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By Dennis D. Embry, Ph.D.
Dianne Perukel submitted the following message on the Office of National Drug Control Policy (ONDCP) listserve on March 5, 2009
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I have been working with several well-meaning traffic safety advocates that would like to print posters with some very graphic pictures of traffic crash victims. I'm having a hard time articulating WHY this is such a bad idea...does anyone know of any articles, research, etc. that would help me?
The question is a good one, and the answers from others on the listserve are correct that scary stuff doesn’t work. Such graphic scare tactics are not effective, and can even have a negative effect on a population level basis.
Now the question is why do such things rebound or not work?
I have to turn to evolutionary findings, neuro-science, anthropology and developmental research to explain.
In the past 40K to 10K years, humans developed certain dopamine receptor gene variations. NIDA and others have funded this research. Drugs are about dopamine, remember all those talks by Dr. Noral Volkow.1 And, she observes that eating and many other survival related behaviors cause the firing of dopamine.2
Now why did these new dopamine genes arise some 10,000 to 40,000 years ago and then spread dramatically and keep spreading? Why are certain dopamine genes positively selected recently by evolution? The clue is that they are associated with human migration across the planet.3
While not complete, genes associated with human migration and risk of substance abuse are generally associated with novelty seeking or sensation seeking,3-13 often higher or “normal” IQ14 15 AND sensitivity to perceived human stressors.16-18 These genes are also associated with increased risk of aggression against other humans.19 20 These genes have been positively selected by evolution, which means they have evolutionary advantages.
Not indulge a bit of “just-so” storytelling to explain what all this might mean to answer the question. Why would humans move from the proverbial Garden of Eden in the Rift Valley where we began?21 There are a couple of interrelated sensible reasons: something bad happened, food became scarce, people died, and people had wars or fight about that food or resources. Almost certainly some of the adolescents left in an aggressive huff rather impulsively, since puberty makes teens more reward dependent than adults and small children. These would not have been the shy, anxious adolescents who would have feared leaving their tribe or clan. These would have most certainly have been the adolescents who were more what we would call, “hyper” today in terms of physical activity—running, jumping, and exploring. They would not have been the timid kids either who followed the adult instructions. And they would have more than likely been somewhat precocious sexually.22 These young humans who left whatever was the current “Eden” founded the next communities some distance away where there was more food and safety. There they mated, and had babies who carried those same genes. If a new bad thing happened of food or fighting problems, the process repeated and the gene penetration for these traits spread across the globe and still is. In fact, one can see the increased prevalence of sensation seeking or thrill seeking all across the frontier—non-farming areas of the United States—on student survey instruments such as the Communities That Care Survey.
Accidentally, these genes conferred an increased risk of substance abuse—especially under conditions of stress as adults or childhood if parenting adults become aggressive or insensitive to the needs of the children who care those genes.18 23-25 These genes get “turned on” when life is hard,16 which is an epigenetic process. This refers to changes in phenotype (appearance) or gene expression caused by mechanisms other than changes in the underlying DNA sequence (hence the name epi - "in addition to" - genetics). These changes may remain through cell divisions for the remainder of the cell's life and may also last for multiple generations. However, there is no change in the underlying DNA sequence of the organism; instead, non-genetic factors cause the organism's genes to behave (or "express themselves") differently.
Why doesn’t the fear mongering work? The scary pictures and scary story approach fails for several scientific reasons: 1) they are not addressing the underlying biological/social predictors; 2) for some, they may engage the epigenetic mechanisms that increase the risk of substance abuse and other risky behaviors; 3) for others who have a heavy loading of sensation seeking and novelty seeking, the “thrills” of such risky behavior are potentially reinforcing; 4) for the small group who have developed such underlying cognitive impulsivity with suicidal thoughts, such fear mongering explicitly shows ways to kill one’s self in a dramatic way; 5) the people who do respond to respond to fear approaches are not likely to have used drugs anyway. The final fatal possibility is that the very fear mongering actually increases the desirability of the deviant behavior and decreases the perceived danger, which is an operant rather than biological causal factor. That is, the social attention (which clearly affects dopamine) one receives for being deviant is highly reinforcing—a fact well documented in prevention science studies for many years.26-29
The recent publications on the Montana Meth Project illustrate the perils of fear appeals.30 The Montana Meth Project showed horrific TV ads, done with the highest production values of dramatic harms of meth. A peer-reviewed, independent study shows: “…the Claims that the campaign is effective are not supported by data. The campaign has been associated with increases in the acceptability of using methamphetamine and decreases in the perceived danger of using drugs.”
References Cited
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2. Volkow ND, Wang G-J, Maynard L, Jayne M, Fowler JS, Zhu W, et al. Brain dopamine is associated with eating behaviors in humans. International Journal of Eating Disorders 2003;33(2):136-42.
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4. Roy A, Adinoff B, Roehrich L, Lamparski D, Custer R, Lorenz V, et al. Pathological gambling. A psychobiological study. Archives of General Psychiatry 1988;45(4):369-73.
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14. Swanson J, Oosterlaan J, Murias M, Schuck S, Flodman P, Spence MA, et al. Attention deficit/hyperactivity disorder children with a 7-repeat allele of the dopamine receptor D4 gene have extreme behavior but normal performance on critical neuropsychological tests of attention. Proceedings of the National Academy of Sciences of the United States of America 2000;97(9):4754-9.
15. Kerns KA, Price KJ. An investigation of prospective memory in children with ADHD. Child Neuropsychology 2001;7(3):162-71.
16. Madrid GA, MacMurray J, Lee JW, Anderson BA, Comings DE. Stress as a mediating factor in the association between the DRD2 TaqI polymorphism and alcoholism. Alcohol 2001;23(2):117-22.
17. Pruessner JC, Champagne F, Meaney MJ, Dagher A. Dopamine Release in Response to a Psychological Stress in Humans and Its Relationship to Early Life Maternal Care: A Positron Emission Tomography Study Using [11C]Raclopride. J. Neurosci. 2004;24(11):2825-31.
18. Lakatos K, Nemoda Z, Toth I, Ronai Z, Ney K, Sasvari- Szekely M, et al. Further evidence for the role of the dopamine D4 receptor (DRD4) gene in attachment disorganization: interaction of the exon III 48-bp repeat and the -521 C/T promoter polymorphisms. Molecular Psychiatry 2002;7(1):27-31.
19. Raine A. Annotation: the role of prefrontal deficits, low autonomic arousal, and early health factors in the development of antisocial and aggressive behavior in children. Journal of Child Psychology & Psychiatry & Allied Disciplines 2002;43(4):417-34.
20. Barkley RA, Smith KM, Fischer M, Navia B. An examination of the behavioral and neuropsychological correlates of three ADHD candidate gene polymorphisms (DRD4 7+, DBH TaqI A2, and DAT1 40 bp VNTR) in hyperactive and normal children followed to adulthood. American Journal of Medical Genetics 2006;Part B, Neuropsychiatric Genetics: the Official Publication of the International Society of Psychiatric Genetics. 141(5):487-98.
21. Broadhurst CL, Cunnane SC, Crawford MA. Rift Valley lake fish and shellfish provided brain-specific nutrition for early Homo.[see comment]. British Journal of Nutrition 1998;79(1):3-21.
22. Charles KE, Egan V. Mating effort correlates with self-reported delinquency in a normal adolescent sample. Personality & Individual Differences 2005;38(5):1035-45.
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27. Dishion TJ, McCord J, Poulin F. When interventions harm: Peer groups and problem behavior. American Psychologist 1999;54(9):755-64.
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29. Dishion TJ, Spracklen KM, Andrews DW, Patterson GR. Deviancy training in male adolescents friendships. Behavior Therapy 1996;27(3):373-90.
30. Erceg-Hurn D. Drugs, Money, and Graphic Ads: A Critical Review of the Montana Meth Project. Prevention Science 2008;9(4):256-63.
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