Substance Use Associated with Short Sleep Duration in Patients with Schizophrenia or Schizoaffective Disorder

Abstract

Study Objectives:

To examine the association between substance use and short sleep duration in individuals with schizophrenia or schizoaffective disorder, depressive type (SADD).

Design:

Cross-sectional, retrospective study.

Setting:

Urban, suburban, and rural centers across the United States.

Participants:

2,462 consented, adult individuals with schizophrenia or schizoaffective disorder, depressive type (SADD). Participants included inpatients in acute or chronic care settings as well as outpatients and residents in community dwellings.

Measurements:

Substance use was assessed with 10 questions adopted from well-validated measures (e.g., CAGE questionnaire) for alcohol, marijuana, and illicit drugs. Short sleep duration was defined as <6 hr of self-reported sleep per night.

Results:

Close to 100% of our sample used nicotine while 83% used substances other than nicotine. More importantly, there was a significant association between substance use and short sleep duration. Interestingly, this association was strongest among African–Americans with schizophrenia or SADD.

Conclusions:

Because psychiatric medications often target chemical receptors involved with both sleep and substance use, understanding the association between short sleep duration and substance use in individuals with schizophrenia and SADD is important. Given that the majority of premature deaths in individuals with psychotic illness are due to medical conditions associated with modifiable risk factors, prospective studies designed to examine the effect of short sleep duration on behaviors like substance use should be undertaken. Finally, analyzing genetic and environmental data in a future study might help illuminate the strong association found between short sleep duration and substance use in African–Americans with schizophrenia and SADD.

INTRODUCTION

Many studies have investigated the effects of substance use on sleep [Stein and Friedmann, 2005; Schierenbeck et al., 2008; Conroy and Arnedt, 2014]. However, few studies have specifically focused on the association between substance use and short sleep duration. In 2008, the National Center for Health Statistics published a report on sleep duration and health risk behaviors using data from the National Health Interview Survey 2004–2006. They found for both men and women, smoking prevalence was substantially higher among those who slept less than 6 hr than among those who slept 7 to 8 hr. The same was true for alcohol consumption with prevalence of the behavior being higher among adults who slept 6 hr or less than among adults who slept 7 to 8 hr [Schoenborn and Adams, 2008]. More recently, with a growing body of evidence that associates short sleep duration with obesity and weight gain [Parks et al., 2006b; Chaput et al., 2010, 2012; Nielsen et al., 2011], a group of researchers decided to look at the association between short sleep duration and alcohol consumption. They found that short sleep duration and disinhibited eating were associated with greater alcohol intake in community-dwelling adults [Chaput et al., 2012].

Sleep disturbances are prevalent in individuals with schizophrenia who have psychosis or a history of psychotic symptoms [Soehner et al., 2013]. A study with 175 clinically stable outpatients with schizophrenia or schizoaffective disorder found that 44% met criteria for clinical insomnia using the Insomnia Severity Index [Palmese et al., 2011; Soehner et al., 2013]. Self-report and polysomnographic investigations of medicated patients with schizophrenia demonstrate prolonged sleep latency, low sleep efficiency, poor sleep quality, and shortened sleep duration [Doi et al., 2000; Monti and Monti, 2005; Xiang et al., 2009; Poulin et al., 2010; Soehner et al., 2013; Afonso et al., 2014]. Finally, a meta-analysis of polysomnographic studies in 321 patients and 331 controls demonstrated that the schizophrenia group experienced increased sleep latency, decreased total sleep time, and reduced sleep efficiency compared to controls [Chouinard et al., 2004; Soehner et al., 2013].

Though the relationship between short sleep duration and schizophrenia is not well-characterized, it is known that severe insomnia is often a sign of impending psychotic decompensation or relapse to psychosis following antipsychotic medication discontinuation [Dencker et al., 1986; Kyung and Douglass, 2010]. Sleep disturbances have been most associated with the exacerbation of positive symptoms that include delusions, hallucinations as well as disorganized thinking and behavior [Soehner et al., 2013]. An actigraphic study found that compared to patients with schizophrenia who experienced mostly negative symptoms on the Positive and Negative Syndrome Scale (PANSS), those with predominantly positive symptoms experienced more sleep-wake disturbances [Afonso et al., 2011; Soehner et al., 2013]. In another study that looked specifically at the relationship between persecutory delusions and insomnia symptoms, more than 50% of a medicated sample of patients experiencing persecutory delusions had moderate to severe insomnia symptoms [Freeman et al., 2009; Soehner et al., 2013].

The lifetime prevalence of substance use and substance dependence among individuals with schizophrenia in the United States has been estimated to be between 47% and 59% compared to 16% in the general population [Regier et al., 1990; Kendler et al., 1996]. Given that 60% of premature deaths in individuals with schizophrenia are due to medical conditions associated with exposures such as alcohol consumption, smoking, and intravenous drug use, recognition and treatment of these modifiable risk factors may have a significant impact on the overall morbidity and mortality of these patients [Parks et al., 2006a; Hartz et al., 2014]. Recently, in one of the largest assessments of substance use among individuals with severe psychotic illness, the odds of smoking as well as alcohol and other substance use were found to be dramatically higher than recent estimates of substance use in a control sample [Hartz et al., 2014].

As mentioned before, recent research has addressed short sleep duration and substance use in the general population. However, little is known about this association in individuals with schizophrenia and/or schizoaffective disorder, depressive type (SADD) with substance abuse and/or substance dependence. Lack of research within this subpopulation is surprising, as many psychiatric medications often target chemical receptors involved with sleep and substance use (dopaminergic, nicotinic, 5-hydroxytrypta-mine). For these reasons, we examined the association between short sleep duration and substance use in a large, systematically ascertained group of individuals (n = 2,462) with schizophrenia or SADD.

MATERIALS AND METHODS

Sample

The Genomic Psychiatry Cohort (GPC) is a multi-institutional resource designed to provide a large, uniformly diagnosed sample for large-scale genomic and other studies on schizophrenia and bipolar disorder. Currently, the 33,000 member GPC includes 10,000 individuals with schizophrenia or schizoaffective disorder, depressive type (SADD) as well as 5,000 individuals with bipolar disorder or schizoaffective disorder, bipolar type (SABP), 3,000 family members, and 15,000 unrelated controls. Participants in the GPC were recruited from urban, suburban, and rural populations across the United States. They included inpatients in acute or chronic care settings as well as outpatients and residents in community dwellings. All recruitment sites received institutional review board approval (Cedars Sinai Medical Center, Emory University, Georgia Regents University, Wright State University, New York University, State University of New York Stony Brook, State University of New York Upstate, Texas Tech University, University of California at Los Angeles, University of North Carolina, and University of Southern California) and informed consent was obtained from all participants. The GPC includes a National Institute of Mental Health-managed repository of DNA and other biological samples as well as clinical and demographic data obtained from these study participants [Pato et al., 2013]. We included individuals with SADD in our sample because it has become common practice to include SADD with schizophrenia in studies as these two illnesses are believed to part of a disease spectrum [Sevy et al., 2001; Etter et al., 2004]. Of the 10,000 individuals with schizophrenia or SADD in the GPC, only 2,462 reported information on sleep duration. Our study focuses on these 2,462 participants. Table I presents our sample characteristics.

TABLE I.

Sample Characteristics

		n = 2,462
Characteristics	n	%
Gender
Male	1,532	62.2
Female	875	35.5
Unknown	55	2.2
Ethnicity
Caucasian, non-Hispanic	1,056	42.9
African-American	864	35.1
White Hispanic	102	4.1
Latino	1	<1.0
Asian	34	1.4
Other (Multiracial)	405	16.5
Diagnoses
Schizophrenia	1,984	80.6
Paranoid	547	22.2
Undifferentiated	982	39.9
Hebephrenic	455	18.5
Schizoaffective disorder, depressive type	478	19.4
Sleep Duration
Short sleep (<6 hr)	227	9.2
≥6 hr	2,235	90.8
Substance Use
Any substance use	2,043	83.0
No substance use	419	17.0
	M ± SD
Age	42.5 ± 12.6

Subject Screening and Diagnosis

Screening questionnaire.

Potential GPC participants were asked to complete a screening questionnaire to assess personal and family psychiatric history as well personal medical history and basic demographics including race and ethnicity. The screening questionnaire was developed using items from well-validated instruments such as the CAGE questionnaire [Ewing, 1984] and included 32 questions on mania, psychosis, depression, anxiety disorders, alcohol, nicotine, and other substance use history [Pato et al., 2013].

Diagnosis.

To confirm psychiatric diagnoses, potential individuals with schizophrenia or SADD were interviewed by trained clinicians using the Diagnostic Interview for Psychosis and Affective Disorders (DI-PAD), a semi-structured clinical interview. The DI-PAD uses questions developed for the Diagnostic Interview for Genetic Studies (DIGS) [Nurnberger et al., 1994]. The DI-PAD also links to the Operational Criteria Checklist for Psychotic Illness (OPCRIT) which is a 90-item checklist and computerized diagnostic algorithm that arrives at diagnoses under various systems [McGuffin et al., 1991; Williams et al., 1996]. Finally, a team of clinicians confirmed diagnoses by reviewing DI-PAD, OPCRIT, and other records. All final diagnoses were made based on DSM-IV criteria.

Substance Use Measurement

As noted, both cases and controls completed a screening questionnaire that included a set of questions on the use of tobacco, alcohol, and other drugs. These questions were adapted from the Diagnostic Interview for Genetic Studies (DIGS) [Nurnberger et al., 1994; Berney et al., 2002] and other validated instruments like the Fagerstrom Test for Nicotine Dependence [Heatherton et al., 1991] and the CAGE questionnaire [Ewing, 1984; Bucholz et al., 1994; Kitchens, 1994]. The exact items from the screening questionnaire that were used in this study are shown in Table II. There were originally 14 items; 10 on substance and alcohol use (Table II) and four on tobacco use. Because nearly 100% of our sample used tobacco in the form of cigarettes, comparison of smokers to non-smokers was uninformative in our analysis and was excluded. In other words, there were too few non-smokers in our study to make any useful comparison to smokers in terms of short sleep duration.

TABLE II.

Substance Use Items

Do you often have more than four drinks in 1 day (for women) or more than five drinks in 1 day (for men)? Have you been under the influence of alcohol three or more times in situations where you could have caused an accident or gotten hurt? (Examples: driving while intoxicated, operating machinery, during sports, or while using a gun) Have you often had a lot more to drink than you intended to have or do you often drink to calm your nerves? Have you ever wanted to quit or tried to cut down on your drinking and found that you couldn’t? Have people annoyed you by criticizing your drinking? Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover (eye-opener)? Have you ever smoked marijuana more than 21 times in a single year? Have you ever used recreational (street) drugs (other than marijuana) or prescription drugs more than 10 times to feel good or get high? (Examples: Vicodin, Xanax, benzos, cocaine, crack, heroin, OxyContin (oxycodone), amphetamines, crystal meth, PCP, or hallucinogens?) Have you ever tried to cut down or quit using drugs and found that you couldn’t? Has your drug use ever caused you any problems? (Examples: physical, emotional, interpersonal, job, school, legal problems)

Two different models were created to characterize substance use. Model 1 characterized substance use as dichotomous; a participant either answered “Yes” to any substance use items listed in Table II or a participant did not mark any of the items. Model 2 characterized substance use as the sum of the items marked “Yes” in Table II. In Model 2, if more items were marked “Yes,” it was hypothesized that there would be a greater “degree” of substance use.

Sleep Measurement

As part of the DI-PAD interview for cases, a single question on normal sleep was asked as part of modules on depression and mania. Specifically, the interview item stated “How many hours do you normally sleep?” and the answer was recorded as 0 to 24 hr per night. Short sleep duration was defined as reporting < 6 hr per night versus ≥6 hr per night. For the subjects we assessed, schizophrenia and SADD were chronic illnesses. When we asked the question “How many hours do you normally sleep?,” we assumed that the information provided reflected the participant’s sleep at baseline for their chronic illness, even though he/she might have a waxing and waning psychosis (schizophrenia or SADD) or depressive episodes (SADD).

Covariates

We included as covariates known correlates of both substance use and sleep: age, gender, and ethnicity. These were also assessed as part of the screening questionnaire.

Analyses

Logistic regression analysis was used to examine the association between substance use and short sleep duration (<6 hr per night). Two different models were run. Model 1 characterized substance use as dichotomous; a participant either answered “Yes” to any substance use items listed in Table II or a participant did not mark any of the items. Model 2 characterized substance use by the total number of substance use items marked “Yes” in Table II. In Model 2, if more items were marked “Yes,” it was hypothesized that there would be a greater “degree” of substance use. Running each of the models included two steps. Step 1 was calculating the unadjusted effect for substance use on short sleep duration. In step 2, a priori covariates age, sex, and race/ethnicity were included and an adjusted effect was calculated. Analyses were performed using SPSS (Version 21); α = 0.05.

RESULTS

Short sleep was reported by 9.2% of our sample (Table I). Most participants (83%) said “Yes” to at least one substance use item (Table I). The average number of substance use items reported was 5.7 ± 4.2 (M ± SD) and the median was 6.

In Model 1, marking any items in Table II “Yes” was used to characterize substance use. Unadjusted, any substance use was a significant risk factor for short sleep duration (Table III). After adjusting for covariates, there was a 58% increased chance of short sleep duration for participants reporting any substance use (Table III). In this model, age and ethnicity were also significant predictors. For every 10 years of age, there was a 20% increase in risk of short sleep (Table III). Additionally, African–American and Other (Multiracial) ethnic groups had a 184% and 161% increased risk of short sleep duration, respectively, compared to Caucasian, non-Hispanics (Table III).

TABLE III.

Odds Ratios (OR) for the Association Between Any Substance Use (Model 1) and Short Sleep Duration (<6 hr)

Unadjusted		Adjusted*
	Crude OR, P-value		Adjusted OR, P-value
Any substance (Y/N)	1.63 (P= 0.004)	Any substance (Y/N)	1.58 (P= 0.010)
		Gendera	0.93 (P= 0.645)
		Age	1.02 (P= 0.007)
		Racea
		African-American	2.84 (P< 0.001)
		White Hispanic	1.19 (P= 0.696)
		Latino	0.00 (p= 1.000)
		Asian	0.65 (P= 0.675)
		Other (Multiracial)	2.61 (P< 0.001)

^*Adjusted for age, sex, and race/ethnicity.

^aComparison for gender was male; comparison for ethnicity was Caucasian, non-Hispanic.

In Model 2, the total number of substance use items marked “Yes” was hypothesized to correspond to the “degree” of substance use. This sum significantly predicted short sleep in both unadjusted and adjusted analyses (Table IV). With each additional item marked, the increase in risk of short sleep duration was 7% in the adjusted analysis (Table IV). For example, a comparison of patients who marked six items “Yes” versus zero items would reflect a risk increase of 42%. Like Model 1, age and ethnicity were significant predictors. However, an interesting difference arose with Model 2, showing that Asian ethnicity (compared to Caucasian, non-Hispanic) was protective for short sleep duration (Table IV). African–Americans and Other (Multiracial) groups showed increased risk as before (Table IV).

TABLE IV.

Odds Ratios (OR) for the Association Between Total Substance Use (Model 2) and Short Sleep Duration (<6 hr)

Unadjusted		Adjusted*
	Crude OR, P-value	Covariates	Adjusted OR, P-value
Total substance	1.08 (P= 0.001)	Total substance use	1.07 (P= 0.003)
		Gendera	0.93 (P= 0.629)
		Age	1.02 (P= 0.013)
		Racea
		African-American	2.81 (P< 0.001)
		White Hispanic	1.16 (P= 0.687)
		Latino	0.00 (P= 1.000)
		Asian	0.66 (P< 0.001)
		Other (Multiracial)	2.67 (P< 0.001)

^*Adjusted for age, sex, and race/ethnicity.

^aComparison for gender was male; comparison for ethnicity was Caucasian, non-Hispanic.

DISCUSSION

Overall, our results showed that substance use among individuals with schizophrenia or SADD was significantly associated with short sleep duration (<6 hr). After further characterization of our participants, we found that African–Americans and individuals self-described as “Other” were at much higher risk for short sleep duration if they used substances. Specifically, African–Americans had a 181–184% increased chance of short sleep duration while individuals of “Other” race/ethnicity had a 161–167% increased chance of short sleep duration compared to non-Hispanic Caucasians, regardless of sex and age.

The finding of “higher” substance use associated with short sleep duration in our sample is similar to other studies that have reports of disinhibited eating behavior or increased alcohol consumption in adults with short sleep duration [Chaput et al., 2012]. Previous studies have looked mostly at disinhibited “food” intake in association with sleep duration and some have looked at disinhibited “drink” or “substance” intake in correlation with sleeping less than 6 hr per night but not in relationship to psychiatric illnesses [Parks et al., 2006b; Chaput et al., 2010, 2012; Nielsen et al., 2011]. Psychiatric symptoms may already make it difficult for subjects to inhibit behaviors like substance use but with additional sleep disturbance there might be further disinhibition. Understanding how sleep might contribute to this disinhibition in future studies may be important in gaining insight into why individuals with schizophrenia are more likely to use substances compared to the general population [Kendler et al., 1996; Regier et al., 1990].

In terms of understanding the increased prevalence of substance use in individuals with schizophrenia or SADD, other factors besides sleep duration should be considered. To date, studies investigating causes of the co-morbidity between schizophrenia and substance use disorder can be categorized into four different models: 1) common factors, 2) secondary mental disorder, 3) secondary substance use, and 4) bidirectional [Mueser et al., 1998; Campbell et al., 2014]. The common factors model hypothesizes that comorbidity results from risk factors common to both schizophrenia and substance use disorder [Campbell et al., 2014]. A shared genetic vulnerability has been proposed to underlie dopaminergic and glutamatergic dysregulation in schizophrenia and substance abuse, supporting this model [Krystal et al., 2006; Chambers et al., 2007; Campbell et al., 2014]. In addition, impaired myelin development has been studied as a possible precursor to both schizophrenia and substance use disorder [Feng, 2008]. The secondary mental disorder model proposes that substance use precedes and precipitates mental disorders [Mueser et al., 1998]. The strongest evidence for this model is findings of a dose-related association between cannabis use and the subsequent onset of schizophrenia [Campbell et al., 2014]. A systematic review of 35 Longitudinal studies found a significantly increased risk of psychosis for those who ever used cannabis compared to those who did not. This same review also found a two-fold increase in the risk of psychosis for people who used cannabis most frequently [Moore et al., 2007]. These results, however, remain controversial and a causative role has not been proven [Campbell et al., 2014]. The secondary substance use model, or the “self-medication hypothesis” posits that individuals with schizophrenia turn to substances to ameliorate their symptoms [Kumari and Postma, 2005; Campbell et al., 2014]. Most studies, however, do not support the self-medication hypothesis [Spencer et al., 2002; Thornton et al., 2012; Campbell et al., 2014]. Finally, the bidirectional model suggests that the presence of either schizophrenia or substance use disorder can contribute to the development of the other over time. This last model is largely theoretical and also lacks supporting evidence from research [Campbell et al., 2014].

Another finding in our study was that African-Americans with schizophrenia and SADD were at much higher risk of experiencing short sleep duration if they used substances. This result was consistent with several recent studies that looked at racial differences in short sleep duration in the general population [Brimah et al., 2013; Jackson et al., 2013]. A 2013 Harvard study found that short sleep generally increased with increasing professional responsibility within a given industry among blacks but decreased with increasing professional roles among whites [Jackson et al., 2013]. Another study published the same year found that African-Americans who reported short sleep had greater odds of being functionally impaired than their white counterparts [Brimah et al., 2013]. The latter finding is relevant to our study in that mental illness may already have a significant impact on functionality without the additional burden of short sleep duration. Because participants in our sample have agreed to be re-contacted, future studies will include additional questions to better understand the factors behind the racial differences in our results. We believe that collecting genetic and environmental data such as number of roommates, living conditions, etc. would help us identify other factors that might affect racial differences in sleep duration in this population.

U.S. African–Americans may be at particularly high risk for insufficient sleep-related morbidity and mortality [Nunes et al., 2008; Ruiter et al., 2011]. Obesity, diabetes and hypertension are found at higher rates in African–Americans [Cossrow and Falkner, 2004] and based on current studies, these morbidities have been shown to be associated with short sleep duration [Gangwisch, 2009]. Experimental studies in the general population have also shown sleep deprivation to decrease leptin, increase ghrelin, increase appetite, compromise insulin sensitivity and raise blood pressure [Gangwisch, 2009]. Disinhibition and eating behavior may be related to these neuroendocrine abnormalities. Conversely, obesity is a strong risk factor for obstructive sleep apnea (OSA) and patients with schizophrenia have high rates of obesity [Peppard et al., 2000; Correll et al., 2010]. In the general population, OSA has been shown to be associated with an increased risk in cardiovascular morbidity and mortality [Monahan and Redline, 2011]. To our knowledge, no large scale study has directly addressed the relationship between short sleep duration and cardiometabolic dys-functions in individuals with schizophrenia and SADD [Ruschena et al., 1998; Appleby et al., 2000]. In addition, the prevalence of OSA and its risk factors in individuals with schizophrenia and SADD is not well-studied [Annamalai et al., 2015]. While antipsychotic medication is often linked to cardiovascular and metabolic perturbations, important cardiometabolic abnormalities have been reported in drug naïve or drug-withdrawn patients with schizophrenia [Newcomer, 2007]. In light of the results of this and previous observational studies, future research should prospectively examine the consequences of short sleep duration on cardiometabolic function in individuals with schizophrenia or SADD.

Little work has been done to explore treatment options for sleep disturbances in individuals with schizophrenia or schizoaffective disorder despite its high prevalence in these illnesses [Soehner et al., 2013]. Currently, treatment of insomnia in patients with schizophrenia tends to be medication-based and most commonly involves antipsychotics and sedative hypnotics [Kantrowitz et al., 2009; Soehner et al., 2013]. With the exception of risperidone which decreases REM sleep, first and second-generation antipsychotics facilitate an increase in total sleep time and/or sleep efficiency [Cohrs, 2008; Krystal et al., 2008; Soehner et al., 2013]. Less is known about the safety and efficacy of hypnotic medications in treating sleep disturbance in this population. No randomized controlled trials of benzodiazepine hypnotics or non-benzodiazepine hypnotics have been conducted in the context of sleep and schizophrenia [Baandrup et al., 2013; Soehner et al., 2013]. Finally, despite the evidence supporting behavioral rather than pharmaceutical interventions for the long-term treatment of insomnia, little is known about the efficacy of these therapies in patients with schizophrenia and SADD [Morin et al., 1999, 2009].

Two sleep intervention studies, one examining the use of melatonin and the other examining the use of adapted Cognitive Behavioral Therapy for Insomnia (CBT-I), offer the best preliminary evidence that correction of sleep disturbances relates to decreased positive symptoms and/or mood [Soehner et al., 2013]. Relative to placebo, melatonin significantly improved sleep quality, reduced the number of nighttime awakenings, increased duration of sleep, and improved mood [Suresh Kumar et al., 2007; Soehner et al., 2013]. The adapted CBT-I intervention which included sleep psycho-education, sleep hygiene recommendations, and a stimulus control intervention reduced insomnia severity and improved sleep quality. In addition, this treatment decreased paranoid thinking as well as anxiety and depression symptoms [Myers et al., 2011; Soehner et al., 2013]. Further studies are needed to clarify the benefits of treating sleep disturbances in psychotic disorders. However, there seems to be growing evidence that the treatment of sleep disturbances may be related to improvement in positive symptoms and quality of life.

Limitations

First, our cross-sectional study design precluded an investigation of causality between substance use and short sleep. This may be overcome by prospectively designed studies. Formal reliability and validity testing of our substance use items also has not been conducted. Despite this, all items were adopted from well-validated measures like the CAGE questionnaire [Ewing, 1984; Nurnberger et al., 1994]. In addition, although we tried to examine the degree of substance use with Model 2, more questionnaire items specifically regarding the amount and frequency of substance use could have allowed us to better assess drug use severity. Finally, substance use items used in this study are not diagnostic of substance use or dependence. Rather, they were used as screening items only and follow-up with in-depth diagnostic interviews (e.g., DIGS Substance Abuse Module [Nurnberger et al., 1994] are planned.

Next, we acknowledge that different substances (alcohol, cannabis, cocaine, etc.) have varied neuropsychiatric effects and interactions with psychotropic medications. Although we wanted to examine each of these substances separately in association with short sleep duration, a very small number of participants indicated the use of only one substance like alcohol or marijuana. Because a large number of participants responded “Yes” to Question 8 in Table II which encompasses Vicodin, Xanax, benzos, cocaine, crack, heroin, OxyContin (oxycodone), amphetamines, crystal meth, PCP, or hallucinogens, we decided to examine substance use in general.

Our study was also limited by the fact that our data was derived from self-reports. It is important to clarify, however, that this wasn’t purely a self-rating but an interviewer’s interpretation of what the patient reports. The interviewer was allowed to clarify any of the self-report data the patient shared to ensure accuracy of what was collected. Compared to self-reported data, actigraphy and polysomnography have been shown to more accurately measure sleep duration [Ancoli-Israel et al., 2003]. However, these methods, especially polysomnography, are limited by their cost and inconvenience as a method for sleep monitoring for more than a few nights [Ancoli-Israel et al., 2003]. In addition, studies examining the correlation between self-reported sleep duration and objective sleep measures have been varied in their results. One such study looking at 669 young adults, found a moderate correlation between self-reported sleep duration and measured sleep duration using wrist actigraphy [Lauderdale et al., 2008]. Another paper compared self-reported sleep duration to actigraphy among postmenopausal women experiencing hot flashes. Mean actigraph sleep over 1 week was 6.3 hr while mean self-reported sleep over 1 week was 6.6 hr [Regestein et al., 2004]. Performing actigraphy or polysomnography on a large sample would require a significant time and financial investment but would provide a more accurate measure of sleep duration. Similarly, objective measures of substance use from biological samples in addition to self-report should be considered in future studies.

Finally, only 2,462 out of 10,000 individuals with schizophrenia/SADD in the Genomic Psychiatry Cohort (GPC) reported information on sleep duration and were included in our study. Because strict random sampling was not employed, there may be biases in the data set that limit extrapolation to larger populations.

CONCLUSIONS

Our study found that substance use among individuals with schizophrenia or SADD (n = 2,462) was significantly associated with short sleep duration (<6 hr). This association was strongest among African–Americans with schizophrenia or SADD. Furthermore, less than 6 hr of sleep was found to be more prominent in those who had an increased degree of substance use (Model 2). Because our sample came from a large cohort of 10,000 individuals with schizophrenia or SADD who agreed to be re-contacted, we plan to do more in-depth, prospective studies that examine the effects of short sleep duration on health behaviors as well as cardiometabolic risk markers (blood pressure, blood sugar, etc.). It is our hope that publication of this preliminary paper will set the stage for the aforementioned research and encourage future collaborations between individuals in the fields of sleep medicine and psychiatry.