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Published in final edited form as: Schizophr Res. 2009 Nov 27;118(1-3):162–167. doi: 10.1016/j.schres.2009.10.028

Developmental instability in social anhedonia: An examination of minor physical anomalies and clinical characteristics

Jack J Blanchard 1, Minu Aghevli 2, Amy Wilson 1, Marsha Sargeant 1
PMCID: PMC2856752  NIHMSID: NIHMS157366  PMID: 19944570

Abstract

Developmental instability (DI) refers to the inability of the developing brain to buffer the effects of genetic and environmental insults. This concept has been invoked to better understand how fetal brain development goes awry in schizophrenia and related spectrum disorders. This study examined one marker of DI, minor physical anomalies (MPAs), and its association with a putative indicator of schizotypy, the trait of social anhedonia. MPAs and clinical symptoms were assessed within a community sample of psychometrically-identified individuals high in social anhedonia and a matched group of healthy controls. Results indicated that, compared to the controls, MPAs were elevated in the social anhedonia group. Additionally, within the social anhedonia group, MPAs were significantly correlated with clinical ratings of schizoid personality disorder characteristics and also showed strong associations with schizotypal personality disorder ratings. These findings indicate a relationship between developmental anomalies and negative schizotypy and suggest that, when combined with psychometrically identified risk, the presence of MPAs may further elevate the probability of clinical manifestations of schizophrenia spectrum characteristics.

Keywords: Social Anhedonia, Schizotypy, Developmental Instability, Minor Physical Anomalies, Schizophrenia, Neurodevelopment

1. Introduction

Schizophrenia and related spectrum disorders such as schizotypy have been viewed from a neurodevelopmental perspective (e.g., Cannon, 1998; Weinberger, 1987; Walker, 1994). This developmental conceptualization proposes that genetic and environmental factors interact to determine fetal brain development and later risk for schizophrenia. In attempting to understand how development may go awry in schizophrenia and other disorders, developmental instability has been invoked as an important concept (Yeo, Gangestad, Thoma, 2007). Developmental instability (DI) refers to an individual's inability to buffer the effects of genetic and environmental stressors on development. The DI model is rooted in the assumption that the ability of an organism to precisely carry out its genetic “design” is an imprecise, epigenetic process. Increased developmental stability acts to “buffer” development, allowing the organism to express its genotype precisely even in the face of adverse environmental conditions (Waddington, 1957; Jantz, Webb, 1980). On the other hand, DI is thought to result in increased developmental imprecision and “noise” in developmental pathways (Yeo et al., 2007). One result of DI is that environmental stressors may have more of an impact on the individual (Yeo et al., 2007).

DI is measured through the assessment of proxy measures or markers of this developmental disturbance (Yeo et al., 2007). Putative markers of DI include minor physical anomalies (MPAs) as well as dermatoglyphic abnormalities. MPAs are morphologic anomalies that are evident in the craniofacial region (e.g., flat or prominent forehead, wide-spaced eyes, asymmetrical ears, narrow or steepled palate) and limbs (e.g., webbed toes). Dermatoglyphic abnormalities can include deviations from symmetry on bilateral traits (e.g., palmar ridge counts) that are symmetric in the general population (Yeo et al., 2007). Deviation from symmetry is thought to represent developmental error either resulting from genetic or environmental disruption of growth (Yeo and Gangestad, 1998).

There is accumulating evidence that, while certainly not unique to schizophrenia, markers of DI are present at higher levels in schizophrenia than in nonpsychiatric control groups (e.g., Compton, Bollini, Mack, Kryda, Rutland, Weiss, Bercu, Esterberg, and Walker, 2007; Edgar, Yeo, Canive, and Miller, 2006; Green, Satz, Gaier, Gazell, and Kharabi, 1989; Lane, Kinsella, and Murphy et al, 1997). With regard to MPAs, in a recent review Compton and Walker (2009) concluded that an accumulation of studies have found MPAs in schizophrenia and that these results are consistent with the neurodevelopmental model of schizophrenia (see also meta-analyses on MPAs by Weinberg, Jenkins, Marazita, and Maher, 2007). Similarly, in a review of studies on dermatoglyphic anomalies Chok, Kwapil, and Scheuermann (2005) found that such anomalies were more prevalent in schizophrenia than in controls (with some exceptions: Cantor-Graae et al., 1988; Rosa et al., 2000).

Given the above findings in schizophrenia, researchers have begun to extend research on neurodevelopmental anomalies to the study of schizotypal traits. Schizotypal traits may represent phenotypic manifestations of genetic liability for schizophrenia (Meehl, 1962). The use of these traits in psychometric high-risk paradigms may afford opportunities to study correlates of schizotypy (Blanchard et al., in press; Chapman et al., 1994; Gooding et al., 2005; Kwapil, 1998) prior to illness onset and free of complicating factors including medication exposure.

A small number of studies have now demonstrated an association between MPAs, dermatoglyphic anomalies and psychometrically identified positive (as indexed by traits such as perceptual aberrations and magical ideation) and negative (relating to physical and social anhedonia) schizotypy traits in nonclinical samples (Barrantes-Vidal et al., 2002; Chok, Kwapil, and Scheuermann, 2005; Chok and Kwapil, 2005; Daly, Gooding, Jessen, and Auger, 2008; Rosa et al., 2000; Thoma et al., 2008). However, there are important limitations to the existing literature. First, although some studies suggest that indices of developmental deviance are related to anhedonia (Daly et al., 2008) and that negative schizotypy is more strongly related to such anomalies than positive schizotypy (Chok and Kwapil, 2005; Rosa et al., 2000) these findings are not consistent across methods and studies. Results vary across measures of DI (e.g., Daly et al., 2008) and there is some evidence that associations between developmental deviance and negative schizotypal traits is most pronounced in males (Daly et al., 2008; Rosa et al., 2000). Further, these developmental deviance findings are not consistent across studies as one study failed to show an association between anhedonia and DI (Thoma et al., 2008). Thus, replication focusing on anhedonia is clearly required.

A second limitation with existing research is that, although MPAs are important indicators of developmental deviance and are present in schizophrenia (Compton, and Walker, 2008), only one published study has examined MPAs in psychometrically assessed schizotypy traits (Thoma et al., 2008). Other studies have focused on various dermatoglyphic anomalies and it is important to determine if these findings generalize to MPAs.

A third concern is that none of the published studies on DI and psychometrically identified schizotypy have directly assessed clinical symptoms of schizophrenia spectrum personality disorders. This is important as not all putative schizotypes will develop clinical symptoms and it would be informative to determine what factors may account for this heterogeneity in outcomes. It may be that greater DI contributes to greater clinical severity within psychometrically identified high-risk samples (i.e., enhancing risk stratification, Compton and Walker, 2009). Relatedly, since DI is not specific to schizophrenia-spectrum disorders (Compton et al., 2009; Lloyd et al., 2008; Yeo et al., 2007) it would be informative to demonstrate that obtained group differences in developmental deviance are actually associated with clinically rated characteristics of personality pathology associated with schizophrenia-spectrum disorders.

A final limitation with the existing literature is that the majority of studies on developmental deviance and schizotypal traits have been conducted in college samples (Chok et al., 2005; Chok, and Kwapil, 2005; Daly et al., 2008; Thoma et al, 2008). Given the potential lack of representativeness of high functioning college students, it would be informative to determine if findings of DI and schizotypy can be replicated in community samples.

To address the above issues, this study sought to examine the incidence of MPAs in a community sample of individuals high in social anhedonia and matched controls. It was hypothesized that MPAs would be more prevalent in social anhedonics compared to controls. We also examined the association between MPAs and clinical ratings of schizophrenia-spectrum personality disorder characteristics. We hypothesized that within the social anhedonia group, MPAs would be related to greater clinical severity as measured by dimensional personality disorder characteristics of schizotypal, schizoid, and paranoid personality disorder. Finally, based on prior findings that DI is more associated with negative schizotypal characteristics in males (Daly et al., 2008; Rosa et al., 2000) we explored gender effects within the analyses.

2. Methods

2.1 Sample

The present study recruited community participants from the larger ongoing Maryland Longitudinal Study of Schizotypy (MLSS; Blanchard et al., in press). The MLSS is a study focusing on social anhedonia as a putative indicator of schizotypy (Meehl, 1962) and the risk for development of schizophrenia and related spectrum disorders. Prior publications on this sample have examined clinical (Blanchard et al., in press), cognitive (Cohen et al., 2006) and behavioral (Collins et al., 2005) features in probands as well as parental characteristics of participants within the MLSS (Cohen, et al., in press; Emmerson et al, 2009).

Full details of MLSS recruitment methodology can be found in Blanchard et al. (in press). Briefly, the MLSS participants were drawn from a larger community sample of 2,434 18- to 19- year-olds recruited by the UMCP Survey Research Center using random digit dial methods. Participants were mailed a consent form and a screening questionnaire that included the Revised Social Anhedonia Scale (SocAnh Scale; Eckblad, 1982), Perceptual Aberrations Scale (PerAb; Chapman, Chapman, and Raulin, 1976), and Magical Ideation Scale (MagicID; Eckblad and Chapman, 1983). A validity scale (The Infrequency Scale; Chapman, 1976) was embedded within the screening questionnaire, and individuals who endorsed three or more items in the unexpected direction were excluded from the study (as in Chapman, 1976).

A subset of the full MLSS social anhedonia participants (n = 36) were recruited to participate in this study focusing on additional assessments of minor physical anomalies. In the full MLSS study, two methods were used to identify participants with extreme scores on social anhedonia. The first method involved identifying individuals at least 1.9 standard deviations above SocAnh Scale mean The second selection method involved using the taxometric method of maximum covariate analysis (MAXCOV-HITMAX; Waller and Meehl, 1998). Individuals with Bayesian probabilities greater than or equal to 0.50 were assigned to the social anhedonia taxon group (see Blanchard et al., 2000, Horan et al., 2004 for a review of this methodology). There were no statistically significant differences between subjects identified through these two procedures for any of the dependent variables examined in the overall MLSS study (Blanchard et al., in press). In either selection method, scores on the PerAb and MagicID scales were not considered in forming the social anhedonia group.

A subset of the full MLSS control participants (N = 41) were recruited to participate in this study. The control group consisted of individuals without elevated scores on the SocAnh Scale, operationalized as a SocAnh score 0.50 standard deviations below the gender and race group derived mean and a Bayesian probability of taxon membership below 0.50. An additional inclusion criterion specified that control participants not score higher than 0.50 standard deviations above the mean on the PerAb or MagicID scales of psychosis proneness.

2.2. Measures

2.2.1 Minor physical anomalies

Minor physical anomalies (MPAs) were assessed using the Manual for Assessing Minor Physical Anomalies (Waldrop, Halverson & Shetterley, 1989), which sets forth guidelines for determining the presence and degree of a variety of MPAs. These include wide-spaced eyes, low-seated ears, single transverse palmer crease, and anomalies of the fingers and toes. This manual is the most popular assessment tool for MPAs (Yeo, Gangestad, and Daniel, 1993). It has been used in many other studies of MPAs, including both those of individuals at genetic risk for schizophrenia, for whom it may be associated with clinical history and outcome (e.g., Shiffman et al., 2002), and those of normal college-age individuals (e.g., Yeo et al., 1997). MPAs as measured by Waldrop and colleagues' manual have been shown to remain stable from birth (Waldrop, 1975). Inter-rater reliability for the overall MPA score has been found to be high (e.g., .70; Waldrop, Pederson and Bell, 1968). Raters were graduate students trained using the Waldrop Manual. All MPA assessments were conducted in the same laboratory room providing consistent lighting for purposes of physical assessment. Discussion of the scoring criteria and group ratings on practice subjects were carried out prior to rating actual subjects in order to ensure agreement about the criteria. In addition, regular discussions about any difficulties in ratings took place during supervision, and periodic checks were conducted in order to ensure ongoing agreement. MPA ratings were conducted blind to group status and clinical ratings.

2.2.2. Schizophrenia-Spectrum Symptom Ratings

The International Personality Disorders Examination (IPDE; Loranger et al., 1995) is a semi-structured interview which yields both categorical and dimensional ratings of Axis II disorders (each symptom item is rated on a 3-point scale: 0 = not present; 1= subthreshold; 2 = threshold). The IPDE was administered to assess schizoid, schizotypal, and paranoid personality disorders, consisting of items related to unusual thinking or beliefs, unusual perceptual experiences, suspicious or paranoid ideation, inappropriate or constricted affect, odd or eccentric behavior or appearance, impaired social relationships, and social anxiety. A number of studies have used the IPDE for the assessment of schizophrenia-spectrum disorders in putatively psychosis-prone individuals (e.g., Chapman et al., 1994; Kwapil et al., 2002; Horan et al., 2007). All diagnostic interviewers were Masters-level doctoral students under the supervision of a licensed clinical psychologist with extensive training and experience in clinical assessment (JJB). A consensus meeting was used to discuss the diagnostic material (ratings and notes), issues raised in an independent video review, and to consult the video tape for further clarification. Final symptom severity ratings and diagnostic decisions were determined within the consensus meeting. IPDE ratings were not available for one control participant (N = 40).

3. Results

Demographic characteristics are presented in Table 1. The groups did not differ in sex X2 (1,77) = .019, p > .05, or race, X2 (4, 77) = 7.76, p > .05.

Table 1.

Demographic Characteristics in Control (n = 41) and Social Anhedonia (n = 36) Groups.

Control
n(%)		 Social Anhedonia
n(%)
Sex:
 Male 20 (48.8%) 18 (48.7%)
 Female 21 (51.2%) 19 (51.4%)
Race:
 White 26 (63.4%) 19 (51.4%)
 Black 10 (24.4%) 16 (43.2%)
 Asian 1 (2.4%) 1 (2.7%)
 Hispanic 3 (7.3%) 1 (2.7%)
 Other 1 (2.4%) 0 (0.0%)
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Group ratings of MPAs are presented in Table 2. A group X sex ANOVA was conducted to examine group differences. The main effect of group was significant, F(1, 73) = 4.34, p = .04, d = 0.45. However, the main effect of sex F(1, 73) = 0.55, and the group by sex interaction F(1, 73) = .001, were not significant, ps > .05. The social anhedonia group had significantly higher MPAs than did the control group.

Table 2.

Desciptive Statistics for Minor Physical Anomolies and Personality Disorder Dimensional Ratings.

Control
Mean (SD)		 Social Anhedonia
Mean (SD)
Minor Physical Anomalies 1.83 (1.75) 2.68 (1.99)*
Schizoid Personality Disorder 0.24 (0.62) 1.49 (2.09)***
Schizotypal Personality Disorder 0.32 (0.69) 1.03 (1.42)**
Paranoid Personality Disorder 0.34 (0.88) 1.08 (1.75)*
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*

p < .05

**

p < .001

***

p < .0001

Group differences in clinical characteristics within the full MLSS sample have been reported elsewhere (Blanchard et al., in press). Personality disorder characteristics were evaluated within the current sample (see Table 2) with separate group X sex ANOVAs conducted on each IPDE spectrum dimensional score. A significant main effect of group for schizoid dimensional scores was obtained, F(1, 73) = 13.75, p = .0001, d = .81. However, the main effect of sex and the sex X group interaction were not significant, Fs(1, 73) = .55, .001, respectively, ps > .05. For schizotypal dimensional scores, there was a main effect for group F(1, 73) = 12.10, p = .001, d = .64. The main effect for sex and the sex X group interaction were not significant, Fs(1, 73) = 1.75, .002, respectively, ps > .05. Finally, a similar pattern emerged for paranoid dimensional scores, with a significant main effect for group, F(1, 73) = 4.60, p = .04, d = .53, with social anhedonia participants having higher scores than control participants. However, the main effect of sex and the sex X group interaction for paranoid scores were not significant, Fs(76) = .07, 0.18, respectively, ps > .05. In summary, consistent with findings from the full MLSS sample, group differences in personality characteristics were found across the IPDE dimensional scores with the social anhedonia group obtaining higher pathological ratings compared to controls.

Correlations between MPAs and IPDE dimensional scores within the Social Anhedonia group are presented in Table 3. MPAs were significantly correlated with schizoid dimensional ratings (r = .39, p = .02). The correlation between MPAs and schizotypal dimensional ratings was not significant (r = .29, p = .09) but the magnitude of the correlation approximated a medium effect size (Cohen, 1992). Paranoid dimensional scores were not correlated with MPAs (r = .09, p = .58). In order to examine if sex of participants contributed to these relationships, partial correlations were conducted. After controlling for sex, correlations between MPAs and personality dimensional scores were essentially unchanged for schizoid (pr = .39, p = .03), schizotypal (pr = .30, p = .08), and paranoid (pr = .10, p = .57) dimensional scores.

Table 3.

Correlations between Minor Physical Anomalies (MPAs) and Personality Disorder Dimensional Ratings in the Social Anhedonia Group (N = 36)

Dimensional Scores MPAs
Schizoid .39*
Schizotypal .29†
Paranoid .09
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*

p < .05

†

p = .09

4. Discussion

The present study sought to examine whether developmental instability was associated with social anhedonia, a putative indicator of risk for schizophrenia and related spectrum disorders. Results indicated that MPAs were higher in the social anhedonia group compared to the control group. This finding is consistent with the proposal that neurodevelopmental aberrations may contribute to the spectrum of schizophrenia liability (Compton, et al., 2009; Yeo, et al., 2007). These results are also consistent with prior findings that other markers of developmental instability are associated with negative schizotypy (Chok,et al., 2005; Daly et al., 2008; Rosa et al., 2000) and extend these findings to MPAs.

The association between MPAs and clinical characteristics were examined within the social anhedonia group. As predicted, greater MPAs within this group were significantly correlated with schizoid personality dimensionality ratings. The correlation with schizotypal ratings was not significant, but a medium effect size was obtained. No relationship was found between MPAs and paranoid personality dimensional ratings. These results suggest that schizotypal and schizoid characteristics may have stronger associations with DI than paranoid characteristics. This later findings was not predicted and caution is warranted in the interpretation of this unexpected result. Overall, these findings are interesting in that they suggest that in association with psychometrically identified risk, the presence of MPAs may further elevate the probability of clinical manifestations of spectrum disorders. This would appear to be consistent with Compton and Walker's (2009) suggestion that DI may enhance risk stratification. These findings require further replication but suggest that the joint use of psychometric measures of schizotypy and indicators of developmental deviance may yield an especially vulnerable high-risk group. Ultimately, longitudinal designs would be required to test this conjecture, but initial validation could come from cross-sectional studies assessing symptom and functional correlates of DI in psychometrically-identified individuals.

Prior research has yielded inconsistent findings with regard to the role of sex in the association between schizotypy and measures of DI. Some studies have found that this association is particularly pronounced in males (Daly et al., 2008; Rosa et al., 2000); however, the present study found no main effects or interactions for sex in MPAs or in personality dimensional scores. Further, sex made no contribution to the correlational findings between MPAs and personality scores within the social anhedonia group. The discrepancy in findings may relate to sample differences in prior studies which used college samples compared to the community sample in the current study. Additionally, most prior studies of psychometrically-identified schizotypy have not included MPAs but have focused on other indices of developmental deviance such as dermotoglyphics. Caution is warranted in interpreting the current results given the modest sample size and limited power to detect small gender differences. However, the current null findings indicate the need to further assess the role of sex in DI and schizotypy.

A limitation to the present findings is that only MPA's were addressed. There are other indicators of DI including fluctuating asymmetries that are found in dermatoglyphics features. Although these various indicators of developmental disturbance are presumed to reflect the same underlying process, findings would suggest that these indicators may be differentially related to schizotypy (e.g., Daly et al., 2008). Thus, caution is warranted in extending the present results with MPAs to other markers of DI. Additionally, different markers of DI may represent anomalies occurring at different periods of development (Yeo et al., 2007) and thus may provide information regarding what period appears to be most related to schizotypy. Finally, neurological soft signs have been used as broad indicators of developmental deviance (e.g, Barrantes-Vidal et al., 2002; Bollini et al, 2007) and were not evaluated in this study. Future studies should include broader assessments of developmental abnormalities to further examine which markers may be most informative in understanding heightened risk in putative schizotypes.

The present findings are limited in that they are cross-sectional. Although there is an accumulation of evidence suggesting that social anhedonia identifies individuals who are at risk for schizophrenia-spectrum personality disorders (Gooding et al., 2005; Kwapil, 1998), it is unclear to what extent participants in this cross-sectional study will ultimately develop schizophrenia-spectrum disorders. Further, the current cross-sectional results with young adults cannot address the conjecture that elevated MPAs will ultimately contribute to longitudinal clinical outcomes during adulthood.

A final interpretive caution concerns the specificity of the current findings. The two-factor DI model of Yeo et al. (2007) proposes that DI is related to a variety of neurodevelopmental disorders other than schizophrenia (e.g., ADHD and dyslexia). Compton et al. (2009) have also noted that, although the study of MPAs in other disorders has been limited, elevated MPAs have been found in psychiatric disorders other than schizophrenia. For example, MPAs have been found to be elevated in affective psychosis (Lloyd et al., 2008). Thus, the mere elevation of DI within any psychometrically identified group does not allow conclusions regarding specific diagnostic outcomes. It would be informative to examine other symptom domains and risk groups to determine the specificity of findings obtained with psychometric measures of schizotypy.

Acknowledgements

This research was supported by NIMH grants R01MH51240 and K02MH079231 to Jack J. Blanchard.

Role of funding source

Funding for this study was provided by NIMH Grants R01MH51240 and K02MH079231; the NIMH had no further role and study design; in the collection, analysis, and interpretation of the data; in the writing of the report; or in the decision to submit the paper for publication.

Footnotes

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Conflict of interest

All authors declare that there are no conflicts of interest to disclose.

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