Essay by PaperNerd ContributorCollege, Undergraduate October 2001

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essayMinor Physical Anomalies, Dermatoglyphic Asymmetries, and Cortisol Levels in Adolescents with Schizotypal Personality Disorder leaves some methodological doubt that carries over into results concerning the relationship between cortisol and schizotypal personality disorder.

This study was conducted over only one day and with some intelligent foresight the authors realized that many of these participants would be taking medications, and so asked those participants in the study to abstain from their medication only one day prior to the study. It probably would have been difficult to get the participants to abstain for more than one day prior to the tests, but the question remains is one day enough when some of those medications have effects that last longer than a couple of days? These medications were also more likely to be given to those with behavioral problems and so if they have some affect on cortisol were more likely to skew schizotypal and the other personality disorders group, rather than the normal group(Weinstein et al.,

619). It turns out in fact that methylphenidate does indeed influence the hypothalamic-pituitary-adrenal axis by increasing plasma ACTH (Appendrodt et al., 415). This increase in ACTH would result in an increase in cortisol release. Methylphenidate concentrations in the blood plasma have been shown to peak at 6.5 hours after ingestion, with not too quick a half life of 32.9 ng.h/mL and 3.9 hours (Modi et al., 379). Hence after 48 hours, 7% of the original methylphenidate would still be present in one’s system. This may or may not be enough to skew the schizotypal personality disorder group, since five of them had taken methylphenidate in the last month, and possibly even under 48 hours prior to the study. Therefore it is questionable whether or not the cortisol increase was due to medication in the schizotypal group or that the group was more likely to have increased cortisol levels.

The long term effects of such medication and its relationship to cortisol also seems to be unstudied. Chronic exposure to methylphenidate has been shown to have long term changes such as lowering the number of dopamine transporters in the rostral caudate putamen (Izenwasser et al., 187). Since such long term effects have been shown on neurotransmitter populations already with chronic methylphenidate exposure, it is not without strong possibility that such chronic exposure could also influence long term cortisol production and output. Hence more doubt is cast on the fact that a cortisol level increase is correlated with schizotypal personality disorder.

Caffeine on the other hand has been shown to stop its cortisol elevation period after 2 hours of ingestion (Lovallo WR et al., 365), so it is unlikely that caffeine use interfered with the study. Another question involving substance abuse to ask, besides how long exactly it has been since the last medication period, is were there any smokers in this group? The illegality of underage smoking does not make its prescience null and void. The other possibility that is raised in response to the increase cortisol levels is that perhaps people with schizotypal personality disorder have a higher cortisol level increase to novelty. Though an intriguing possibility, a test needs to be devised, such as a novel sound test in which random sounds are generated and the cortisol level response is measured among the participants. Yet still this would not eliminate the possibility of medicinal interference with cortisol response.

In order to fix such confusion between medicinal effects and natural effects, a new experiment should be conducted in which the exact dates of medication are known, and a longer period of abstinence from such medications are required. The best solution would be to find an un-medicated population for sampling so that all of this doubt could be eliminated.

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