as a teachable moment for quit attempts,” said Dr. Warner. “The scheduling of children for surgery may present us with an opportunity to provide tobacco interventions to parents, who are apparently more motivated to at least try to quit – but who need assistance to succeed.”

Shi, Y., & Warner, D. (2011). Pediatric Surgery and Parental Smoking Behavior Anesthesiology, 115 (1), 12-17 DOI: 10.1097/ALN.0b013e3182207bde

Photo Credit: http://special-needs.families.com/... Read more »

  • April 3, 2011
  • 06:26 PM
  • 756 views

When Smokers Move

by Dirk Hanson in Addiction Inbox


Is your new house a thirdhand smoke reservoir?

In the first published examination of thirdhand smoke pollution and exposure, researchers at San Diego State University discovered that non-smokers who move into homes purchased from smokers encounter significantly elevated nicotine levels in the air and dust of their new homes two months or more after moving in.

100 smoking households and 50 non-smoking households participated in the study, which was published in Tobacco Control. The researchers tested for surface nicotine levels in living rooms and bedrooms, took finger nicotine concentrations, collected dust and air samples, and measured urine concentrations of the nicotine breakdown product cotinine.

So, what faces non-smoking new homeowners when they take up residence in a smoker’s former home? “Air nicotine concentrations were 35-98 times higher than those found in non-smoker homes,” the investigators write. “Dust and surfaces showed nicotine levels approximately 12-21 and 30-150 times higher, respectively, than the reference levels in non-smoker homes.”

The homes had been vacated a median of 62 days, and tests on the new residents were conducted a median of 34 days after the move. “Nicotine levels found on the index fingers of non-smokers residing in former smoker homes were 7-8 times higher” than those residing in non-smoking homes. What makes this even more noteworthy is that most of the smokers’ homes “underwent cleaning and many were repainted and had carpets replaced before new occupants moved in.” In addition, “smoker homes remained vacant for on average an extra month,” all of which suggests that smoking has a host of economic side effects we are only beginning to pin down.

“In summary,” say the researchers, “these findings demonstrate that smokers leave behind a legacy of thirdhand smoke (THS) in the dust and on the surfaces of their homes that persists over weeks and months.” But do these numbers rise to the level of a legitimate health and safety concern?  After all, an exposure of 150 times more cigarette smoke than the background nicotine pollution level of essentially zero doesn’t necessarily mean a hazardous layer of leftover smoke. 

Unless, possibly, you happen to be a small child who likes to crawl around on everything you can reach, wearing only your diapers, while licking absolutely everything you come across and simultaneously “ingesting non-food items,” as the researchers put it. In that case, your exposure to the nicotine, phenol, cresols, naphthalene, formaldehyde, and tobacco-specific nitrosamines (all combining in unknown ways with other pollutants and oxidants in the home environment), and the potential effect of that exposure on your immature immune system, might be high enough to raise the concern level of your parents.

Matt, G., Quintana, P., Zakarian, J., Fortmann, A., Chatfield, D., Hoh, E., Uribe, A., & Hovell, M. (2010). When smokers move out and non-smokers move in: residential thirdhand smoke pollution and exposure Tobacco Control, 20 (1) DOI: 10.1136/tc.2010.037382

Photo Credit: quit-smoking-central.... Read more »

Matt, G., Quintana, P., Zakarian, J., Fortmann, A., Chatfield, D., Hoh, E., Uribe, A., & Hovell, M. (2010) When smokers move out and non-smokers move in: residential thirdhand smoke pollution and exposure. Tobacco Control, 20(1). DOI: 10.1136/tc.2010.037382  

  • May 13, 2010
  • 09:30 PM
  • 735 views

Cocaine Treatment and the Stroop Test

by Dirk Hanson in Addiction Inbox


Treatment dropouts do poorly on color/word match.
It’s commonly used to demonstrate behavioral inhibition, but it’s also a nifty parlor game. It is called the Stroop Test, and it plays off the fact that people are far better at reading words than they are at intentionally ignoring them. To prove it, John Ridley Stroop’s 1935 Ph.D. thesis showed how difficult it is to interfere with the automatic processing of words. In the basic Stroop test, a list of color names is presented. However, the word green might be printed in red ink, and the word red might be printed in blue ink. The task is to quickly name not the word itself, but the color of the word. As an example, for the word “green” printed in red ink, the correct verbal answer is “red.” Because of a phenomenon called directed attention, this is hilariously difficult to do. The subject must actively inhibit the automatic response—reading the word—in order to do something else.
What’s all this got to do with drug addiction?
Psychologists have known for some time that drug craving focuses attention on drug-related stimuli in the environment, and draws attention away from environmental cues unrelated to drugs. Naturally, researchers began to wonder whether the Stroop test could be brought to bear on the matter of addiction, and employed as a tool with which to predict the likelihood of relapse among the addict population. 
As researchers at the University of Wales have pointed out,  “Decisions about drinking and drug use can be highly automatic, with users being unaware of the factors that influence their decisions.” At the same time, addicts are hyper-aware of addiction-related environmental stimuli, compared to non-addicts. As a result, “the automatic processing of addiction-related stimuli might elicit conditioned responses such as withdrawal… or they might invoke automatic patterns leading to substance use.”
In a recent study of treatment dropouts among 74 cocaine-addicted subjects, published in Neuropsychopharmacology, Dr. Chris Streeter and coworkers at the Boston University School of Medicine and Harvard University provide strong evidence for the use of the Stroop Test as a diagnostic tool in addiction treatment.  Variations on the Stroop Test were better predictors of dropout than addiction severity, depression, and other clinical variables.  Dropouts took 24 per cent longer, on average, to finish the tests than cocaine addicts who stuck with treatment, the researchers reported.  “These finding suggest that the Stroop test can be used to identify cocaine-dependent subjects at risk for treatment dropout,” say the researchers, and that it can serve as another instrument with which to “identify and tailor interventions of at risk individuals in the hope of improving treatment compliance.”
Furthermore, other studies suggest that attentional bias may serve as a useful predictor of opiate relapse and smoking cessation failure as well.
Streeter, C., Terhune, D., Whitfield, T., Gruber, S., Sarid-Segal, O., Silveri, M., Tzilos, G., Afshar, M., Rouse, E., Tian, H., Renshaw, P., Ciraulo, D., & Yurgelun-Todd, D. (2007). Performance on the Stroop Predicts Treatment Compliance in Cocaine-Dependent Individuals Neuropsychopharmacology, 33 (4), 827-836 DOI: 10.1038/sj.npp.1301465
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Streeter, C., Terhune, D., Whitfield, T., Gruber, S., Sarid-Segal, O., Silveri, M., Tzilos, G., Afshar, M., Rouse, E., Tian, H.... (2007) Performance on the Stroop Predicts Treatment Compliance in Cocaine-Dependent Individuals. Neuropsychopharmacology, 33(4), 827-836. DOI: 10.1038/sj.npp.1301465  

  • July 8, 2010
  • 11:31 PM
  • 731 views

Consider the CB(2) Receptor

by Dirk Hanson in Addiction Inbox


A different destination for cannabinoids.
THC and its organic cousin, anandamide, do what they do by locking into both the CB1 receptor, discovered in 1988, and the CB2 receptor (as it is commonly written in shorthand), discovered 5 years later. THC and anandamide are CB receptor agonists, meaning they activate the receptors in question. (An antagonist blocks the receptor’s action.)
CB1 is a very common receptor in the central nervous system, and, when stimulated by an agonist, is responsible for the well-known roster of alleged medical effects, such as pain relief and nausea from chemotherapy--along with the typical marijuana high. (For more on this, see the excellent 2007 post by Dr. Joan Bushwell.) Conversely, blocking CB1 activity with an antagonist like rimonabant is one controversial avenue being explored in the search for new weight loss drugs. (CB1 antagonists can also produce anxiety and depression.)
However, CB2 was long considered a “peripheral” cannabinoid receptor, meaning that scientists hadn’t managed to find CB2 receptors in the central nervous system. They were, however, plentiful in the immune system, and seemed to be involved in inflammation as well as pain responses. CB2 receptors were in fact eventually discovered in the central nervous system, and are active in the brain during certain kinds of inflammatory responses.
There is a straightforward commercial incentive for tracking the extent of CB2 expression in brain neurons. As the authors of a cannabinoid receptor study wrote in the June issue of the British Journal of Pharmacology:
“As CB(2) is an attractive therapeutic target for pain management and immune system modulation without overt psychoactivity, defining the extent of its presence in neurons will have a significant impact on drug discovery.”
Translated, this means that there are a number of new molecules that are selective for CB2 receptors. Since people don’t get a strong traditional marijuana-style buzz from CB2 receptor activation, and given the active involvement of CB2 receptors in things like immune responses and inflammatory reactions, the possibility exists of finding lucrative spinoffs like pain pills or anti-inflammatory medications.  So drug researchers would like to know exactly where those receptors are, and what they do, in the event that they end up attempting to make a medicine that stimulates or blocks  them artificially. (Credit to Vaughan Bell of Mind Hacks for highlighting this study.) 
The psychologists at Indiana University who produced the paper did their best to shed light on where the CB(2) receptor is hiding, and what, exactly, it does.  But there is still not enough known about how various substances react with this somewhat elusive receptor for cannabinoids. In 2008, scientists at the University of Madrid published research in the Journal of Biological Chemistry indicating that activation of the CB2 receptor reduced nerve cell loss in animals suffering from a disease similar to multiple sclerosis. Researchers point to the possibility that a safe drug for M.S. patients could be one of the results of CB2 research.
Atwood, B., & Mackie, K. (2010). CB2: a cannabinoid receptor with an identity crisis British Journal of Pharmacology, 160 (3), 467-479 DOI: 10.1111/j.1476-5381.2010.00729.x
Graphics Credit: www.cnsforum.com... Read more »

Atwood, B., & Mackie, K. (2010) CB2: a cannabinoid receptor with an identity crisis. British Journal of Pharmacology, 160(3), 467-479. DOI: 10.1111/j.1476-5381.2010.00729.x  

  • June 25, 2011
  • 04:46 PM
  • 726 views

That Pesky Gambling Question

by Dirk Hanson in Addiction Inbox


The DSM-V is set to label problem gambling an addiction.

Nobody has ever bet enough on the winning horse.
— Unknown wise person

I used to gamble. Back when I did, I was also an active alcoholic and a chain smoker. Camel filters, if you’re wondering. And we had a running joke, my wife and I, although the humor leaked out of it for her pretty quickly. We would breach the doors of the gambling palace, and plunge into the dark, icy interior of a casino at Las Vegas or Tahoe, and stand on the edge of the gaming room, taking it all in for a moment. “Ah,” I would say, surveying the roomful of cigarette smokers with drinks in their hands, making bets or hitting buttons at one o’clock in the morning, “my kind of people.”

Gambling can be defined as an activity in which something of value is put at risk in a situation where the outcome is uncertain. That’s really all there is to it. Howard J. Shaffer and Ryan Martin, whose article in the Annual Review of Clinical Psychology, “Disordered Gambling: Etiology, Trajectory and Clinical Considerations,” takes on all the interesting questions about gambling as an addictive disease, have chosen to favor the term “disordered gambling.” Just as there are divisions between alcoholic drinking, heavy drinking, and social drinking, there are similar states we can call pathological gambling, excessive gambling, and social gambling. On the problematic end of the scale, pathological or problem gambling has proven to be “a more complex and unstable disorder than originally and traditionally thought.” No kidding. Once the neurophysiology of the gambling state of mind came under scrutiny, the parallels with addiction cropped up so rapidly that investigators have been hard pressed to come up with suitable explanations for it all.

The new DSM-V proposes to shift pathological gambling from “impulse control disorder” to the new category of “addiction and related disorders.” So it’s a good time to rethink the question along with the psychiatric community.

In the traditional view, pathological gambling was a matter of exposure to the proper stimuli—it could happen to anyone. But as more and more gambling outlets and opportunities bloomed in Nevada, on reservations and riverboats, and in convenience stores, that view began to fall out of favor, because a funny thing happened. According to Shaffer and Martin, the prevalence of pathological gambling has remained stable over the past 35 years, even as opportunities to gamble have exploded. The lifetime prevalence rate of pathological gambling in the U.S. in the mid-1970s was 0.7%, say the authors, and by 2005, U.S. lifetime rates had actually fallen slightly, to 0.6% or less. Where was the concomitant explosion in the number of pathological gamblers?

Next, researchers got technical, wondering whether certain types of gambling, or certain types of gambling machines, were more “addictive” than others. They quickly ran into the same kind of trouble substance abuse researchers got into when they first tried ranking drugs according to strict hierarchies of addictiveness. In so doing, the staggering metabolic diversity of the human animal got lost in the shuffle, as did the fact that my metabolism and my behavior when taking drugs, or knocking one back, or losing money in a casino, is going to be different from yours.

Then came Internet gambling. In 1996, the first online casino to accept real money began operation, and by 2001, there were more than a thousand. Previously, researchers had to rely mostly on the time-honored but not always accurate system of self-reporting. If you ask people why they gamble, they tend to answer that they do it for the fun, the excitement, the challenge, and the chance to win some money. But what gamblers can’t recall very well are specific patterns of play over time that might benefit researchers. For example, in a 2009 study in which observers actually watched gamblers gambling, one long-standing observation from the self-report literature—gamblers become more liberal risk takers as they approach the end of a gambling session in a behavior called “chasing”—didn’t prove out. When researchers watched actual gamblers in action on the Internet, or playing lotteries, they found that problem gamblers in fact began betting more conservatively as they approached the end of their gambling, the authors write.

Another approach is to consider risk factors of all kinds—neurobiological, psychological, and social—and look for similarities between those for substance addiction, and those for “activity-based expressions of addiction.” The “syndrome model,” or what I usually call the umbrella model, derives from neurobiological research suggesting that “addictive disorders might not be independent: each outwardly unique addiction disorder might be a distinctive expression of the same underlying addiction syndrome…. The specific objects of addiction play a less central role in the development of addiction than previously thought….”

 All of this opens the door to some informed speculation about a broader range of disorders that may lurk beneath the umbrella of the addictive disease concept. Among these are such conditions as body dysmorphic disorder, bulimia, depression, and extreme PMS, which are all found more often in addict populations. In addition, impulsivity and low “harm avoidance” are behavioral traits often found in association with addiction. Shaffer and Martin call these “shadow syndromes,” and they are found to be associated with BOTH substance and behavioral addictions.

But what, exactly, is the high in gambling? The researchers believe that, “similar to ingesting stimulants, there is evidence that gambling is associated with autonomic arousal including elevated blood pressure, heart rate, and mood.” That's not very specific, and could also describe a craving for teddy bears. But recently, fascinating evidence of neurobiological influences on gambling arose when Parkinson’s’ patients on strong dopamine agonist treatments, with no history of gambling whatsoever, began behaving for all the world like pathological gamblers. I cannot imagine a better suggestion of neurogenetic involvement than this unexpected finding. Previous research had shown that dopamine-active drugs were capable of increasing the incidence of other addictions, too. Shaffer and Martin list compulsive eating, compulsive sexual behaviors, and compulsive shopping as activities that can also be boosted with dopamine agonists or diminished by lowering dopamine activity. 

And it does not strike me as surprising to learn that, yes, gambling problems tend to run in families, or that twins studies show that pathological gambling is higher among twins born to pathological gamblers than twins born to non-gamblers. It is the same evidence anyone can bring forth to bolster the argument for neurobiological influences on alcoholism, heroin addiction, and the like. “In sum” Shaffer and Martin conclude, “genetic influences might not determine the development of specific expression of addiction; however, genetics does influence the risk of addiction in general.”

If all of this is true, we should expect to see a corresponding connection between pathological gambling and substance abuse disorders. Some degree of overlap would be good evidence. And we have it in spades. Pathological gamblers are five and a half times more likely to have suffered from a substance abuse disorder. “75% of PGs (pathological gamblers) have had an alcohol disorder, 38% have had a drug use disorder and 60% have had nicotine dependence.” Also, “PGs are 4 times more likely than non-PGs to experience a mood disorder in their lifetime….”

So when I used to stand on the edge of the casino floor, as an alcoholic and a nicotine addict, casually calling those gamblers my kind of people, I think I was more right than I ever could have guessed.

Does all this mean that playing games on the Internet is an addictive behavior if making bets with real money is involved? The authors crunched the studies on that question, and discovered that maybe 1% of the Internet population has used the Internet for gambling purposes, and that “the case of Internet gambling provides little evidence that exposure is the primary driving force behind the prevalence and intensity of gambling…. The relationship between the extent of gambling ‘involvement’ is a better predictor of disordered gambling than any particular game that people play.”

By gambling involvement, the authors mean the number of different kinds of games a gambler plays. The more he or she plays, the more likely they are, or are likely to become, problem gamblers. However, it’s not hard to see where the online notion came from. Gambling folklore has alw... Read more »

  • July 5, 2011
  • 07:42 PM
  • 697 views

The Undiagnosed Epidemic of Incarceration

by Dirk Hanson in Addiction Inbox


Prison once again a place for addicts and the mentally ill.

Readers may remember the dark day of January 1, 2008, when the U.S. set an all-time record: One out of every 100 adults was behind bars. That’s more than 2.3 million people. That’s 25% of all the prisoners in the world—and the world includes some very nasty nations. What gives?

You know the answer: drug crimes. Can it really be a coincidence that over the past 40 years, ever since President Richard Nixon first declared war on drugs, the number of people housed in U.S. prisons has gone up by more than 600%? Are we really just that much more vicious and larcenous than we used to be? 600% more unlawful than we were as a people in 1971? Last month, a group of medical professionals from the Division of Infectious Diseases at Brown Medical School, and the Center for Prisoner Health and Human Rights, both in Providence, Rhode Island, co-authored an article for the New England Journal of Medicine entitled “Medicine and the Epidemic of Incarceration in the United States.” The investigators conclude that the explosion in the prison population is a direct result of “our country’s failure to treat addiction and mental illness as medical conditions. The natural history of these diseases often leads to behaviors that result in incarceration.” Packed prisons are also the result of a broader movement over the past 40 years to shift the burden of care for addiction and mental illness over to the prison system. “Deinstitutionalization of the mentally ill over the past 50 years and severe punishment for drug users starting in the 1970s have shifted the burden of care for addiction and mental illness to jails and prisons,” the authors argue.

Do the social costs of this massive transfer of addicts and the mentally ill to the U.S. prison system outweigh the benefits? According to the NEJM article by Josiah D. Rich and co-workers, “more than 50% of inmates meet the DSM-IV criteria for drug dependence or abuse, and 20% of state prisoners have a history of injection-drug use.” Rich estimates that up to a third of all heroin users pass through the criminal justice system each year. These figures are shockingly high, compared to the general population, even allowing for a higher level of drug use among the criminal population.

“The largest facilities housing psychiatric patients in the United States are not hospitals but jails,” they write. “More than half of inmates have symptoms of a psychiatric disorder… yet correctional facilities are fundamentally designed to confine and punish, not to treat disease.” Furthermore, as most people are aware, the punishment is not meted out equally: “By middle age, black men in the United State are more likely to have spent time in prison than to have graduated from college or joined the military and they are far more likely than whites to be sent to prison for drug offenses despite being no more likely that whites to use drugs.”

And there is one aspect of the sorry situation that receives almost no attention at all: Most prisoners are eventually released. This post-release period, says the NEJM article, “presents extraordinary risks to individuals and costs to society.” In the first two weeks after release, former inmates are 129 times more likely to die from a drug overdose than the average man or woman on the street. They are 12 times more likely to die, period. And here’s a nice touch: Most of them don’t have Medicaid or other medical insurance, and there is usually no primary care follow-up to assure that they have access to affordable medications, if they need them. Inevitably, these are among the people who make the local emergency room their primary care facility, at great cost to everyone involved.  As the article states: "Addressing the health needs of this vulnerable population is thus not only an ethical imperative, but also of crucial importance from both a fiscal and a public health perspective."

State spending on correctional institutes is now the second fastest growing sector of government spending, after Medicaid. According to the authors, five states now spend more on prisons than they spend on higher education. “Locking up millions of people for drug-related crimes has failed as a public-safety strategy and has harmed public health in the communities to which these men and women return.”

The authors make it clear that, for addicts, drug and mental health treatment programs are humane and sensible alternatives to incarceration. They are also cost-effective: In Rhode Island, for example, the price for putting someone behind bars for a year is $41,000—or $110,000, if we are talking about the new super maximum-security facilities. Why haven’t politicians seized on all of this as a budgeting issue; as a cost-effective way to address drug and alcohol addiction without clogging up the criminal justice system, and creating embarrassing rates of incarceration? The authors have an answer: the fear of being tagged as “soft on crime.” If addiction is a craven failure of will power leading to the violation of social norms, as so many citizens seem to think, than prison is where addicts belong. The result: political pandering on the drug issue, by politicians suffering from a craven failure of will.


Here is where President Obama’s Affordable Care Act could really end up making a difference. Former prisoners will have a good shot at health coverage, and a policy that links together community health centers and academic medical centers could radically improve care during the critical post-release period. As Rich and colleagues argue: “Such access could redirect many people with serious illnesses away from the revolving door of the criminal justice system, thereby improving overall public health in the communities to which prisoners return and decreasing the costs associated with reincarceration due to untreated addiction and mental illness.”

Rich JD, Wakeman SE, & Dickman SL (2011). Medicine and the epidemic of incarceration in the United States. The New England journal of medicine, 364 (22), 2081-3 PMID: 21631319

Pic http://scrapetv.com ... Read more »

Rich JD, Wakeman SE, & Dickman SL. (2011) Medicine and the epidemic of incarceration in the United States. The New England journal of medicine, 364(22), 2081-3. PMID: 21631319  

  • June 20, 2010
  • 02:00 PM
  • 689 views

Vitamin B6 May Lower Risk of Lung Cancer

by Dirk Hanson in Addiction Inbox

Large European study confirms earlier findings.

It doesn’t mean you should start popping handfuls of B vitamins if you are a smoker or a former smoker (those who never smoked rarely get the disease). What it appears to mean is that people with the highest levels of vitamin B6 in their bodies may have as little as half the risk of developing lung cancer as people with very low levels of B6--also known as pyridoxine.

In a June 16 article in the Journal of the American Medical Association (JAMA) , dozens of researchers from around the world deconstructed a European medical database from the 1990s, containing medical data and blood test results for more than 380,000 people. They were looking for meaningful statistical correlations having to do with the 899 people in the study who eventually developed lung cancer.

According to Nathan Seppa in Science News, the international research team found that “people with vitamin B6 levels ranking in the top one-fourth of all the samples taken had less than half the risk of lung cancer as those with the lowest vitamin B6. A similar comparison found that people with high levels of [the amino acid] methionine seemed to have almost half the cancer risk of people with low levels. High folate levels seemed to give less protection.” The researchers calculated that having high levels of all three compounds could reduce lung cancer risk by as much as two-thirds.

Much remains unknown. Can smokers use B6 vitamin supplements to protect against lung cancer, or are the protective effects, if verified, due to a B6 level that reflects diet and other metabolic factors at work over decades? And, as always, there is the question of B6 from vitamin supplements vs. B6 from B6-rich foods like fish, beans, and grains.

A smaller prospective study undertaken in 2001 came up with similar results. Published in the American Journal of Epidemiology, the study involved 300 lung cancer patients in Finland between 1985 and 1993. The researchers looked at B6, B12, and folate, and found “significantly lower risk of lung cancer among men who had higher serum vitamin B6 levels. Compared with men with the lowest vitamin B6 concentration, men in the fifth quintile had about one half of the risk of lung cancer.” The researchers speculate that one of the mechanisms by which B6 could influence carcinogenesis is the role the vitamin plays in homocysteine metabolism. B6 is involved in the complex process of metabolizing homocysteine, another amino acid. Absent sufficient B6, homocysteine levels can build up in the body, causing heart disease and other ailments.

Mattias Johansson, et. al. (2010). Serum B Vitamin Levels and Risk of Lung Cancer Journal of the American Medical Association, 303 (23), 2377-2385

Graphics Credit: http://helios.hampshire.edu/... Read more »

Mattias Johansson, et. al. (2010) Serum B Vitamin Levels and Risk of Lung Cancer. Journal of the American Medical Association, 303(23), 2377-2385. info:/

  • January 7, 2011
  • 02:59 PM
  • 687 views

Marijuana and Testicular Cancer

by Dirk Hanson in Addiction Inbox


NIDA touts controversial 2009 study.

After 50 years of rumor, study, and argument in the research community, the National Institute on Drug Abuse (NIDA) has come out squarely behind the assertion that marijuana use in men “may increase their risk for developing testicular cancer.”

But a problem exists. The evidence just isn’t that good. Especially if you base the conclusion on a single small study, as NIDA is apparently doing.

Writing in NIDA Notes for December, 2010, Lori Whitten highlights a study of 369 men from the Seattle area with testicular cancer, and a control group of 979 disease-free men. “The researchers found that the odds of having testicular cancer were 70 percent higher among men who reported current marijuana use compared with nonusers…. They also found that the odds for testicular cancer among men who used marijuana at least weekly were twice that of nonusers.”

The hypothesis supporting this statistical correlation is not terribly robust: Testicular cancer has doubled in the past 50 years in the U.S. So has the percentage of the population that smokes pot. And since cannabinoid receptors are found on the cell membranes of the testes, and chronic marijuana use is associated with decreased testosterone plasma levels and reduced spermatogenesis, marijuana smoking must somehow interfere with the growth of germ cells in the testes. The result: cancer.

But wait, there’s more. Whether or not this contention can be considered true and proven remains quite arguable, but the study does appear to show a statistical association between marijuana use and one particular form of the disease. Marijuana smoking was strongly associated with only one form of testicular cancer, called nonseminomas, a fast growing type representing 40% of all testicular germ cell tumors (TGCT). The other type—seminomas—accounts for the other 60%.

Dr. Sudhansu Dey, a NIDA-funded researcher involved in the study, published in Cancer, told NIDA Notes that the association between marijuana smoking and nonseminomas, but not seminomas, is “difficult to explain.”

Here’s one possibility: Testicular cancer is too rare, and the study in question too small, to be anything but suggestive. It does not show a direct linkage between testicular cancer and pot smoking, and the authors do not claim that it does. In fact, they point to several limitations of their own study. The researchers were only able to directly interview a little more than half of the eligible cases and controls. And the study relied on self-report questionnaires, which, in the case of an illegal drug like marijuana, can skew the results. For example, “patients with cancer may be expected to more accurately admit to the use of an illegal substance than individuals in a control group.”

Specifically, the report states that “the incidence of seminoma from 1973 to 1998 in the US was 64% compared with an increase of only 24% for nonseminoma…. If the increase in nonseminomas was caused in part by an increase in the use of marijuana, then some other increasing exposures must account for the higher incidence of seminomas over time.” The point, as the researchers acknowledge, is that “none of these explanations likely would be specific to nonseminomas. Indeed, if the association is true, then new avenues of research will be needed to address the specificity of the association to nonseminomas.”

In other words, the argument that pot smoking might increase cases of one particular kind of testicular cancer is not accompanied by an explanation of the biological mechanism by which marijuana would be capable of exerting such effects.  The primary risk factor for testicular cancer seems to be a family history of the disease, followed by abnormal development of the testicles or undescended testes.

“If these interesting findings are replicated in a large, national representative group of participants,” Dr. Vishnudutt Purohit of NIDA’s Division of Basic Neuroscience and Behavioral Research told NIDA Notes, “then future research should delve into the molecular mechanism underlying the association.”

At present, that is a very big “if.”

Daling, J., Doody, D., Sun, X., Trabert, B., Weiss, N., Chen, C., Biggs, M., Starr, J., Dey, S., & Schwartz, S. (2009). Association of marijuana use and the incidence of testicular germ cell tumors Cancer, 115 (6), 1215-1223 DOI: 10.1002/cncr.24159
Graphics Credit: http://testicularcanceronline.info/... Read more »

Daling, J., Doody, D., Sun, X., Trabert, B., Weiss, N., Chen, C., Biggs, M., Starr, J., Dey, S., & Schwartz, S. (2009) Association of marijuana use and the incidence of testicular germ cell tumors. Cancer, 115(6), 1215-1223. DOI: 10.1002/cncr.24159  

  • June 10, 2010
  • 08:21 PM
  • 663 views

Choline for Fetal Alcohol Spectrum Disorders?

by Dirk Hanson in Addiction Inbox


Common supplement may reduce cell death in pregnancies.
A common dietary supplement markedly decreases defects in the skull and brain formation of  lab mice born to mothers exposed to alcohol, say researchers at the Medical College of Georgia.
Among the grisly list of potential effects caused by alcohol consumption during pregnancy, one involves a relatively obscure lipid called ceramide. Ceramide can markedly increase the rate of programmed cell death—a process known as apoptosis—and may be involved in the characteristic cranial defects seen in fetal alcohol syndrome.
In the study, 25 % of the mouse embryos exposed to alcohol showed characteristic defects in skull development, including diminished growth in the multi-layered membrane—the meninges--covering the brain.  Biochemists Erhard Bieberich and Guanghu Wang, in an article published in Cell Death and Disease, found that the supplement CDP-choline decreased cell death and protected the fetal cranium from damage due to maternal drinking episodes. According to Dr. Bierberich in a press release from the Medical College of Georgia, the result of alcohol on pregnancy is “a snowball effect. The neural crest is damaged, the meninges doesn’t develop properly and tissue like bone and brain that are regulated by the meninges don’t develop properly either.”
Choline is a precursor to the neurotransmitter acetylcholine. In addition, it has been known for decades that alcohol increases choline requirements. Choline is already added to some baby formulas and prenatal vitamins. Choline’s effects on stroke and traumatic brain injury are also being investigated.
A similar discovery twenty years ago concerning folic acid led the U.S. Public Health Service (USPHS) to recommend that all women thinking of becoming pregnant should consume supplemental folic acid daily in order to reduce their risk of having a pregnancy affected by spina bifida or other neural tube defects. The rate of occurrence of this kind of birth defect has been dropping ever since.
The researchers believe that “there is just a little window” four weeks after conception—while neural cells are forming numerous organs--when the alcohol-related cranial damage is likely to occur. Unfortunately, this window of disaster opens before many women have discovered that they are pregnant. 
Since warnings about the dangers of drinking during pregnancy are either not known or are ignored in many cases, researchers are always on the lookout for medications that could be given after exposure to alcohol--or even after birth of a baby to an alcoholic mother.  As early as 2005, researchers at Tripler Army Medical Center in Honolulu demonstrated that adding choline to the pre-natal diet of pregnant alcoholic rats suppressed physiological symptoms of fetal alcohol syndrome in the offspring. In a press release from the American Physiological Society, lead researcher John Claybaugh asserted that the results “are consistent with the hypothesis that supplemental dietary choline fed to the pregnant dam can prevent the alcohol-induced partial diabetes insipidus seen in the young adult offspring.”
The American Psychological Association, in the wake of a 2007 study published in Behavioral Neuroscience, announced that “giving choline to infants who were exposed in the womb to alcohol may mitigate some of the resulting problems” related to learning, attention, and motor skills. The researchers gave choline to rat pups exposed to alcohol during the third trimester. Alcohol-related hyperactivity and learning deficits decreased, the researchers say. “The data suggest that early dietary interventions may reduce the severity of some fetal alcohol effects, even when administered after birth."
 Despite such optimism, the issue is whether a choline supplement would be capable of rescuing cells after alcohol exposure, or whether choline would need to be taken ahead of time as a supplement.
What is not at issue is that pregnant women should not drink, and should be aware that fetal damage can occur very early in a pregnancy.
Graphics Credit: http://www.cholineinfo.org/
Wang, G., & Bieberich, E. (2010). Prenatal alcohol exposure triggers ceramide-induced apoptosis in neural crest-derived tissues concurrent with defective cranial development Cell Death and Disease, 1 (5) DOI: 10.1038/cddis.2010.22... Read more »

  • October 3, 2010
  • 03:34 PM
  • 663 views

Marijuana and Memory

by Dirk Hanson in Addiction Inbox


Do certain strains make you more forgetful?
Cannabis snobs have been known to argue endlessly about the quality of the highs produced by their favorite varietals: Northern Lights, Hawaiian Haze, White Widow, etc. Among dedicated potheads, debates about the effects of specific cannabis strains are often overheated, and, ultimately, kind of boring. It's a bit like listening to a discussion of whether the wine in question evinces a woody aftertaste or is, instead, redolent of elderberries. For most people, the true essence of wine drinking is pretty straightforward: a drug buzz, produced by a 12 to 15 % concentration of ethyl alcohol derived from grapes, which can be had in a spectrum of varietal flavors.
However, there is no doubting that, unlike the case of wine, different strains of marijuana can have markedly different psychoactive effects. With weed, it's not just a matter of taste.
Over the past couple of years, the cannabis debate has taken a nasty turn, after British scientists published several controversial studies suggesting that high-THC "skunk" cannabis was responsible for increased mental problems among young people--including an increased risk of developing the symptoms of schizophrenia. British drug policy makers have continued to lead the charge on this, with mixed results. See my earlier post.
Recently, a study published in the British Journal Of Psychiatry concluded that marijuana high in THC--including so-called "skunk" cannabis--caused markedly more memory impairment than varieties of marijuana containing less THC.
In an article at Nature News, Arran Frood spelled out the details of the study:
"Curran and her colleagues traveled to the homes of 134 volunteers, where the subjects got high on their own supply before completing a battery of psychological tests designed to measure anxiety, memory recall and other factors such as verbal fluency when both sober and stoned. The researchers then took a portion of the stash back to the laboratory to test how much THC and cannabidiol it contained....  Analysis showed that participants who had smoked cannabis low in cannabidiol were significantly worse at recalling text than they were when not intoxicated. Those who smoked cannabis high in cannabidiol showed no such impairment."
The two main ingredients in cannabis are THC and cannabidiol (CBD). CBD shows less affinity for the two main types of cannabis receptors, CB1 and CB2, meaning that it attaches to receptors more weakly, and activates them less robustly, than THC.  The euphoric effects of marijuana are generally attributed to THC content, not CBD content. In fact, there appears to be an inverse ratio at work. According to a paper in Neuropsychopharmacology, "Delta-9-THC and CBD can have opposite effects on regional brain function, which may underlie their different symptomatic and behavioral effects, and CBD's ability to block the psychotogenic effects of delta-9-THC."
So, CBD specifically does not produce the usual marijuana high with accompanying euphoria and forgetfulness and munchies. What the researchers found was that pot smokers suffering memory impairment and those showing normal memory "did not differ in the THC content of the cannabis they smoked. Unlike the marked impairment in prose recall of individuals who smoked cannabis low in cannabidiol, participants smoking cannabis high in cannabidiol showed no memory impairment."
As far as memory goes, THC content didn't seem to matter. It was the percentage of CBD that controlled the degree of memory impairment, the authors concluded. "The antagonistic effects of cannabidiol at the CB1 receptor are probably responsible for its profile in smoked cannabis, attenuating the memory-impairing effects of THC. In terms of harm reduction, users should be made aware of the higher risk of memory impairment associated with smoking low-cannabidiol strains of cannabis like 'skunk' and encouraged to use strains containing higher levels of cannabidiol."
The idea that cannabidiol may protect against THC-induced memory loss is still quite speculative.  Other research has suggested that a paucity of CB1 receptors may be protective against memory impairment. Marijuana growers select for high-THC strains, not high-CBD strains, and thus there is little data available about the CBD levels of most marijuana.
An earlier study in Behavioural Pharmacology by Aaron Ilan and others at the San Francisco Brain Research Institute did not find any connection between memory and CBD content. However, Ilan speculated in the Nature News article that the difference might have been due to methodology: In Britain, the subjects were studied using marijuana of their own choosing.  In the U.S., National Institute of Health research policy has decreed that marijuana for official research must be supplied by the National Institute on Drug Abuse (NIDA). And if there is one thing many researchers seem to agree on, it is that NIDA weed "is notorious for being low in THC and poor quality."
But CBD still does something, and that something just might be pain relief.  Lester Grinspoon, a long-time marijuana researcher at Harvard Medical School, thinks that if the study proves out, it could have an important impact on the medical use of marijuana. Also quoted in Nature News, Grinspoon said: "Cannabis with high cannabidiol levels will make a more appealing option for anti-pain, anti-anxiety and anti-spasm treatments, because they can be delivered without causing disconcerting euphoria."

Morgan, C., Schafer, G., Freeman, T., & Curran, H. (2010). Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: naturalistic study The British Journal of Psychiatry, 197 (4), 285-290 DOI: 10.1192/bjp.bp.110.077503
Graphics Credit: http://sites.google.com
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  • March 18, 2010
  • 08:12 PM
  • 661 views

Germs in Tobacco

by Dirk Hanson in Addiction Inbox


Bacteria found in major cigarette brands.
It’s not enough that smoking causes all manner of cardiopulmonary complications, or that more than 3,000 chemicals and heavy metals have been identified as additives. Now comes evidence that tobacco particles extracted from cigarettes contain markers for hundreds of known bacteria. Lung infections in some smokers may be caused by germs on shredded tobacco, rather than the act of smoking itself.
According to a report by Janet Raloff in Science News, Amy Sapkota and a team of researchers at the University of Maryland screened tobacco flakes from cigarettes for bacterial DNA using known markers. In an online paper for Environmental Health Perspectives, the scientists explored the bacterial metagenomics of cigarettes using standard cloning and sequencing processes. The team provided evidence for the presence of Campylobacter (a cause of food poisoning), E. coli, several Staphylococcus varieties, as well as a number of bacteria, such as Clostridium, which is directly associated with pneumonia and other infections. Fifteen different classes of bacteria in all, with no significant variation from one cigarette brand to another. 
The time has come, Sapkota and coworkers conclude, “ to further our understanding of the bacterial diversity of cigarettes,” given the more than 1 billion smokers worldwide.  Smoking is now recognized as a risk factor for a basketful of respiratory illnesses, including influenza, asthma, bacterial pneumonia, and interstitial lung disease. In light of this, the authors have advanced their study as solid evidence that “cigarettes themselves could be the direct source of exposure to a wide array of potentially pathogenic microbes among smokers and other people exposed to secondhand smoke.”
In 2008, researcher John Pauly and coworkers at the Roswell Park Cancer Institute in Buffalo, New York, helped provide early evidence by conducting a tobacco flake assay and publishing the results in the journal Tobacco Control. The scientists opened a package of cigarettes “within the sterile environment of a laminar flow hood. A single flake of tobacco was collected randomly and aseptically from the middle of the cigarette column and placed onto the surface of a blood agar plate. The test cigarettes included eight different popular brands, and these were from three different tobacco companies.”
And the results? “After 24 hours of incubation at 37 degrees C, the plates showed bacterial growth for tobacco from all brands of cigarettes. Further, more than 90% of the individual tobacco flakes of a given brand grew bacteria.” Pauly believes that “the results of these studies predict that diverse microbes and microbial toxins are carried by tobacco microparticulates that are released from the cigarette during smoking, and carried into mainstream smoke that is sucked deep into the lung.”

In a recent study published in Immunological Research , Pauly and others expanded on their findings, writing that “Cured tobacco in diverse types of cigarettes is known to harbor a plethora of bacteria (Gram-positive and Gram-negative), fungi (mold, yeast), spores, and is rich in endotoxin (lipopolysaccharide).” This time out, the researchers conclude that “lung inflammation of long-term smokers may be attributed in part to tobacco-associated bacterial and fungal components that have been identified in tobacco and tobacco smoke.”
Cigarette manufacturers already use antibacterial washes during the curing process in order to reduce infection by fungi and bacteria.
If the findings are sound, they could place the argument over secondhand smoke in a vastly different light—cigarettes smoke may be taking the rap for respiratory infections cause by extant bacteria. With smoking rates in the U.S. holding at a steady 21 percent of the population, the issue is not trivial.
Graphics Credit: http://commons.wikimedia.org/
Sapkota, A., Berger, S., & Vogel, T. (2009). Human Pathogens Abundant in the Bacterial Metagenome of Cigarettes Environmental Health Perspectives, 118 (3), 351-356 DOI: 10.1289/ehp.0901201
Pauly, J., Smith, L., Rickert, M., Hutson, A., & Paszkiewicz, G. (2009). Review: Is lung inflammation associated with microbes and microbial toxins in cigarette tobacco smoke? Immunologic Research, 46 (1-3), 127-136 DOI: 10.1007/s12026-009-8117-6

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  • October 21, 2010
  • 02:40 PM
  • 660 views

Does Ketamine Cause Bladder Damage?

by Dirk Hanson in Addiction Inbox


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://onlinelibrary.wiley.com... Read more »

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  

  • August 5, 2011
  • 12:56 PM
  • 651 views

Cigarette Sadness

by Dirk Hanson in Addiction Inbox


The chemistry of sorrow during nicotine withdrawal.

When you smoke a cigarette, nicotine pops into acetylcholine receptors in the brain, the adrenal glands, and the skeletal muscles, and you get a nicotine rush. Just like alcohol, a cigarette alters the transmission of several important chemical messengers in the brain. “These are not trivial responses,” said Professor Ovide Pomerleau of the University of Michigan Medical School. “It’s like lighting a match in a gasoline factory.”

Experiments at NIDA’s Addiction Research Center in Baltimore have confirmed that nicotine withdrawal not only makes people irritable, but also impairs intellectual performance. Logical reasoning and rapid decision-making both suffer during nicotine withdrawal. Acetylcholine appears to enhance memory, which may help explain a common lament voiced by many smokers during early withdrawal. As summarized by one ex-smoker, “I cannot think, cannot remember, cannot concentrate.”

But there is another, less widely discussed aspect of nicotine withdrawal: profound sadness. Profound enough, in many cases, to be diagnosed as clinical unipolar depression.

 Of course, people detoxing from addictive drugs like nicotine are rarely known to be happy campers. But quitting smoking, for all its other withdrawal effects, reliably evokes a sense of acute nostalgia, like saying goodbye to a lifelong friend. The very act of abstinence produces sadness, joylessness, dysphoria, melancholia—all emotional states associated with unipolar depression.

Work undertaken by Dr. Alexander Glassman and his associates at the New York State Psychiatric Institute has nailed down an unexpectedly strong relationship between prior depression and cigarette smoking, and the findings have been confirmed in other work. This sheds important light on the question of why some smokers repeatedly fail to stop smoking, regardless of the method or the motivation.  The problem, as Glassman sees it, is “an associated vulnerability between affective [mood] disorders and nicotine.”

Now a group of Canadian researchers, working out of the Centre of Addiction and Mental Health (CAMH), and the Department of Psychiatry at the University of Toronto, believe they have isolated the specific neuronal mechanisms responsible for the profound sadness of the abstinent smoker.

Writing in the Archives of General Psychiatry, the investigators, who had access to what the CAMH proudly calls the only PET scanner in the world dedicated to mental health and addiction research, gave PET scans to 24 healthy smokers and 24 healthy non-smokers. Non-smokers were scanned once, while heavy and moderate cigarette smokers were scanned after smoking a cigarette, and also after a period of acute withdrawal. Earlier research of this kind had focused on nicotine’s effect on dopamine release. But Ingrid Bacher and her coworkers in Toronto were measuring MAO-A levels in the prefrontal and anterior cingulate regions, two areas known to be involved in “affect,” or emotional responses. When patients suffering from major depressive disorders get scanned, they tend to show elevated levels of MAO-A. The so-called MAO-A inhibitors Marplan, Nardil, Emsam, and Parnate are still in use as antidepressant medications. In general, the higher the levels of MAO-A, the lower the levels of various neurotransmitters crucial to pleasure and reward. A high level of MAO-A would suggest that the enzyme was significantly altering the activity of serotonin, dopamine, and norepinephrine in brain regions involved in mood.

The researchers found that smokers in withdrawal had 25-35% more MAO-A binding activity than non-smoking controls. “This finding may explain why heavy smokers are at high risk for clinical depression," says Dr. Anthony Phillips, Scientific Director of the Canadian Institutes of Health Research's (CIHR's) Institute of Neurosciences, Mental Health and Addiction, which funded this study.

Although researchers involved in these kinds of drug studies almost always claim that the work is likely to lead to new pharmacological therapies, the plain truth is that such immediate spinouts are rare. But in this case, it does seem like the study provides a clear incentive to investigate the clinical standing of MAO-A inhibitors as an adjunct therapy in stop-smoking programs. “Understanding sadness during cigarette withdrawal is important because this sad mood makes it hard for people to quit, especially in the first few days,” said Dr. Jeffrey Meyer, one of the study authors.

As one addiction researcher noted, an associated vulnerability to depression “isn’t going to cover everybody’s problem, and it doesn’t mean that if you give up smoking, you’re automatically going to plunge into a suicidal depression. However, for people who have some problems along those lines, giving up smoking definitely complicates their lives.”


Bacher, I., Houle, S., Xu, X., Zawertailo, L., Soliman, A., Wilson, A., Selby, P., George, T., Sacher, J., Miler, L., Kish, S., Rusjan, P., & Meyer, J. (2011). Monoamine Oxidase A Binding in the Prefrontal and Anterior Cingulate Cortices During Acute Withdrawal From Heavy Cigarette Smoking Archives of General Psychiatry, 68 (8), 817-826 DOI: 10.1001/archgenpsychiatry.2011.82

Photo Credit:http://jenniferonmars.wordpress.com
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  • January 26, 2011
  • 02:16 PM
  • 650 views

Khat to the Chase

by Dirk Hanson in Addiction Inbox


Of mephedrone, bath salts, and impaired driving.

 Automobile accidents are the ninth leading cause of death worlwide, according to the World Health Organization (WHO). More than a million people are killed on roads annually, and that number could rise to 2.5 million by 2020. WHO estimates that traffic accidents cost developing countries an astonishing 1-2 % of their gross domestic product (GDP).

For years now, police and public health officials have puzzled over the alarming number of traffic accidents in East Africa. In terms of sheer numbers, Asian countries have the highest total traffic fatalities, according to figures compiled by the Global Road Safety Partnership (GRSP), a consortium including the World Bank, the Red Cross and other aid agencies (PDF HERE). That is not surprising, since these nations contain the majority of the world’s drivers.

However, beyond the picture of traffic fatalities in terms of sheer numbers, or on a per population basis, there is another revealing measure—traffic deaths per motor vehicle. And when the GRSP measured nations by that yardstick, the four worst countries in the world for traffic deaths—judging by the number of fatalities per 10,000 licensed vehicles—were Ethiopia, Tanzania, Lesotho, and Kenya—all East African nations.

Moreover, these are all African countries in which the use of khat--an amphetamine-like plant drug that is the natural precursor of the designer drug known as mephedrone--is legal and common. The major khat-using countries in Africa are commonly listed as: Somalia, Kenya, Yemen, Ethiopa, Tanzania, Lesotho. Note the overlap. Khat, as one online article put it, is “the legal high of east Africa.”

On the tiny island nation of Mauritius, just off the southeast African coast, Touria Prayag writes at allAfrica.com that drivers “zoom past you, zigzag on the roads, nervously changing to the left lane to swiftly veer back on your side without any warning…. brazenly flouting the Highway Code in every imaginable dangerous manner…. And the carnage continues….”

In Ethiopia, annual road crash fatalities account for 114 deaths per 10,000 vehicles, compared to one death per 10,000 vehicles in Great Britain, and an average of 60 deaths per 10,000 vehicles across 39 sub-Saharan African countries. A report in the Bulletin of the World Health Organization (PDF HERE)  notes that Ethiopian truck drivers “are regarded as so dangerous that their trucks are commonly referred to across Ethiopia as ‘al Qaeda.’” Anecdotally, Ethiopians told WHO officials that khat “increased driver confidence and vehicle speed while also making drivers irritable and impairing concentration,” and that high levels of khat could lead to hallucinations.

A Kenya forum on TripAdvisor asks: Are matatus [local taxes piloted by khat-chewing Kenyans] safe?” 

Since khat is legally available in most of East Africa, and comprises a significant part of the social fabric of local cultures, the use of khat is similar to the use of alcohol in higher-income nations. But does khat present the same threat of driving impairment as alcohol? Bolivia is now arguing its right to allow citizens to chew coca leaves in the traditional manner. Is it safe to drive and chew coca leaves? In all of these cases, the challenge is to determine what constitutes a “safe” dose of the drug; a dose that does not endanger people on or near the highway. There is not enough research on khat to answer that question. Nor is there a way to administer roadside tests for khat. The best evidence, African police officers say, is green teeth.

The active ingredients in khat—cathine and cathinone—are similar in structure to amphetamines, and chemically similar to the ingredients used in the manufacture of mephedrone powder. Mephedrone is sold as 4-MMC, Meow Meow, M-Cat, and other nicknames. Cathine and cathinone ramp up dopamine, serotonin and noradrenaline levels in a manner very similar to amphetamine, with many of the same positive effects (mild euphoria, reduced hunger, increased energy) and the same negative effects (depression, fatigue, lack of appetite, drug craving). It is thought that chronic use of khat results in dopamine D2 depletion in areas of the brain involved in goal-directed action.

The current fervor over mephedrone being disguised as bath salts or plant food for black market sales purposes in the U.S and U.K. demonstrates that this question is not academic for developed western nations. Sold as Ivory Wave, or Bliss, or White Lightning, mephedrone and other products containing cathinone are increasingly available across the U.S. states. In 2008, police seized 600 pounds of fresh khat—in Fargo, North Dakota.

A recent paper published in Frontiers in Psychology, authored by a group of Dutch and Spanish psychologists, appears to show that khat users exhibit a specific cognitive deficit: On stop-signal tasks, stop signal reaction time (SSRT) was significantly slower for the khat users. Such tests typically involve rapidly pressing a green “go” button upon seeing an arrow in certain positions, or abruptly aborting the response when the arrow turns red. The test measures “individual ability to stop a planned or ongoing motor response in a voluntary fashion.” For example, someone with Parkinson’s disease would score at the very high end of the SSRT scale.

The study itself involved 20 regular khat users recruited from the immigrant populations of Leiden and The Hague, and matched against 20 khat-free controls. All of the khat users met four or more of the 7 DSM-IV criteria for addiction, and did not consume alcohol the night before the test. The investigators speculate that this reduced level of inhibitory control “may even be involved in the emergence of addiction: the more a drug is used, the less able users are to prevent themselves from using it.”

The parallels to traffic signals and stop signs are obvious, and apt. The authors state that the findings of their study are “rather worrying because, first, many real-life situations require active inhibition of prepotent actions, as in the case of traffic lights turning red, or of criminal actions.” The obvious conclusion is that the chronic chewing of khat leaves “may indeed lead to a marked deterioration of cognitive functions (as inhibitory control) implicated in driving behavior.” Studies by NIDA director Nora Volkow and others have show that cocaine users suffer similar reductions in dopamine D2 receptors and “need significantly more time to inhibit responses to stop signals than non-users.” In general, stimulant drugs taken regularly at high doses appear to disrupt response inhibition due to alterations in dopamine functioning. (Although some studies have shown a facilitation of inhibitory control at lower doses).

The usual caveats apply: It is impossible to rule out pre-existing propensities for impulsivity, disinhibition, and the like. Some health researchers do not agree that the case for driving impairment on khat has yet been made. In the Bulletin of the World Health Organization, Anita Feigin of the Centre for Population Health in Australia writes that, so far, much of the information is anecdotal, “and, as yet, there is no clear evidence of a causal relationship between the use of khat and traffic accidents.” African taxi drivers who immigrate to Australia use khat “to stay awake and alert.” However, Feigin notes that the use of khat has deeply divided the members of east African migrant communities.

It is an interesting conundrum. The developed West has its entrenched tradition of alcohol as a legal high, despite its side-effects, which frequently result in mayhem on the highways. On the other hand, the drinking nations must now contend with demands from other cultures for the decriminalization of khat and coca leaf, which, along with coffee and tea, make up a category we might call the “soft” stimulants.

Because of the connection with mephedrone and other amphetamine-like designer drugs, these questions will not be going away until more research provides some solid answers. Such research may not be long in coming: The NIH-funded Khat Research Program (KRP) at the University of Minnesota, for example, brings American researchers together with a br... Read more »

Colzato, L., Ruiz, M., van den Wildenberg, W., Bajo, M., & Hommel, B. (2011) Long-Term Effects of Chronic Khat Use: Impaired Inhibitory Control. Frontiers in Psychology. DOI: 10.3389/fpsyg.2010.00219  

  • January 30, 2011
  • 03:52 PM
  • 647 views

Smoking and the Slave Trade

by Dirk Hanson in Addiction Inbox


To Africa and back again.

[Queen Nzinga (smoking a pipe) with Her Entourage, Kingdom of Kongo, 1670s]--------->

In the 17th Century, tobacco, the prototypical New World stimulant, was introduced to Africa by European traders. By 1607, tobacco was being cultivated in Sierra Leone, and in 1611 a Swiss doctor commented on how the soldiers of the “Kingdom of Kongo” fought hunger by grinding up tobacco leaves and setting them on fire, “so that a strong smoke is produced, which they inhale.”

It did not take long for the true motivations behind this botanical boon to be revealed. Tobacco served two crucial functions for the slave traders of the Middle Passage: Once Africans had acquired the smoking habit, tobacco could be used in lieu of cash as payment for purchasing slaves. In addition, tobacco was frequently handed out to slaves during the horrific Atlantic voyage. This was not done out of altruism, or common decency, of course. In an article for Slavery and Abolition Journal, Jerome S. Handler writes: “European slavers apparently believed that such measures were useful in their efforts to control their ‘cargo’ and avoid or minimize social unrest and revolts—or even put the enslaved in a better mood prior to their being sold or transshipped from one American port to another."

How did the slaves smoke the tobacco enroute? With clay pipes supplied by the slave traders. The Europeans had introduced an easily grown, highly addictive plant drug, so it was inevitable that white traders would use that addictive property to their advantage. And they were happy to create an additional market in paraphernalia.

Handler, writing in the African Diaspora Archaeology Network Newsletter, notes that, while Africans produced their own pipes, “white clay pipes of Europeans manufacture, particularly English and Dutch, were commonly used to purchase slaves…. In general it appears that European pipes were often preferred to African ones.” The pipes came in long and short versions, the long “elbow bend” pipes being preferred on shore, with the short pipe being preferred for use onboard. Jean Barbot, an agent for the French Royal African Company, reported that the slaves onboard were occasionally given “short pipes and tobacco to smoak upon deck by turns.”

However humane the practice might sound, the motivations of the traders “were the same as those which prompted them to distribute beads and allow African board games aboard the ships, that is, an attempt to mollify or placate the captives in situations that were always fraught with tension and possibilities of insurrection.” Presumably, it also diminished hunger and helped keep the slaves on their feet during auction in the New World.

Not every ship’s captain went along with the pipes. A French slave ship captain wrote that “for fear of fire, tobacco should be grated and given as a powder.”  Handler, a Senior Scholar at the Virginia Foundation for the Humanities, notes that “there are no data on whether the enslaved were allowed to keep the pipes they received aboard the slave ships. “

Probably not. “Chances are that pipes were collected by the ship’s crew after each use to be re-used at another time,” according to Handler. But it is likely enough that at least some pipes were successfully smuggled ashore. And while most of the white clay pipes found in African descendant archaeological sites in America were probably local in origin, “it may be that an occasional pipe was brought by some enslaved African via the Middle Passage.”

Handler, J. (2009). The Middle Passage and the Material Culture of Captive Africans Slavery and Abolition, 30 (1), 1-26 DOI: 10.1080/01440390802673773

Graphics Credit: Virginia Foundation for the Humanities and the University of Virginia Library,
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