Socioeconomic status of origin and the clinical expression of Schizophrenia

Socioeconomic status of origin and the clinical expression of Schizophrenia

Schizophrenia Research 75 (2005) 417 – 424 www.elsevier.com/locate/schres Socioeconomic status of origin and the clinical expression of Schizophrenia...

111KB Sizes 2 Downloads 55 Views

Schizophrenia Research 75 (2005) 417 – 424 www.elsevier.com/locate/schres

Socioeconomic status of origin and the clinical expression of Schizophrenia Brooke Parrott*, Rich Lewine1 Department of Psychological and Brain Sciences, University of Louisville, Louisville, KY 40292, United States Received 10 August 2004; received in revised form 24 November 2004; accepted 3 December 2004 Available online 7 January 2005

Abstract The concentrated focus on biology during the bdecade of the brainQ has resulted in decreased attention to the indisputable influence of psychosocial and sociocultural factors in the expression of schizophrenia. The aim of this study was to evaluate the relationship between the socioeconomic background of the origin and the clinical manifestation of schizophrenia. Parent socioeconomic information and clinical symptom data from 120 (84 men and 36 women) schizophrenia and schizoaffective patients were analyzed. Results suggested that higher parental SES (socioeconomic status) is associated with decreased symptom severity in female patients, but with increased symptom severity and decreased global functioning in male patients. Possible interactions between socioeconomic status and sex of patient are discussed, as well as suggestions for further study. D 2004 Elsevier B.V. All rights reserved. Keywords: Parent socioeconomic status; Sociocultural factors; Schizophrenia expression

1. Introduction The study of psychosocial and sociocultural factors associated with schizophrenia during the bdecade of the brainQ has been largely restricted to the study of stress and the differential use of services. With respect to stress, for example, it has been suggested that large urban areas associated with poverty and physical

* Corresponding author. Tel.: +1 502 852 3395. E-mail addresses: [email protected] (B. Parrott)8 [email protected] (R. Lewine). 1 Tel.: +1 502 852 3243. 0920-9964/$ - see front matter D 2004 Elsevier B.V. All rights reserved. doi:10.1016/j.schres.2004.12.006

hardship contribute to raising stress in individuals with a genetic vulnerability to schizophrenia, thereby contributing to the disorder’s onset (Leff, 1992). This is, of course, the well-known diathesis-stress model of schizophrenia. Sociocultural factors such as race and social class have been found to correlate with different patterns and levels of mental health services use (Chow et al., 2003; Cheung and Snowden, 1990; Hu et al., 1991; Neighbors et al., 1992; Snowden and Hu, 1997). As the decades-long battle between bsocial causationQ and bsocial driftQ hypotheses of schizophrenia seems finally to have been settled convincingly on the side of social drift (Johnson et al., 1999), it is not surprising that much of our attention during

418

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

the past two decades has been focused on the biological underpinnings of schizophrenia (Berger et al., 2002; Brunello et al., 1995; Kapur, 2003; Watson, 1996; Weinberger, 1999). It is quite clear, however, that even the most basic biological processes take place within a sociocultural and psychosocial milieu. Consider as examples the salience of IQ heritability as a function of socioeconomic status (Turkheimer et al., 2003), the role of a nonshared environment in schizophrenia (Plomin and Daniels, 1987), and the influence of the family environment via expressed emotion (Brown et al., 1972; Hooley, 1998; King and Dixon, 1995). Over the past several years, we have undertaken a program of research that has focused on the role of socioeconomic status in schizophrenia. As indicated above, the study of social context, usually socioeconomic status and sociodemographic features, in schizophrenia has primarily been of the individuals with the disorder. Patient socioeconomic status is not, however, informative on two accounts. First, approximately 80–90% of all schizophrenia patients are unemployed at any given time (Beautrais et al., 1998; Becker et al., 1998; Bell and Lysaker, 1996). Second, the process of bsocial driftQ in schizophrenia (Johnson et al., 1999) creates a superficial sociocultural homogeneity that actually camouflages a diverse group of individuals. That is, the neuropsychological and interpersonal impairments of schizophrenia cause individuals from a broad range of backgrounds to bdriftQ into lower socioeconomic conditions resulting in a superficial commonality. To better understand how individuals respond to schizophrenia it is as important to understand from whence they’ve come as to understand where they are. With few exceptions, family of origin is not generally included in schizophrenia studies as an independent variable, if it is included at all. An interesting exception is a study by Mueser et al. (2001) in which the authors found that the educational level of the patient’s mother predicted the patient’s competitive work status at follow-up. In our analyses to date we have found that parental education (a significant component of socioeconomic status) explained what appeared to be race differences in neuropsychological performance among schizophrenia patients (Lewine and Caudle, 2000). The fewer years of education the parents had, the lower the

neuropsychological performance of their adult offspring with schizophrenia. A recent pilot study (Lewine, in press) found that parent socioeconomic status was significantly correlated with adult sons’ vocational expectations, which in turn was significantly correlated with hopelessness. That is, the higher the parental socioeconomic status, the higher the sons’ expectations for work and the greater their hopelessness. This may be a function of the unwillingness of those from more advantaged backgrounds, especially males, to accept blow statusQ jobs (Parrott et al., 2004). The current study was designed to assess the relationship between socioeconomic status (SES) of origin and the clinical expression of schizophrenia. Parental SES was used to determine the socioeconomic status in which patients were reared. In view of the diathesis-stress model of schizophrenia, we hypothesized that SES would negatively correlate with symptom severity if it were assumed that growing up in a lower SES environment is more stressful than growing up in a higher SES environment. Schizophrenia research has yielded several studies indicating clear sex differences in the expression and onset of the illness (Goldstein and Lewine, 2000). However, this research does not predict that parent SES would have a differential effect for males and females. Studies examining the relationship between parental SES and offspring occupational choice do suggest a possible difference between the way in which male and female patients respond to psychosocial factors. For example, in a study investigating the relationship between job expectations, social class, and gender, Sinclair et al. (1977) found that the occupational choice of seventh to tenth grade students was significantly related to social class, as defined by the neighborhood in which they lived (presumably with their parents). This relationship was reflected differently in boys and girls. Significantly fewer boys from lower SES neighborhoods expected to enter scientific/technical jobs than boys from higher SES neighborhoods. Lower SES boys were more likely to expect a craftsman position than higher SES boys. Girls from lower SES neighborhoods were less likely to expect social aid positions (teacher, lawyer, psychologist) than girls from higher SES neighborhoods and were more likely to expect white-collar

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

occupations (secretary, clerical worker). While these sex differences likely reflect gender roles rather than social class, the interaction effect between gender and social class was not examined in this study. Also, in the previously cited study by Parrott et al. (2004), it was found that fathers’ SES significantly negatively correlated with son’s acceptance of low prestige jobs in an undergraduate population. A similar significant relationship was not found for daughters. Although there is no obvious link between job expectation or acceptability and symptoms of schizophrenia, these studies provide some evidence to suggest that socioeconomic factors in family of origin may not affect male and female offspring similarly. Therefore, in the current analysis we attempted to investigate the possibility of differential parental influence as a function of the sex of the patient. In exploring these relationships we hope to gain a clearer understanding of the influence of family environment and socioeconomic background on the clinical expression of schizophrenia.

2. Methods 2.1. Participants Data from a larger research project on sex differences in schizophrenia (Lewine et al., 1996, 1997) were analyzed from 96 (69 men and 27 women) schizophrenia patients and 24 (15 men and 9 women) schizoaffective patients for whom we had adequate information to calculate family of origin socioeconomic status. All patients chosen for analysis were under the age of 55 as to focus the study on patients most influenced by their social background and to minimize confounding variables associated with aging. Participants in the larger study were recruited through the Clinical Research Program and Schizophrenic Disorders Program in the Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine. Patients were also recruited from a broad range of public and private facilities, from the Georgia Alliance for the Mentally Ill, and by word of mouth (i.e. volunteers completing the study who spoke to others about it). The study was approved by a local IRB and written, informed consent was obtained.

419

2.2. Measures Diagnoses of schizophrenia or schizoaffective disorder were made using the Schedule for Affective Disorders and Schizophrenia—Lifetime Version (SADS-L), which was administered by a trained clinical psychologist, a doctoral-level social worker, or a nurse specialist supervised in weekly meetings by a senior clinician (R.R.J.L.), who conducted approximately 50% of the interviews himself. While blind to all study results, that senior clinician assigned a final diagnosis based on review of all clinical information. Widely used semi-structured interviews, rating scales, and questionnaires were administered to assess symptoms of schizophrenia. Positive symptoms of schizophrenia were measured using Andreasen’s Scale for the Assessment of Positive Symptoms (SAPS), a 34-item rating scale assessing the presence and severity of hallucinations, delusions, bizarre behavior, and thought disorder (Andreasen, 1984). Andreasen’s Scale for the Assessment of Negative Symptoms (SANS), a 24-item rating scale assessing the presence and severity of affective flattening, alogia, apathy, anhedonia, and attention, was used to measure negative symptoms of schizophrenia (Andreasen, 1983). The Brief Psychiatric Rating Scale (BPRS), an 18-item rating scale, was used to assess the severity of positive symptoms, general psychopathology, and affective symptoms (Overall and Gorham, 1962). Depression was measured via two instruments: The Hamilton Depression Rating Scale (HDRS), a structured interview for the assessment of depressive symptoms (Hamilton, 1960), and the Beck Depression Inventory (1973 Revision), a self-report questionnaire (Beck, 1972). The Global Assessment of Functioning Scale (GAF) was used to measure overall social and occupational functioning (American Psychiatric Association, 1987). The senior clinician (R.R.J.L.) trained all interviewer/raters to an interrater reliability (intraclass correlation) of .80 or higher on interview-based rating scales. He reviewed all ratings during weekly assessment meetings, and completed ratings for the majority of patients. Age at first hospitalization and parent data were collected via patient self-report and hospital records when available. Mother’s and father’s SES were coded using Watt’s Amherst Modification (Watt, 1976) of the Hollings-

420

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

head–Redlich Two-Factor Index of Social Position (Hollingshead and Redlich, 1958). This modification provides a table that converts education and occupation, the two factors in the Hollingshead–Redlich index, to estimates of bsocial classQ that incorporate a weighting for residence, a third factor in social class estimates in earlier instruments. These weights are derived from the two known factors, education and occupation. The conversion table yields social class estimates from blowQ (134, unskilled labor, b6 years of schooling) to bhighQ (20, professional occupation, graduate degree). These estimates can be used as continuous variables or as categories. For the current analysis, estimates of SES were used as continuous variables. For accurate interpretation of correlational data, it should be strongly emphasized to the reader that higher values in Watt’s scale reflect lower socioeconomic status. [A copy of education and occupations codes and the conversion table is available from the authors on request.] 2.3. Procedures Correlational analyses were conducted using schizophrenia symptom data and parental SES in order to examine the relationship between symptomology and sociocultural background. Additional correlational analyses were conducted separately on male and female patients in order to investigate the possibility of a differential pattern of parental influence as a function of patient sex.

3. Results 3.1. Full Sample Descriptive statistics for the entire sample are summarized in Table 1. Table 2 lists descriptive statistics by sex of patient. Sample cell sizes vary due to missing data. Table 3 summarizes the results of the correlational analysis of SES and clinical characteristics. Strikingly, mothers’ SES is significantly associated with anxiety/ depression, withdrawal/retardation, SAPS, and GAF score. These correlations suggest that increasing socioeconomic status of the mother is associated with increasing positive symptoms, withdrawal/retardation,

Table 1 Sample descriptive statistics Age at first hospitalization BDI total score BPRS score BPRS thinking disorder BPRS anxiety/depression BPRS withdrawal/retardation BPRS hostility/suspiciousness Global assessment of functioning score Hamilton depression score SANS total score SAPS total score Mother SES Father SES

N

Mean

SD

119 96 81 81 81 81 81 103 98 111 108 122 122

21.42 11.33 32.78 7.01 6.11 6.72 5.09 47.32 7.02 8.51 5.05 68.85 58.49

6.617 9.663 8.929 3.397 2.962 3.179 2.476 12.167 5.576 4.752 3.414 30.654 31.077

and decreasing anxiety/depression and global performance. In contrast, father’s SES is not statistically significantly associated with any of the variables. To determine the contribution of illness severity to the relationship between mothers’ SES and symptoms and global functioning, we calculated partial correlations, partialling out age at first hospitalization (an indicator of illness severity). The correlation between SES and GAF actually increased to .29 ( p=.038), while the other three correlations remained virtually unchanged: .21 ( p=.068), .29 ( p=.01), and .17 ( p=.09) for anxiety/depression, withdrawal/retardation, and total SAPS, respectively. 3.2. Sex differences We repeated the analyses separately by patient sex to explore whether our initial results varied according to the sex of the offspring. Tables 4 and 5 summarize the findings for male and female patients, respectively. Mothers’ SES is significantly correlated with three of their sons’ clinical characteristics (age at first hospitalization, withdrawal/retardation, and global functioning), while fathers’ SES is significantly correlated with sons’ negative symptoms scores (SANS). As the mothers’ SES increases, their sons’ AFH decreases, their withdrawal/retardation increases, and their overall functioning decreases. Greater negative symptoms in sons are associated with higher SES of the father. In contrast to the pattern for mothers and sons, mothers’ SES is only significantly associated with anxiety/depression in their daughters, with anxiety/ depression being lower the higher the mother’s

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

421

Table 2 Descriptive statistics by sex of patient Female Age at first hospitalization BDI total score BPRS score BPRS thinking disorder BPRS anxiety/depression BPRS withdrawal/retardation BPRS hostility/suspiciousness Global assessment of functioning score Hamilton depression score SANS total score SAPS total score Mother SES Father SES

Male

N

Mean

SD

N

Mean

SD

35 25 22 22 22 22 22 27 28 32 31 34 34

21.80 12.40 32.09 6.23 6.95 6.55 4.95 48.78 8.39 9.38 5.26 81.41 71.41

7.30 8.47 8.01 2.99 2.97 3.19 2.84 12.51 4.41 4.99 3.00 29.96 29.35

83 69 57 57 57 57 57 74 68 77 75 78 81

21.23 11.03 33.33 7.37 5.86 6.91 5.21 46.27 6.62 8.22 5.04 69.88 56.22

6.38 10.11 9.26 3.55 2.95 3.18 2.36 11.64 5.94 4.66 3.58 25.25 29.28

socioeconomic status. Father’s SES is significantly correlated with daughters’ BPRS Thinking Disorder and approaches statistical significance for total BDI. In both instances, higher SES is associated with lower symptom scores. Interestingly, statistical analysis of the relationship between sex of offspring and parental SES strongly suggests that higher parental SES is associated with lower levels of symptoms in daughters and higher levels of symptoms in sons. More specifically, increased parental SES is associated with lower anxiety/depression and less severe thinking disorder

in daughters and more severe withdrawal/retardation and overall illness severity in sons. Given the number of correlations reported, it is likely that at least one significant finding was found by chance. In fact, we obtained six statistically significant correlations. Some readers may choose to ignore marginally significant findings (i.e. p= .058; .056, .075). We chose not to use the Bonferroni procedure in setting a level of statistical bsignificance,Q as it is well-known to be extremely conservative. While some caution about statistical testing is in order as indicated above, particularly compelling in this study is the fact that socioeconomic

Table 3 Correlations between parental SES and symptom severity

Table 4 Relationship between parental SES and male patient symptom severity Mother SES Father SES

Mother SES Father SES Age at first hospitalization BDI total score (1–21) BPRS Score (1–18) BPRS thinking disorder BPRS anxiety/depression BPRS withdrawal/retardation BPRS hostility/suspiciousness Global assessment of functioning score Hamilton depression score (1–21) SANS total score SAPS total score Mother SES Father SES a b c

pb.05. pb.01. Marginally significant p=.058.

– – – – .245a .286b – .187c – – .190a – –

– – – – – – – – – – – – –

Age at first hospitalization BDI total score (1–21) BPRS score (1–18) BPRS thinking disorder BPRS anxiety/depression BPRS withdrawal/retardation BPRS hostility/suspiciousness Global assessment of functioning score Hamilton depression score (1–21) SANS total score SAPS total score Mother SES Father SES a b c

pb.05. pb.01. Marginally significant p=.056.

.239a – – – – .368b – .228a – – – – –

– – – – – – – – – .217c – – –

422

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

Table 5 Relationship between parental SES and female patient symptom severity Mother SES Father SES Age at first hospitalization BDI total score (1–21) BPRS score (1–18) BPRS thinking disorder BPRS anxiety/depression BPRS withdrawal/retardation BPRS hostility/suspiciousness Global assessment of functioning score Hamilton depression score (1–21) SANS total score SAPS total score Mother SES Father SES b c d

– – – – .403d – – – – – – – –

– .355b – .464c – – – – – – – – –

Marginally significant p=.075. pb.05. Marginally significant p=.056.

status of origin and symptom expression had the opposite relationship for women and men.

4. Discussion Consistent with a large body of literature on sex differences in schizophrenia (see Goldstein and Lewine, 2000 for review), it appears from the results of this analysis that the association of socioeconomic class of origin and the expression of schizophrenia differs as a function of patient sex. We found that the higher the parental SES of female patients, the less severe the illness appeared as judged by thought disorder ratings. This finding in women is consistent with the diathesis-stress model of schizophrenia. That is, females from higher socioeconomic backgrounds assumed to be under less stress and exhibit fewer and less severe symptoms of schizophrenia than those from lower socioeconomic standing. In contrast, the opposite was found for males: the higher the parental SES, the more severely ill the patient as judged by age at first hospital admission, symptoms, and global functioning. These findings could be consistent with the view presented by Goldstein and Lewine (2000) that schizophrenia in women is a familial (or, diathesis-stress) type, while in men it is a sporadic type. While this is a correlational finding and therefore not a legitimate

basis for causal interpretation, there are several processes that this sex difference in social class of origin and clinical expression suggests for future study. Higher social status of origin may serve as a significant source of stress for men predisposed to schizophrenia, while functioning as a source of support (or at least is neutral) for women so predisposed. We have suggested elsewhere (Lewine, in press) that advantaged social class of origin is associated with higher job expectations and greater hopelessness in young male schizophrenia patients than in those from less advantaged social origins. The finding that negative symptoms increased among male schizophrenia patients from more advantaged SES of origin in this study is consistent with the bparadox of advantageQ perspective. That is, increased severity of negative symptoms and emotional withdrawal may reflect the hopelessness felt by male patients who are having difficulty fulfilling their high vocational expectations determined by their socioeconomic status of origin. This withdrawal and lack of motivation may, in turn, result in a decline of social and occupational functioning. Furthermore, it may be that men from more advantaged backgrounds are less willing to work in low prestige jobs than are men from less advantaged backgrounds (Parrott et al., 2004). Coupled with the cognitive, emotional, and interpersonal deficits of schizophrenia, an unwillingness to accept low prestige jobs may fuel hopelessness. We are currently pursuing a course of study examining the role of perceived parental expectations in the perpetuation and exacerbation of hopelessness in schizophrenia patients. It is hypothesized that schizophrenia diminishes the ability of an individual to fulfill the wishes and goals they believe their parents have set for them. A sense of disappointment, guilt, or embarrassment may result, possibly leading to increased depression, withdrawal, or suicidal ideation. These reactions present obstacles that impede treatment. Whether or not this phenomenon is particular to male patients with higher socioeconomic backgrounds is under investigation. The pervasiveness of culturally-defined gender roles may also explain why advantaged social background adversely affects male patients and not female patients. A review article by Page (1987) suggests that clinicians view the bmasculineQ personality as the prototype for mental health, whereas feminine char-

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

acteristics are interpreted as more indicative of psychopathology. Further, it is suggested that clinicians and others infer psychopathology from behaviors deemed gender incongruent. Perhaps increased negative symptoms and decreased global functioning in male patients result from the patient’s perceived failure to meet the expectations of his gender role, as the symptoms and consequences associated with schizophrenia appear to him and others as more stereotypically bfeminine.Q For example, a socially advantaged male patient unable to work would feel more stigmatized than a female patient because it is less culturally acceptable and expected for him to be bsickQ and unemployed than it is for her. Earlier age at first admission as a function of higher parental SES among male schizophrenia patients may reflect a social class difference in access to and use of mental health resources (Chow et al., 2003). Thus, rather than reflecting a more severe form of schizophrenia, a younger age at first hospitalization may reflect earlier formal intervention among those with the resources to do so. As there was virtually no relationship between SES of origin and first admission among female schizophrenia patients (r= .066 and .003 for mothers’ and fathers’ SES, respectively), we are still faced with a sex difference. This sex difference may arise from the fact that men are more likely to be living with their families of origin at time of schizophrenia onset than are women. That is, the failure of family of origin SES and admission age to correlate significantly among female patients might arise because of well-documented sex differences in the onset age (Goldstein and Lewine, 2000; Lewine, 1980) rather than differential expectations of or response to schizophrenia in men and women. In examining the magnitude of the significant correlations (effect sizes) between family SES and patient illness expression, we find that the mean effect size among female patients (.403) is a little more than 50% greater than that among male patients (.263). The mean of the significant correlations was comparable for mothers (.409) and fathers (.361), as well as those calculated for parent by patient sex (.278, .217, .403, and .409 for mothers/sons, fathers/sons, mothers/ daughters, and fathers/daughters, respectively). Put more colloquially, while an advantaged socioeconomic background may be a negative factor for male schizophrenia patients, at least the magnitude of its

423

beffectQ is less than that for female schizophrenia patients (for whom it is positive). This effect size interpretation contradicts our earlier speculation about male schizophrenia being of a sporadic (nonfamilial) sort and that for women being a familial (or diathesisstress sort) as we would expect socioeconomic background to have a greater role in sporadic than familial cases of schizophrenia. This is a conundrum to be resolved with further study. The results of this study are admittedly subject to all of the limitations of correlational research. Our speculations about sociocultural processes that may differentially affect the expression of schizophrenia in women and men must be examined in studies designed for that purpose. (Although we can also point out that socioeconomic status of origin is not obviously confounded by the impairments of schizophrenia that clearly contribute to social class of the patient.) Further, there is no way to determine which of the myriad of factors associated with SES of origin (i.e. money, education, cognitive ability, marital status, time spent at home, household stressors, etc.) are involved in any of the reported associations. A replication study may strive toward equal numbers of male and female patients; in the current study there were many more male patients than female patients, perhaps biasing the results. Further, the data did not indicate whether patient SES was static throughout childhood, with which parent the patient was reared, or if the patient lived with their parent(s) at all. For patients reared in a one-parent household, it is highly likely that they lived with their mother. Perhaps the number of correlations associated with mother’s SES reflects this imbalance. Finally, the most intriguing finding in our analysis is the pattern of the results: that advantaged parent SES was associated with greater symptom severity in male patients and lesser symptom severity in female patients. Further research is needed to explore the specific pathways by which SES influences symptom severity, some of which we have provided in preliminary form in the discussion above.

Acknowledgments This study was supported, in part, by NIMH Grant #MH44151 and funds from the Grawemeyer Award in Psychology endowment, University of Louisville.

424

B. Parrott, R. Lewine / Schizophrenia Research 75 (2005) 417–424

References American Psychiatric Association, 1987. Diagnostic and Statistical Manual of Mental Disorders, (3rd ed., revised). American Psychiatric Association, Washington, DC. Andreasen, N.C., 1983. Scale for the Assessment of Negative Symptoms (SANS). The University of Iowa, Iowa City. Andreasen, N.C., 1984. Scale for the Assessment of Positive Symptoms (SAPS). The University of Iowa, Iowa City. Beautrais, A.L., Joyce, P.R., Mulder, R.T., 1998. Unemployment and serious suicide attempts. Psychol. Med. 28, 209 – 218. Beck, A.T., 1972. Measuring depression: the depression inventory. In: Williams, T.A., Katz, M.M., Shields, J.A. (Eds.), Recent Advances in the Psychobiology of Depressive Illnesses. Government Printing Office, Washington, pp. 299 – 302. Becker, D.R., Drake, R.E., Bond, G.R., Xie, H., Dain, B.J., Harrison, K., 1998. Job terminations among persons with severe mental illness participating in supported employment. Community Ment. Health J. 34, 71 – 82. Bell, M., Lysaker, P., 1996. Levels of expectation for work activity in schizophrenia: clinical and rehabilitation outcomes. Psychiatr. Rehabil. J. 19, 71 – 76. Berger, G.E., Wood, S.J., Pantelis, C., Velakoulis, D., Wellard, R.M., McGorry, P.D., 2002. Implications of lipid biology for the pathogenesis of schizophrenia. Aust. N.Z. J. Psychiatr. 36, 355 – 366. Brown, G.W., Birley, J.L.T., Wing, J.K., 1972. Influence of family life on the course of schizophrenic disorders: a replication. Br. J. Psychiatry 121, 241 – 258. Brunello, N., Masotto, C., Steardo, L., Markstein, R., et al., 1995. New insights into the biology of schizophrenia through the mechanism of action of clozapine. Neuropsychopharmacology 13, 177 – 213. Cheung, F., Snowden, L., 1990. Community mental health and ethnic minority populations. Community Ment. Health J. 26, 277 – 291. Chow, J.C., Jaffee, K., Snowden, L., 2003. Racial/ethnic disparities in the use of mental health services in poverty areas. Am. J. Publ. Health 93, 792 – 797. Goldstein, J.M., Lewine, R.R.J., 2000. Overview of sex differences in schizophrenia: where have we been and where do we go from here? In: Castle, D., McGrath, J., Kulkarni, J. (Eds.), Women and Schizophrenia. Cambridge University Press, Cambridge, pp. 111 – 144. Hamilton, M., 1960. A rating scale for depression. J. Neurol. Neurosurg. Psychiatry 23, 56 – 62. Hollingshead, A.B., Redlich, F.C., 1958. Social Class and Mental Illness: A Community Study. John Wiley and Sons, New York. Hooley, J.M., 1998. Expressed emotion and psychiatric illness: from empirical data to clinical practice. Behav. Ther. 29, 631 – 646. Hu, T., Snowden, L., Jerrell, J., Nguyen, T., 1991. Ethnic populations in public mental health: services choice and level of use. Am. J. Publ. Health 81, 1429 – 1434. Johnson, J.G., Cohen, P., Dohrenwend, B.P., Link, B.G., Brook, J.S., 1999. A longitudinal investigation of social causation and social selection processes involved in the association between

socioeconomic status and psychiatric disorders. J. Abnorm. Psychology 108, 490 – 499. Kapur, S., 2003. Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. Am. J. Psychol. 160, 13 – 23. King, S., Dixon, M.J., 1995. Expressed emotion, family dynamics and symptom severity in a predictive model of social adjustment for schizophrenic young adults. Schizophr. Res. 14, 121 – 132. Leff, J., 1992. Over the edge: stress and schizophrenia. New Sci. 4, 30 – 33. Lewine, R.R.J., 1980. Sex differences in age of symptom onset and first hospitalization in schizophrenia. Am. J. Orthopsychiatr. 50, 316 – 322. Lewine, R.R.J., in press. Social class of origin, lost potential, and hopelessness in schizophrenia. Schizophr Res. Lewine, R.R.J., Caudle, J., 2000. Racial effects on neuropsychological functioning in schizophrenia. Am. J. Psychiatr. 157, 2038 – 2040. Lewine, R.J., Walker, E.F., Shurett, R., Caudle, J., Haden, C., 1996. Sex differences in neuropsychological functioning among schizophrenic patients. Am. J. Psychiatr. 153, 1178 – 1184. Lewine, R., Haden, C., Caudle, J., Shurett, R., 1997. Sex-onset effects on neuropsychological function in schizophrenia. Schizophr. Bull. 23, 51 – 61. Mueser, K.T., Salyers, M.P., Mueser, P.R., 2001. A prospective analysis of work in schizophrenia. Schizophr. Bull. 27, 281 – 296. Neighbors, H., Bashshur, R., Price, R., Donavedian, A., Selig, S., Shannon, G., 1992. Ethnic minority mental health service delivery: a review of the literature. Res. Community Ment. Health 7, 55 – 71. Overall, J.E., Gorham, D.R., 1962. The brief psychiatric rating scale. Psychol. Rep. 10, 799 – 812. Page, S., 1987. On gender roles and perception of maladjustment. Can. Psychol. 28, 53 – 60. Parrott, B., Lewine, R., Cadle, C., Wilson, T., Adkins, C., 2004. Job acceptability and socioeconomic status of origin: clinical implications. Poster presented at the 16th annual convention of the American Psychological Society, Chicago, Illinois. Plomin, R., Daniels, D., 1987. Why are children in the same family so different from one another? Behav. Brain Sci. 10, 1 – 16. Sinclair, K., Crouch, B., Miller, J., 1977. Occupational choices of Sydney teenagers: relationships with sex, social class, grade level, and parent expectations. Aust. J. Educ. 21, 41 – 54. Snowden, L., Hu, T., 1997. Ethnic differences in mental health services use among the severely mentally ill. J. Commun. Psychol. 25, 235 – 247. Turkheimer, E., Haley, A., Waldron, M., D’Onofrio, B., Gottesman, I.I., 2003. Socioeconomic status modifies heritability of IQ in young children. Psychol. Sci. 14, 623 – 628. Watson, S.J. (Ed.), Biology of Schizophrenia and affective disease. American Psychiatric Press, Washington, DC. Watt, N., 1976. Two-factor index of social position: amherst modification. Unpublished manuscript, University of Massachusetts at Amherst. Weinberger, D.R., 1999. Cell biology of the hippocampal formation in schizophrenia. Biol. Psychol. 45, 395 – 402.