The students in my classes sometimes argue that, even though they have an "occasional" cigarette, they are not really "hooked" or dependent upon the nicotine they are inhaling. My response has usually been to suggest that they try to go without a cigarette for a week and come back to tell me about their lack of addiction. None has ever come back. Now, I understand why they don't ever return.

In a new clinical study reported in the July, 2007 issue of the Archives of Pediatric and Adolescent Medicine, the researchers followed 1246 sixth-grade students in Massachusetts for four years. By the end of their study, 217 of their participants reported inhaling while smoking. So, how many of these 10th graders could now be considered dependent on nicotine? Using the "Hooked on Nicotine Checklist" as the measure of loss of autonomy over tobacco and the ICD-10's definition of tobacco dependence, the results were startling. More than half these adolescents (N = 127; 54.5% of smokers) had lost their autonomy over tobacco use and 83 inhalers (38.2% of smokers) were fully tobacco dependent. Further, the speed with which autonomy loss was reached was extremely fast: 10% of these smokers had lost their autonomy within 2 days of beginning to smoke and 25% within the first month of first inhaling. Of those who were tobacco dependent, half had reached that condition by the time they were smoking just 46 cigarettes per month, i.e., one and a half cigarettes per day. The authors conclude

[t]he most susceptible youths lose autonomy over tobacco within a day or 2 of first inhaling from a cigarette. The appearance of tobacco withdrawal symptoms and failed attempts at cessation can precede daily smoking; ICD-10-defined dependence can precede daily smoking and typically appears before consumption reaches 2 cigarettes per day.

These data ought to speak loud and clear (though I know they won't) to teenagers and young adults who think that a couple of cigarettes every once in a while mean nothing. The ease with which tobacco use hooks its addicts is simply amazing.

Target article: DiFranza, J. R., Savageau, J. A., Fletcher, K., O'Loughlin, J., Pbert, L., Ockene, J. K., McNeill, A. D., Hazelton, J., Friedman, K., Dussault, G., Wood, C, & Wellman, R. J. (2007). Symptoms of tobacco dependence after brief intermittent use: The development and assessment of nicotine dependence in Youth-2 study. Archives of Pediatric and Adolescent Medicine, 161, 704-710. [Link to abstract]

Newspaper report: Bakalar, N. (2007, July 31). Nicotine addiction is quick in youths, research finds. New York Times [Electronic version]

The image above is Copyright © Wellcome Images, but has been altered into a Derivative Work by the author by a colorization change.

In his volume on memory, the German evolutionary biologist, Richard Semon (1859-1918), postulated that the result of encoding an experience in memory would result in a specific physical trace of that experience in the brain's cells, or what he termed an "engram" (Semon, 1904, 1921 [in English]; see Cherkin, 1966, note 1 for a brief explanation of Semon's argument). The famed American neuropsychologist, Karl S. Lashley (1890-1958), searched in vain for evidence of such engrams or memory traces in his Harvard laboratory and went on to propose a countertheory of memory as function of non-localized "mass action" across the brain.

Following upon the work of Ramon y Cajal and Sherrington, the Canadian neuropsychologist, Donald O. Hebb (1904-1985), disagreed with Lashley and argued for a mechanism by which memories could be localized, i.e., his proposal for the "Hebbian synapse" on the neuron and collections of such synapses across associated neurons in the form of "cell assemblies" (see Brown & Milner, 2003, for a longer appreciation of Hebb's contributions). For the past four decades, the focus for identifying Hebbian synapses has been undertaken under the overarching research concern for long-term potentiation (LPT), that is, the assumption that "information is storied in the brain as changes in synaptic efficiency..." and that "the location of storage, the engram of learning and memory, must therefore be found among those synapses which support activity-dependent changes in synaptic efficiency" (Bliss & Collingridge, 1993, p. 31).

In a report published in the Journal of Neuroscience, a group of researchers at the University of California at Irvine have reported the first direct visual and physical evidence for a memory trace. As the press release from the UCI describes their breakthrough work

the study shows that synaptic connections in a region of rats' brains critical to learning change shape when the rodents learn to navigate a new, complex environment. In turn, when drugs are administered that block these changes, the rats don’t learn, confirming the essential role the shape change plays in the production of stable memory...Working with advanced microscopic techniques called restorative deconvolution microscopy, the UC Irvine team found that the LTP-related markers appear during learning and are associated with expanded synapses in the hippocampus. Because the size of a synapse relates to its effectiveness in transmitting messages between neurons, the new results indicate that learning improves communication between particular groups of brain cells.  (UC Irvine scientists, 2007, July 25).

So, more than a century after Semon proposed a role for a physical trace in the brain's cell in the establishment of a memory, laboratory research has appeared to confirm this finding.

Target article: Fedulov, V., Rex, C. S., Simmons, D. A., Palmer, L., Gall, C. M., & Lynch, G. (2007). Evidence that long-term potentiation occurs within individual hippocampal synapses during learning. Journal of Neuroscience, 27(30), 8031-8039. [Link to abstract]

Press release: UC Irvine scientists unveil the 'face' of a new memory [Press release]. (2007, July 24). Today@UCI. Retrieved July 31, 2007 from the UCI website: http://today.uci.edu/news/release_detail.asp?key=1638

References

Bliss, T. V. P., & Collingridge, G. L. (1993, Jan 7). A synaptic model of memory: Long-term potentiation in the hippocampus. Nature, 361(6407), 31-39.

Brown, R. E., & Milner, P. M. (2003). The legacy of Donald O. Hebb: More than the Hebb synapse. Nature Reviews Neuroscience, 4, 1013-1019. Retrieved July 31, 2007 from http://www.nature.com/nrn/journal/v4/n12/full/nrn1257_fs.html

Cherkin, A. (1966, Jan 15). Toward a quantitative view of the engram. Proceedings of the National Academy of Sciences of the United States of America, 55(1), 89-91.

Hebb, D. O. (1949). The organization of behavior: A neuropsychological theory. New York: Wiley. (Reprinted by Lawrence Erlbaum Associates, 2002.)

Semon, R. (1904). Die Mneme als erhaltendes Prinzip im Wechsel des organischen Geschehens. Leipzig, Germany: Wilhelm Engelmann.

Semon, R. (1921). The mneme. London: Allen and Unwin.

The Wellcome Trust has made available both its historical and contemporary image library for biomedical topics. Read More...

The debate over the effects of marijuana (cannabis) and its principal psychoactive ingredient, Δ^9-tetrahydrocannabinol (THC), has raged for many decades. During the 1930s as the nation was coping with the effects of the Depression, the Federal Government promoted the notion that marijuana was a dangerous narcotic which led straight to psychiatric madness. The most infamous version of this belief came in the 1936 film, Reefer Madness (originally known as Tell Your Children). The criminalization of marijuana use at the federal level was put in place with the passage of the Marihuana Tax Act of 1937 and was further refined by the Comprehensive Drug Abuse Act of 1970. During the 1960s and 1970s as the use of marijuana became more widespread within the general American culture, a shift in public opinion led to a decreased fear of the substance and a call for the decriminalization of the drug. In the later years of the 20th century, the argument by its supporters held that there was little to no evidence that marijuana had any lasting delerious effect and that, compared with the legally-available substances of alcohol and tobacco, marijuana use was innocuous. This view was never endorsed by the government nor by most medical organizations.

A new meta-analysis published in British medical journal, The Lancet, argues that the use of cannabis is not at all an innocent pleasure. Rather, in a review of the combined results of 35 population-based longitudinal observational studies of the relationship between the use of cannabis and psychiatric disorders in later life, the authors found an overall increased risk of 41% in the development of any psychosis among individuals who had used marijuana in the past. The summary of their findings reports:

There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio=1·41, 95% CI 1·20–1·65). Findings were consistent with a dose-response eff ect, with greater risk in people who used cannabis most frequently (2·09, 1·54–2·84). Results of analyses restricted to studies of more clinically relevant psychotic disorders were similar. Depression, suicidal thoughts, and anxiety outcomes were examined separately. Findings for these outcomes were less consistent, and fewer attempts were made to address non-causal explanations, than for psychosis. A substantial confounding effect was present for both psychotic and affective outcomes.

These results were so persuasive that the editors of The Lancet editorialized as follows:

In 1995, we began a Lancet editorial with the since much-quoted words: “The smoking of cannabis, even long term, is not harmful to health.” Research published since 1995, including Moore's systematic review in this issue, leads us now to conclude that cannabis use could increase the risk of psychotic illness. ("Rehashing the evidence...," 2007)

So, has the question been settled? Is it clear that marijuana is a dangerous drug which can cause irreparable harm to its users? It would be stretching the scientific arguments advanced by Moore and her colleagues (2007) to use this study's findings as having settled this question in a definitive way. My reactions to this article include these thoughts:

• It is likely that using marijuana increases the risk of psychotic illness in later life for some small percentage of the population. And, since psychotic illness can be quite debilitating and tends to follow a chronic course, the danger may be substantial that some marijuana users are putting their later life in real jeopardy.
• Correlation, as our basic research theories tell us, can never prove causation. All of the studies examined by Moore et al. (2007) were correlational in nature. Further, the additional use of meta-analytic grouping techniques cannot turn correlational data into experimental data no matter how sophisticated the statistics. This means that, while the trends and the thrust of the data seems to make marijuana a very promising explanatory causal factor in the development of some of the psychoses that these research participants developed, such a link has not been conclusively demonstrated. And, while the gross odds ratio speaks of a 41% increased risk, the authors themselves acknowledge the impact of confounding and other variables in lowering the risk percentage in the studies they examined. Hence, we are left without a good estimate of what the actual increased risk might be.
• This last point is related to a fundamental set of questions about causality in the area of drug risk research. The primary question concerns how much the decision to use marijuana (in earlier life) and the development of a psychotic illness (in later life) might BOTH be causally related to an underlying third factor. Might it be possible that there is a genetic determinant or a genetic x environmental interactive determinant that could explain a large proportion of the relationship identified in this study? Alternatively, since we know that psychosis tends to emerge in adulthood rather than adolescence, might it be possible that pre-psychotic adolescents might be "self-medicating" or using marijuana to ward off their sense of an increasingly unstable or deteriorating psychological state and this would then serve to explain the sequence of drug use preceeding the appearance of tangible psychotic symptoms? Such questions demand further study.

Target article: Moore, T. H. M., Zammit, S., Lingford-Hughes, A., Barnes, T. R. E., Jones, P. B., Burke, M., Lewis, G. (2007, July 28-August 3). Cannabis use and risk of psychotic or affective mental health outcomes: A systematic review. The Lancet, 370, 319-328.
  
Press release: Cannabis could increase risk of psychotic illness in later life by over 40 percent [Press release]. (2007, July 26). EurekAlert!.

References

Nordentoft, M., & Hjorthøj, C. (2007, July 28-August 3). Cannabis use and risk of psychosis later in life. The Lancet, 370, 293-294. (Commentary)

Rehashing the evidence on psychosis and cannabis [Editorial]. (2007, July 28-August 3). The Lancet, 370, 292.
  
====================
Update 7/30/07 11:30 pm

A respondent to Andrew Sullivan's excellent blog has posted a detailed argument why cannabis is not congenial to the mental health of many of its users. I found the posting persuasive and have posted a link to it here.

The New York Times reports that the founder of "rational-emotive behavior therapy," Albert Ellis, has died at age 93. Ellis was both an incredibly influential figure in his challenge to the orthodoxy of Freudian theory in the 1950s and 1960s, but also one of the great characters in psychology. His belief that people are prone to think like they were crazy (and thereby makes themselves nuts) and that people believe all sorts of nonsense prompted him to rail and challenge both patients and critics alike. I only saw Ellis once or twice at the annual meeting of the American Psychological Association, but to hear him preach the "Gospel of St. Albert" as the New York Times obit writer put it was a bracing experience. In class, lectures and discussions about Ellis' approach to therapy in my experience often bring out passionate statements in support and opposition. But, they are always fun.

Target article: Kaufman, M. T. (2007, July 25). Albert Ellis, influential psychotherapist, dies at 93. New York Times. Retrieved July 24, 2007 from the New York Times website.

Resources: Albert Ellis Institute | Albert Ellis (@ Wikipedia)

The latest issue (July 21, 2007) of the British medical journal, The Lancet, reports on a startling case of a 44-year-old French man who came to the hospital complaining of weakness in his left leg. In giving his medical history, he noted that he had had a ventricular shunt inserted for a while in his head when he was 9 years old. The shunt had been removed 5 years later when he was 14 years old. The doctors at the hospital decided, therefore, to take a look at the man's adult brain by taking an MRI. They were startled with what they found:
  

(Image taken from Wired Science blog)

The interior of the man's brain consisted mostly of fluid-filled ventricles with highly compressed brain tissue. Somehow, as the man grew up and the brain structure grew increasingly small, the brain was able to compensate. The man's IQ level was in the borderline range (full IQ = 75; verbal IQ = 84; performance IQ = 70), but permitted him to marry, father two children, and maintain a job as a government worker. (Read more at ScienceDirect).

Target article: Feuillet, L., Dufour, H., & Pelletier, J. (2007, July 21). Brain of a white-coloar worker. The Lancet, 370, 262.

A new story by Adam Liptak in the New York Times (behind the TimesSelect wall) entitled, "Story of Wrongful Convictions Raises Questions Beyond DNA" points once again to the weakness of "eyewitness" testimony. As the story notes:

Brandon L. Garrett, a law professor at the University of Virginia, has, for the first time, systematically examined the 200 cases, in which innocent people served an average of 12 years in prison. In each case, of course, the evidence used to convict them was at least flawed and often false — yet juries, trial judges and appellate courts failed to notice.“A few types of unreliable trial evidence predictably supported wrongful convictions,” Professor Garrett concluded in his study, “Judging Innocence,” to be published in The Columbia Law Review in January.

The articles goes on to say that

The leading cause of the wrongful convictions was erroneous identification by eyewitnesses, which occurred 79 percent of the time. In a quarter of the cases, such testimony was the only direct evidence against the defendant.

Once again, naive belief in the accuracy or superiority of so-called "eyewitness" testimony is shown to be dangerous and grossly misplaced.

Target Article: Liptak, A. (2007, July 23). Study of wrongful convictions raises questions beyond DNA. New York Times (Electronic version).

I am beginning this blog, Storied Conduct, anew as a place to highlight news and recent information in the fields of psychology and the allied social and natural sciences. I recently got RapidWeaver software to help me compose materials for online publishing. So, I am hoping that I can begin to use this blog as a mechanism to share with my classes and anyone else coming here what I have found to be intriguing or exciting in the areas I teach and read.