In a study examining Insomnia and the attribution process, the two authors Storms and Nisbett (1970) cautiously

warned, in their discussion, that they have no definitive means of showing that the sleep onset changes were produced by the differential attribution of arousal symptoms. Because of the inherent pitfalls in their experiment, Storms and Nisbetts study has been severely criticized on methodological grounds and could not be replicated in four other studies (Reisenzen, 1983). This critique will draw light upon the pitfalls of the study while also offering a host of alternative explanations. Experimental Overview Preceding the experiment it was hypothesized that (a) insomniacs given placebo pills, which they will believe capable of arousing them, will attribute their naturally occurring arousal to the pill, will therefore experience less intense emotions and will fall asleep more quickly than usual and (b) insomniacs given placebo pills, which they believe capable of calming them, will attribute more than their naturally occurring arousal to emotionally toned cognitions, will therefore experience more intense emotions and will fall asleep less quickly than usual. There is one independent variable, attribution, and three conditions: aroused, relaxed, and control. This manipulation varied according to which description of the placebo the participant was told. For those in the control condition, no placebo was administered. The chief dependent variable in the study was sleep onset. Arousal was also measured preexperimental and experimental nights in order to determine the extent to which arousal symptoms were experienced at bedtime. Methodological errors In a quasi-experimental research design, forty-two subjects were recruited by signs posted on the campus of Yale University. Ages of the subjects ranged from 19-26 and thirty-three of the 42 subjects were male and all but 2 were students. The recruitment process and screening process in this study is suspect at best. It should be noted that the majority of the participants were male students. It is possible then that this sample is more disposed to the sort of cognitive and attributional exertions that presumably underlie the reverse placebo effect; as replication studies using a more representative sample have failed to yield the same results (Bootzin, 1976). It is then possible that the misattribution phenomenon is more prevalent among hyper reflective undergraduates (Bootzin, 1976). Following suit, the study lacks generalizability to the larger population. Furthermore, no objective definition of insomnia was provided on the recruitment

posters, the signs were headed Insomniacs wanted for psychological research on dreams. This opens the door to a host of errors. The recruitment process allows for self-selection and selfdiagnosis, as such one must proceed with caution in interpreting the results, as we will see, the sample may not have contained true insomniacs. As a suggestion, medically diagnosed insomniacs should have been requested on recruitment flyers. This would have eliminated the error associated with someone having a false diagnosis. There are two types of insomnia: acute and chronic. Acute insomnia is insomnia persisting for a period less than a month and is more often attributed to stress and environmental factors (Peters, 2013). The researchers should have been clearer in their intent as to which type of insomnia they were focusing and this intent should have followed suit on recruitment posters, with the medical definition explicitly stated to avoid acute sufferers from taking part if it was chronic insomniacs they desired to study. Because chronic insomnia is a long-term condition, it is more likely to be a primary disorder for the individual as opposed to it being caused by stress or environmental factors. The conclusion is then justifiable that there is a difference between the two conditions, cognitively, emotionally, and biologically speaking and it is maybe this underlying difference that results in the prevalence of the misattribution phenomena depending on the type of insomnia. Secondly, there exists a sleep disorder that would heavily confound results. Sleep state misperception (SSM) is the medical term used for people who mistakenly perceive their sleep as wakefulness (Edinger, 1992). While most people with this condition will report not having slept the previous night at all or having slept very little, clinical recordings demonstrate normal sleeping patterns (Edinger, 1992). Furthermore, patients severely overestimate the time they took to fall asleep. Because the recruitment process employed by Storm and Nisbett did not request medically diagnosed insomniacs, people suffering from sleep state misperception could have confounded the data. The chief dependent variable in the experiment was sleep onset latency as estimated by the participant- a variable that is significantly overestimated by individuals suffering from SSM. Even more alarming is that SSM is believed to be most prevalent among young to middle-aged adults (Kushida, 2008), which is the entirety of our sample. Finally, the study should have discluded individuals who have chronic medical problems that may contribute to sleeping conditions, as done by Egeren et al (1983) in a study examining presleep cognitions and attributions in sleep-onset insomnia. Because both of our dependent variables, sleep-onset latency and arousal, are reported via self-report it is critical that the experimenter tries to reduce error variance attributable to unreliability of self-reports (Egeren et al 1983) No such effort was made on behalf of the experimenters. Storms and Nisbetts study would have greatly benefited had it followed more stringent screening criteria as seen in the study by Egeren at al. In their study

recruitment of subjects involved a three-stage process, each of which included either a questionnaire or an interview. Any significant discrepancies (10%>) among a subjects three reports resulted in exclusion from the study. Since our dependent variables are self-reported we have no control on the reliability of them. At a minimum we could have increased the reliability by filtering out candidates who are inconsistent in their preexperimental assessments. However, it appears the experiments had some success in generating a believable cover story as seen in the follow up discussion but at the cost of unreliable self-reported data. The design of the study was quasi-experimental, more specifically an interrupted series design. The drawback of this design is that it is not particularly strong at controlling for threats to internal validity. An interrupted time series design with a comparison group may have helped to provide a check with some of the threats to internal validity. Errors in Measuring the Dependent Variable All of the data gathered in this experiment is self-reported data- this is troublesome as none of it can be verified. The chief dependent variable is the subtraction of two estimated measures: when they went to bed what they fell asleep. Therefore our chief dependent variable is automatically erroneous as all our data are estimates, with the accuracy of these estimates greatly unknown. It is plausible that individuals exaggerated or under estimated these actual times. Also, an individual can never accurately report the time they fell asleep unless they have another individual there or have the assistance of technology. Further detracting from the accuracy of the measured dependent variables is the fact that these estimates were given up to thirty-six hours after the fact. Participants answered pre-experimental questions on Wednesday about their sleep on Tuesday and Monday night and Friday, after the experimental portion, about their sleep on Wednesday and Thursday night. Estimating the time you went to bed and the time you feel asleep is difficult enough but doing it thirty-six hours after the fact becomes extremely difficult. It is hard to find any generalizability in this study and in the treatment as our measure of the chief dependent variable is inherently flawed. The other dependent variable, arousal symptoms, also faces the same flaws. Participants were asked to determine the extent to which arousal symptoms were experienced at bed up to thirty-six hours after the fact. It is hard seeing the validity and reliability in these measures of arousal. Questions such as how warm or cold did you feel? were asked. Because so much time has elapsed since the event it is nave to think this self-reported measure of arousal can be reliable especially considering the trivial nature of the

questions. Answering questions like How much did your mind race? using a scale is also difficult and subjective. As a suggestion, both dependent variables should have been asked upon awaking the very next morning. The time they went to bed could have even been recorded that very night to ensure maximum reliability. This would have decreased the reliance on recall and thus produced heightened sensitivity and reliability (Kellog & Baron 1975). A more elaborate cover story could have been postulated and participants could have been made to sleep in sleep laboratory with the excuse that their brain waves needed to be monitored. This would allow for accurate objective measures of the sleep-onset latency. A habituation period could be provided to counter any experimental effects the participants may face sleeping in a novel environment. To further demonstrate the unreliability of the participants self reports, in a similar study conducted by Egeren et al (1983) objective measure of sleep onset latency were recorded as well as objective measures (self-report). A discrepancy was found between objective and subjective indices of sleep-onset latency. For each subject there was a difference between their estimated and the measured sleep onset latency. Since both dependent variables rely on the participant we have a weak operationalization of the dependent variables, as there is much discrepancy between subjective responses. Lastly, it was instructed that participants could continue taking medication as usual. This opens a host of confounds as many medications/drugs influence sleep behavior including those popular on campus- caffeine, alcohol, and marijuana. There is a chance that any of these three could have been at play. Because of the design of the experiment there is little internal validity. Students drug consumption behaviors could have confounded results as well as environmental stressors such as exams as well as their presleep rituals.

Hypothesis Revisited There were three components to the hypotheses. Only one of the components was effectively measured- the time taken to fall asleep. The second component, attribution was assumed to be effectively manipulated, by creating the arousal and relaxed conditions but was never verified. The third component of the hypotheses emotional intensity was never explicitly checked either. To establish whether subjects in one condition attributed their arousal internally or to the pill, one could have debriefed them following the study and handed them a questionnaire to establish the focus of their attribution. Secondly, the difference in emotional experience was

never checked in either condition. It seems paradoxical now to believe the hypothesis was satisfied when two of its three components were not explicitly measured and verified. The power of the study would have benefited had the researchers randomly selected from a pool of participants with varying sleep-onset latencies. This gives rise to the rival hypothesis of selection, as noted by Huck & Sandler (1979), because there was no random assignment the resultant treatment effects are confounded with group differences. Threats to Internal Validity There is no mention of random assignment to the conditions. Failure to assign subjects randomly to the conditions possibly leads to treatment effects being confounded with group differences. This is problematic as hinted by the inequality of the two groups during preexperimental nights. During so, the group in the arousal condition took 53 minutes to fall asleep versus the thirty-four in the control and the thirty-six in the sedation condition. Even though this difference is not statistically significant, it could be biologically significant, as we will see in the alternative hypotheses section, it is possible the participants in the arousal condition fell asleep faster in the experimental condition to compensate for the reduced amount of sleep in the previous nights. The independent variable in the study was attribution and the two conditions of interest were relaxed and aroused. The credibility of the experiment begins to collapse here, as we will see the experiment failed in successfully manipulating the independent variable all together. In analysis of their arousal manipulation, Storm and Nisbett found insignificant differences in reported arousal for preexperimental and experimental nights. If they failed in manipulating arousal between the two conditions it is logical to assume that they failed to generate different emotional intensities between the two groups as well. How they could justify their hypotheses when clearly they failed to manipulate the independent variable seems paradoxical. With a failed manipulation of the independent variable (attribution) and absence of differing emotional intensities between the groups we are left wondering if it is really the hypotheses that was tested. How could misattribution then cause the effects even though the conditions necessary for the error to occur seem to be absent in the experiment (arousal + emotional intensity). However, it is ignorant to believe that manipulating attribution is an easy feat. Some credit must be given to Nisbett and Storm for the attempt. The difficulty lies in that the variable is ultimately always in control of the participant. The participant consciously or unconsciously has the control when

attributing their arousal to an external or internal source. According to the two factor theory of emotion, emotion is felt when a physiological arousal occurs and the person searches the immediate environment for cues to label the arousal, but since there was no change in arousal it is unlikely this external search occurred, therefore it unlikely that misattribution towards the pill could have been made. Subjects knew that their actual experience of insomnia symptoms was about the same as it usually was because of their own past experience with insomnia (Bootzin, 1976) and since arousal levels did not change as a result of the manipulation no misattribution to the pill could have logically been made. If patients are familiar enough with their symptoms to recognize the pill is not having the originally intended effects (as seen in the manipulation check); it follows that these patients would have had enough experience to recognize the symptoms as the same ones they have been chronically experiencing; These (participants), it seems, would hardly be the ones to begin suddenly attributing their symptoms to a novel pill in the face of a long standing tendency to attribute them to endogenous factors (Bootzin, 1976). The experiment assumes that when participants fail to experience the effects of the drug; they will automatically infer something damaging about themselves however it is also likely that they could infer something damaging about the drugs for like they did not work or they were not given a high enough dose. As discussed by critics of the Storm and Nisbett study (Ross & Olson, 1981) it is possible that sleep onset latency, the intended target behavior, as a variable might not be easily influenced by a misattribution manipulation. In addition it could be argued that target behaviors such as sleep onset latencies are quite removed from any emotional state purportedly mediating those behaviors; as Ross and Olson (1981) point out such behavioral variables should not be expected to be as easily by a misattribution manipulation. In light of this, it is possible that the experiment was not measuring misattribution but introspection with respect to present and past symptomology. Only to the extent that subjects are led to dwell on their symptoms are they likely to engage in the chain of reasoning and comparative analysis that forms the basis for the reverse placebo effect (Bootzin, 1976) Ethics, Power, and Statistics When looking at experimental biases, no demand characteristics were present as noted in the results section of the study. In terms of experimenter bias, the experimenters knew the hypothesis and the conditions of the assigned participants, but this is insignificant as all of the data was collected vie self-report which eliminates researcher biases. The sample size of the study was small and could have been increased to increase power, however in the other studies

examining the same phenomenon the sample size Storms and Nisbett use are typical. Storms and Nisbett failed to report any of their measures in terms of standard deviations, which would be needed for meta-analysis. The statistical significant was confirmed with an ANOVA and the results were significant at the 0.02 level. Furthermore, an analysis of covariance revealed regression did not account for treatment effects (Storms & Nisbett, 1970) Storms and Nisbett failed to mention many of the ethical protocols that should have been in place. No mention of harm was made prior to the study as well as confidentiality of results. Deception was used, however no mention of consent form following the debriefing was made. During the debriefing it is unclear whether participants were told why the deception was necessary or if further contact information of the researchers/ethics committee was given

Alternate hypothesis There are a few alternative hypotheses at play that could have been at play. It is well documented that there is significant night to night variability in sleep quality experienced by insomniacs (e.g., Edinger et al 1991; Coates 1981) Maybe some people were suffering a bad bout of insomnia, while others slept better because they were recovering from a bad bout. This nightto-night variability could have confounded the results because of the biological significance in loss of sleep. There is also the wait and relief hypothesis, maybe both conditions were waiting for effects of pill to kick in, and those in the arousal condition fell asleep faster because they were relieved that they did not experience an increase in arousal while the ones waiting for the relaxing effects were more distressed when they didnt feel intended effect of drug. Finally, there is also the distraction hypothesis. Worchel and teddie (1976) found that the experience of crowding was significantly reduced in a close interaction situation if the room contained a number of presumably distracting pictures and posters; studies in different experimental contexts suggest in addition that distraction can be effective in reducing various types of stress reactions. In Nisbett and storms experiment, this distraction could have risen in the participants selfscanning in attending to expected pill effects.

Quantitative Research Article Critique

Arash Randjbar 100790730 PSYC3001

Presented to: Matt Murdoch

December 10th 2013

References
Bootzin, R. R., Herman, C. P., & Nicassio, P. (1976). The power of suggestion: Another examination of misattribution and insomnia. Journal of Personality and Social Psychology, 34(4), 673-679. doi:http://dx.doi.org/10.1037/00223514.34.4.673 Edinger, J., & McCall, W. (1992). Subjective total insomnia: an example of sleep state misperception. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1557596 Huck, S.W., & Sandler, H. M. (1979). Rival hypotheses: Alternative interpretations of data based conclusions. New York: Harper & Row.

Kellogg, R., & Baron, R. S. (1975). Attribution theory, insomnia, and the reverse placebo effect: A reversal of storms and nisbett's findings. Journal of Personality and Social Psychology, 32(2), 231-236. doi:http://dx.doi.org/10.1037/0022-3514.32.2.231

Kushida, C. (2008). Handbook of sleep disorders. (p. 32). Peters, B. (n.d.). What is acute insomnia? difficulty falling or staying asleep may go away. Retrieved from http://sleepdisorders.about.com/od/commonsleepdisorders/a/Acute_Insomnia.htm

Reisenzein , R. (1983). The schachter theory of emotion: Two decades later. Free University Berlin, Retrieved from http://www.phil.unigreifswald.de/fileadmin/mediapool/psychologie/lehrstuhl_allg2/Reisenzein1983_Schachter_Theory.pdf Storms, M. D., & Nisbett, R. E. (1970). Insomnia and the attribution process, Journal of Personality and Social Psychology, 16(2), 319-328. Van Egeren, L., Haynes, S. N., Franzen, M., & Hamilton, J. (1983). Presleep cognitions and attributions in sleep-onset insomnia.Journal of Behavioral Medicine, 6(2), 217-232. Retrieved from http://search.proquest.com/docview/616845812?accountid=9894 Worchel, S., & Teddie, C. (1976). The experience of crowding: A two-factor theory. Journal of Personality and Social Psychology,34(1), 30-40. Retrieved from http://search.proquest.com/docview/616087799?accountid=9894