Cheryl L Sisk

Michigan State University, East Lansing, Michigan, United States

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Publications (105)416.7 Total impact

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    ABSTRACT: Changes in ovarian hormones predict changes in emotional eating across the menstrual cycle. However, prior studies have not examined whether the nature of associations varies across dysregulated eating severity. The current study determined whether the strength and/or nature of hormone/dysregulated eating associations differ based on the presence of clinically diagnosed binge episodes (BEs). Participants included 28 women with BEs and 417 women without BEs who provided salivary hormone samples, ratings of emotional eating, and BE frequency for 45 days. Results revealed stronger associations between dysregulated eating and ovarian hormones in women with BEs as compared to women without BEs. The nature of associations also differed, as progesterone moderated the effects of lower estradiol levels on dysregulated eating in women with BEs only. Although hormone/dysregulated eating associations are present across the spectrum of pathology, the nature of associations may vary in ways that have implications for etiological models and treatment.
    Clinical psychological science : a journal of the Association for Psychological Science. 09/2014; 2(4):545-559.
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    ABSTRACT: Previous research has shown that fluctuations in ovarian hormones (i.e., estradiol and progesterone) predict the changes in binge eating and emotional eating across the menstrual cycle. However, the extent to which other eating disorder symptoms fluctuate across the menstrual cycle and are influenced by ovarian hormones remains largely unknown. This study sought to examine whether the levels of weight preoccupation vary across the menstrual cycle and whether the changes in ovarian hormones and/or other factors (i.e., emotional eating and negative affect) account for menstrual cycle fluctuations in this eating disorder phenotype.
    International Journal of Eating Disorders 06/2014; · 3.03 Impact Factor
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    ABSTRACT: Mean-levels of thin-ideal internalization increase during adolescence and pubertal development, but it is unknown whether these phenotypic changes correspond to developmental changes in etiological (i.e., genetic and environmental) risk. Given the limited knowledge on risk for thin-ideal internalization, research is needed to guide the identification of specific types of risk factors during critical developmental periods. The present twin study examined genetic and environmental influences on thin-ideal internalization across adolescent and pubertal development.
    International Journal of Eating Disorders 06/2014; · 3.03 Impact Factor
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    ABSTRACT: Binge eating is a significantly heritable phenotype, but efforts to detect specific risk genes have fallen short. Identification of animal strain differences in risk for binge eating could highlight genetic differences across individuals of the same species that can be exploited in future animal and molecular genetic research. The current study aimed to explore strain differences in risk for binge eating in Sprague-Dawley versus Wistar female rats using the Binge Eating Resistant/Binge Eating Prone model. A sample of male Sprague Dawley rats, a known low-risk group for binge eating, was included as a comparison group. A total of 83 rats (23 Wistar female, 30 Sprague-Dawley female, 30 Sprague-Dawley male) completed a protocol of intermittently administered, palatable food. Binge eating prone (BEP) and binge eating resistant (BER) rats were identified using a tertile approach. Sprague-Dawley female rats consumed the highest amount of palatable food and were more likely to be classified as BEP compared to Wistar female and Sprague-Dawley male rats. Wistar female rats were not significantly different from Sprague-Dawley male rats in their palatable food intake and tendency to be classified as BER rather than BEP. Sprague-Dawley female rats appear to be a particularly vulnerable genotype for binge eating. Comparisons between this group and others could help identify specific genetic/biological factors that differentiate it from lower risk groups. The reward system, linked to binge eating in humans, is a possible candidate to explore. Strain differences in the reward system could help increase understanding of individual differences in risk for binge eating in humans.
    Physiology & Behavior 01/2014; · 3.03 Impact Factor
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    ABSTRACT: Testosterone may be a biological factor that protects males against eating disorders. Elevated prenatal testosterone exposure is linked to lower levels of disordered eating symptoms, but effects emerge only after mid-puberty. Whether circulating levels of testosterone account for decreased risk for disordered eating in boys after mid-puberty is currently unknown; however, animal data support this possibility. In rodents, prenatal testosterone's masculinizing effects on sex-differentiated behaviors emerge during puberty when circulating levels of testosterone increase and 'activate' the expression of masculinized phenotypes. This study investigated whether higher levels of circulating testosterone predict lower levels of disordered eating symptoms in adolescent boys, and in particular whether effects are associated with advancing pubertal maturation. Participants were 213 male twins from the Michigan State University Twin Registry. The Minnesota Eating Behavior Survey and Eating Disorder Examination Questionnaire assessed several disordered eating symptoms. The Pubertal Development Scale assessed pubertal status. Afternoon saliva samples were assayed for testosterone using enzyme immunoassays. Consistent with animal data, higher levels of circulating testosterone predicted lower levels of disordered eating symptoms in adolescent boys and effects emerged with advancing puberty. Results were not accounted for by several important covariates, including age, adiposity, or mood/anxiety symptoms. Findings suggest that elevated circulating testosterone may be protective and underlie decreased risk for eating pathology in males during/after puberty, whereas lower levels of testosterone may increase risk and explain why some, albeit relatively few, males develop eating disorders.
    Psychological Medicine 01/2014; · 5.43 Impact Factor
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    ABSTRACT: Previous research indicates that borderline personality disorder (BPD) is well conceptualized as a dimensional construct that can be represented using normal personality traits. A previous study successfully developed and validated a BPD measure embedded within a normal trait measure, the Minnesota Borderline Personality Disorder Scale (MBPD). The current study performed a further validation of the MBPD by examining its convergent validity, external correlates, and heritability in a sample of 429 female twins. The MBPD correlated strongly with the Structured Clinical Interview for DSM-IV Axis II Personality Disorders (SCID-II) screener for BPD and moderately with external correlates. Moreover, the MBPD and SCID-II screener exhibited very similar patterns of external correlations. Additionally, results indicated that the genetic and environmental influences on MBPD overlap with the genetic and environmental influences on the SCID-II screener, which suggests that these scales are measuring the same construct. These data provide further evidence for the construct validity of the MBPD. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    Personality Disorders: Theory, Research, and Treatment 12/2013; · 3.54 Impact Factor
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    ABSTRACT: Adolescence involves shifts in social behaviors, behavioral flexibility, and adaptive risk-taking that coincide with structural remodeling of the brain. We previously showed that new cells are added to brain regions associated with sexual behaviors, suggesting that cytogenesis may be a mechanism for acquiring adult-typical behaviors during adolescence. Whether pubertal cell addition occurs in brain regions associated with behavioral flexibility or motivation, and whether these patterns differ between pubertal and adult animals had not been determined. Therefore, we assessed patterns of cell proliferation or survival in the prefrontal cortex and nucleus accumbens. Pubertal and adult male rats were given injections of bromo-deoxyuridine (BrdU). To assess cell proliferation, half of the animals from each group were sacrificed 24 hours following the last injection. The remaining animals were sacrificed 30 days following the last injection to evaluate cell survival. Adult animals had significantly lower densities of BrdU-immunoreactive (ir) cells in the prefrontal cortex, irrespective of post-BrdU survival time, whereas in the nucleus accumbens, adult animals had a lower density of BrdU-ir cells at the short survival time, but the density was equivalent in pubertal and adult animals at the longer survival time. These data provide evidence that cell addition during puberty may contribute to the remodeling brain regions associated with behavioral flexibility and motivation, and this cell addition continues into adulthood, albeit at lower levels. Higher levels of cell proliferation or survival in younger animals may reflect a higher level of plasticity, possibly contributing to the dynamic remodeling of the pubertal brain. © 2013 Wiley Periodicals, Inc. Develop Neurobiol, 2013.
    Developmental Neurobiology 12/2013; · 4.42 Impact Factor
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    ABSTRACT: Animal studies indicate that gonadal hormones at puberty have an effect on the development of masculine and feminine traits. However, it is unknown whether similar processes occur in humans. We examined whether women with anorexia nervosa (AN), who often experience primary amenorrhea, exhibit attenuated feminization in their psychological characteristics in adulthood due to the decrease/absence of gonadal hormones at puberty. Women with AN were compared on a number of psychological characteristics using general linear models on the basis of the presence/absence of primary amenorrhea. Although women with primary amenorrhea exhibited lower anxiety scores than those without primary amenorrhea, in general, results did not provide evidence of attenuated feminization in women with AN with primary amenorrhea. Future research should utilize novel techniques and direct hormone measurement to explore the effects of pubertal gonadal hormones on masculine and feminine traits. Copyright © 2013 John Wiley & Sons, Ltd and Eating Disorders Association.
    European Eating Disorders Review 10/2013; · 1.38 Impact Factor
  • Cheryl L Sisk, Sheri A Berenbaum
    Hormones and Behavior 07/2013; · 4.51 Impact Factor
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    ABSTRACT: The interpretation of social cues must change during adolescence in order to promote appropriate social interactions in adulthood. For example, adult, but not juvenile, male Syrian hamsters find female pheromones contained in vaginal sections (VS) rewarding, and only adult hamsters engage in sexual behavior with a receptive female. We previously demonstrated that the rewarding value of VS is both testosterone- and dopamine-dependent. Additionally, VS induces Fos expression throughout the mesocorticolimbic circuit in adult but not juvenile hamsters. In this study, we determined whether or not treatment of juvenile male hamsters with testosterone is sufficient to promote adult-like neural responses to VS. Juvenile and adult male hamsters were gonadectomized and given empty or testosterone-filled subcutaneous capsules for one week. Hamsters were then exposed to either clean or VS-containing mineral oil on their nares, and brains were collected one hour later for immunohistochemistry to visualize Fos and tyrosine hydroxylase immunoreactive cells. Testosterone-treatment failed to promote adult-typical patterns of Fos expression in juvenile hamsters; indeed, in some brain regions, juveniles exposed to VS expressed less Fos compared to age-matched controls while, as expected, adults exposed to VS expressed greater Fos compared to age-matched controls. Age-related changes in tyrosine-hydroxylase expression were also observed. These data indicate that testosterone cannot activate the adult-typical pattern of Fos expression in response to female social cues in prepubertal males, and that additional neural maturation during adolescence is required for adult-typical mesocorticolimbic responses to female pheromones. © 2013 Wiley Periodicals, Inc. Develop Neurobiol, 2013.
    Developmental Neurobiology 07/2013; · 4.42 Impact Factor
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    ABSTRACT: This article is part of a Special Issue "Puberty and Adolescence". Sexual differentiation is the process by which the nervous system becomes structurally and functionally dissimilar in females and males. In mammals, this process has been thought to occur during prenatal and early postnatal development, when a transient increase in testosterone secretion masculinizes and defeminizes the developing male nervous system. Decades of research have led to the views that structural sexual dimorphisms created during perinatal development are passively maintained throughout life, and that ovarian hormones do not play an active role in feminization of the nervous system. Furthermore, perinatal testosterone was thought to determine sex differences in neuron number by regulating cell death and cell survival, and not by regulating cell proliferation. As investigations of neural development during adolescence became more prominent in the late 20th century and revealed the extent of brain remodeling during this time, each of these tenets has been challenged and modified. Here we review evidence from the animal literature that 1) the brain is further sexually differentiated during puberty and adolescence; 2) ovarian hormones play an active role in the feminization of the brain during puberty; and 3) hormonally modulated, sex-specific addition of new neurons and glial cells, as well as loss of neurons, contribute to sexual differentiation of hypothalamic, limbic, and cortical regions during adolescence. This architectural remodeling during the adolescent phase of sexual differentiation of the brain may underlie the known sex differences in vulnerability to addiction and psychiatric disorders that emerge during this developmental period.
    Hormones and Behavior 07/2013; 64(2):203-10. · 4.51 Impact Factor
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    ABSTRACT: Research suggests that prenatal testosterone exposure may masculinize (i.e., lower) disordered eating (DE) attitudes and behaviors and influence the lower prevalence of eating disorders in males versus females. How or when these effects become prominent remains unknown, although puberty may be a critical developmental period. In animals, the masculinizing effects of early testosterone exposure become expressed during puberty when gonadal hormones activate sex-typical behaviors, including eating behaviors. This study examined whether the masculinizing effects of prenatal testosterone exposure on DE attitudes emerge during puberty in 394 twins from opposite-sex and same-sex pairs. Twin type (opposite sex vs. same sex) was used as a proxy for level of prenatal testosterone exposure because females from opposite-sex twin pairs are thought to be exposed to testosterone in utero from their male co-twin. Consistent with animal data, there were no differences in levels of DE attitudes between opposite-sex and same-sex twins during pre-early puberty. However, during mid-late puberty, females from opposite-sex twin pairs (i.e., females with a male co-twin) exhibited more masculinized (i.e., lower) DE attitudes than females from same-sex twin pairs (i.e., females with a female co-twin), independent of several "third variables" (e.g., body mass index [BMI], anxiety). Findings suggest that prenatal testosterone exposure may decrease DE attitudes and at least partially underlie sex differences in risk for DE attitudes after mid-puberty. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    Journal of Abnormal Psychology 05/2013; 122(2):420-432. · 4.86 Impact Factor
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    ABSTRACT: OBJECTIVE: Several efforts are underway to model binge eating in animals in order to advance neurobiological models of risk. However, knowledge of sex differences in these models is currently lacking. The goal of the present study was to examine sex differences in binge eating phenotypes using a well-established rodent model (i.e., the binge eating resistant/binge eating prone model). METHOD: Thirty male and 30 female adult Sprague-Dawley rats were exposed to feeding tests consisting of intermittent access to palatable food (PF). Rats were then categorized as binge eating prone (BEP) based on the amount and consistency of PF consumption across tests. RESULTS: Across multiple methods for BEP classification, rates of BEP phenotypes were two to six times higher in female than male rats. DISCUSSION: Findings provide support for sex differences in rodent models of binge eating and highlight the promise of the BER/BEP model for understanding neurobiological mechanisms underlying sex differences in risk. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013).
    International Journal of Eating Disorders 04/2013; · 3.03 Impact Factor
  • Kayla De Lorme, Margaret R. Bell, Cheryl L. Sisk
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    ABSTRACT: Maturation of social cognition and a gain in social proficiency are universal aspects of adolescent development that prepare individuals for adulthood. Social cognition involves the perception and interpretation of social cues, followed by the generation of a behavioral response. Social proficiency is acquired through the ability to make behavioral adaptations as one learns from social experience; increased social proficiency facilitates successful social interactions. In males, the neuroendocrine bases of these developmental changes involve both activational and organizational influences of testicular hormones. Using the male Syrian hamster as a model, this review provides evidence that social stimuli acquire rewarding properties during adolescence via activational effects of pubertal testosterone, whereas the adolescent gain in social proficiency depends on organizational actions of pubertal testosterone.
    Current Directions in Psychological Science 04/2013; 22(2):128-133. · 3.93 Impact Factor
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    ABSTRACT: Within-person changes in estradiol and progesterone predict changes in binge eating tendencies across the menstrual cycle. However, all women have menstrual-cycle fluctuations in hormones, but few experience binge eating. Personality traits may be critical individual difference factors that influence who will engage in emotional eating in the presence of a vulnerable hormonal environment. Women (N=239) provided self-reports of emotional eating and saliva samples for hormone measurement for 45 consecutive days. Negative urgency and negative emotionality were measured once and were examined as moderators of hormone-emotional eating associations. Consistent with prior research, within-person changes in the interaction between estradiol and progesterone predicted emotional eating. Neither negative urgency nor negative emotionality interacted with changes in estradiol and progesterone to predict changes in emotional eating. Additional factors, other than the two personality traits examined, may account for individual differences in within-person associations between hormones and emotional eating.
    Eating behaviors 04/2013; 14(2):161-6.
  • Margaret A Mohr, Cheryl L Sisk
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    ABSTRACT: During puberty, the brain goes through extensive remodeling, involving the addition of new neurons and glia to brain regions beyond the canonical neurogenic regions (i.e., dentate gyrus and olfactory bulb), including limbic and hypothalamic cell groups associated with sex-typical behavior. Whether these pubertally born cells become functionally integrated into neural circuits remains unknown. To address this question, we gave male Syrian hamsters daily injections of the cell birthdate marker bromodeoxyuridine throughout puberty (postnatal day 28-49). Half of the animals were housed in enriched environments with access to a running wheel to determine whether enrichment increased the survival of pubertally born cells compared with the control environment. At 4 wk after the last BrdU injection, animals were allowed to interact with a receptive female and were then killed 1 h later. Triple-label immunofluorescence for BrdU, the mature neuron marker neuronal nuclear antigen, and the astrocytic marker glial fibrillary acidic protein revealed that a proportion of pubertally born cells in the medial preoptic area, arcuate nucleus, and medial amygdala differentiate into either mature neurons or astrocytes. Double-label immunofluorescence for BrdU and the protein Fos revealed that a subset of pubertally born cells in these regions is activated during sociosexual behavior, indicative of their functional incorporation into neural circuits. Enrichment affected the survival and activation of pubertally born cells in a brain region-specific manner. These results demonstrate that pubertally born cells located outside of the traditional neurogenic regions differentiate into neurons and glia and become functionally incorporated into neural circuits that subserve sex-typical behaviors.
    Proceedings of the National Academy of Sciences 03/2013; · 9.81 Impact Factor
  • Kayla C De Lorme, Cheryl L Sisk
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    ABSTRACT: Pubertal testosterone programs the level of aggressive behavior displayed by male Syrian hamsters during resident-intruder interactions. To further explore the pubertal programming of adult male agonistic behaviors, the current study investigated the formation, stability, and maintenance of dominant-subordinate relationships in males that either did (T@P) or did not (NoT@P) experience testicular hormones during adolescent development. NoT@P males were gonadectomized prepubertally and T@P males were gonadectomized in adulthood. Four weeks after gonadectomy, all males received testosterone-replacement. Two weeks later, two males of the same hormonal history were given a 60min introductory trial in a neutral arena, followed immediately and again 24h later by three 5-min trials. During the introductory trial, each male was deemed dominant, subordinate, or no-status. Brains were collected 1h after the last trial and sections were stained for Fos-immunoreactivity. Dominant T@P males flank marked more frequently than subordinate and no-status T@P males; this difference was not found in NoT@P males. NoT@P males showed an increase in the number of offensive postures the day after the first series of tests, whereas T@P males did not. Dominant T@P males had significantly more Fos expression than no-status T@P males in anterior cingulate cortex; this relationship was not observed in NoT@P males. Additionally, dominant T@P males had higher Fos expression than dominant NoT@P males in lateral septum. Thus, pubertal testosterone does not organize the formation or stability of male-male relationships, but does program the behavioral strategies used to maintain these relationships over time and the neural correlates of status.
    Physiology & Behavior 02/2013; · 3.03 Impact Factor
  • Margaret R Bell, Cheryl L Sisk
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    ABSTRACT: Adolescent maturation of responses to social stimuli is essential for adult-typical sociosexual behavior. Naturally occurring developmental changes in male Syrian hamster responses to a salient social cue, female hamster vaginal secretions (VS), provide a good model system for investigating neuroendocrine mechanisms of adolescent change in social reward. Sexually naïve adult, but not juvenile, males show a conditioned place preference (CPP) to VS, indicating that VS is not rewarding before puberty. In this series of experiments, the authors examined the roles of testosterone and dopamine receptor activation in mediating the adolescent gain in positive valence of VS. Experiment 1 showed that testosterone replacement is necessary for gonadectomized adult hamsters to form a CPP to VS. Experiment 2 showed that testosterone treatment is sufficient for juvenile hamsters to form a CPP to VS, and that the dopamine receptor antagonist haloperidol blocks formation of a CPP to VS in these animals. Experiments 3 and 4 demonstrated that the disruption of VS CPP with low doses of haloperidol is the result of a reduction in the attractive properties of VS and not attributable to aversive properties of haloperidol. Together, these studies demonstrate that the unconditioned rewarding properties of a social cue necessary for successful adult sociosexual interactions come about as the result of the pubertal increase in circulating testosterone in male hamsters. Furthermore, this social reward can be prevented by dopamine receptor antagonism, indicating that hypothalamic and/or mesocorticolimbic dopaminergic circuits are targets for hormonal activation of social reward.
    Endocrinology 01/2013; · 4.72 Impact Factor
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    ABSTRACT: Negative urgency (i.e., the tendency to engage in rash action in response to negative affect) has emerged as a critical personality trait contributing to individual differences in binge eating. However, studies investigating the extent to which genetic and/or environmental influences underlie the effects of negative urgency on binge eating are lacking. Moreover, it remains unclear whether negative urgency-binge eating associations are simply a result of the well-established role of negative affect in the development/maintenance of binge eating. The current study addresses these gaps by examining phenotypic and etiologic associations between negative urgency, negative affect, and dysregulated eating (i.e., binge eating, emotional eating) in a sample of 222 same-sex female twin pairs from the Michigan State University Twin Registry. Negative urgency was significantly associated with both dysregulated eating symptoms, even after controlling for the effects of negative affect. Genetic factors accounted for the majority (62-77%) of this phenotypic association, although a significant proportion of this genetic covariation was due to genetic influences in common with negative affect. Nonshared environmental factors accounted for a relatively smaller (23-38%) proportion of the association, but these nonshared environmental effects were independent of negative affect. Findings suggest that the presence of emotion-based rash action, combined with high levels of negative affect, may significantly increase genetic risk for dysregulated eating. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    Journal of Abnormal Psychology 01/2013; · 4.86 Impact Factor
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    ABSTRACT: OBJECTIVE: Associations between within-person changes in ovarian hormones and dysregulated eating (binge eating, emotional eating) have been observed across the menstrual cycle. However, studies have not examined moderators that may contribute to differential associations between individuals. We investigated body-weight regulation variables [body mass index (BMI), dietary restraint] that have theoretical relevance by virtue of their associations with both phenotypes. METHOD: Women (N = 196) provided emotional eating ratings and saliva samples for 45 days. BMI and restraint were assessed at three time points and averaged. RESULTS: Results showed significant estradiol × progesterone interactions in the prediction of within-subject changes in emotional eating. Neither BMI nor restraint moderated these relationships, although a trend-level dietary restraint × estradiol interaction was observed where estradiol's effects were enhanced in high restraint scorers. DISCUSSION: Findings confirm a role for hormones in changes in emotional eating and suggest that restraint might enhance hormone effects in severegroups. © 2013 by Wiley Periodicals, Inc.
    International Journal of Eating Disorders 01/2013; · 3.03 Impact Factor

Publication Stats

2k Citations
416.70 Total Impact Points


  • 1987–2014
    • Michigan State University
      • Department of Psychology
      East Lansing, Michigan, United States
    • Northwestern University
      • Department of Neurobiology
      Evanston, Illinois, United States
  • 2013
    • University of Chicago
      • Department of Psychiatry and Behavioral Neuroscience
      Chicago, IL, United States
  • 2009
    • University of Colorado
      Denver, Colorado, United States