Jenna R. Cummings

Bio: Jenna R. Cummings is an academic researcher from University of Michigan. The author has contributed to research in topics: Medicine & Food addiction. The author has an hindex of 8, co-authored 23 publications receiving 281 citations. Previous affiliations of Jenna R. Cummings include National Institutes of Health & University of California, Los Angeles.

Time Doesn’t Change Everything: The Longitudinal Course of Distress Tolerance and its Relationship with Externalizing and Internalizing Symptoms During Early Adolescence

Abstract: Although distress tolerance is an emerging construct of empirical interest, we know little about its temporal change, developmental trajectory, and prospective relationships with maladaptive behaviors. The current study examined the developmental trajectory (mean- and individual-level change, and rank-order stability) of distress tolerance in an adolescent sample of boys and girls (N = 277) followed over a four-year period. Next we examined if distress tolerance influenced change in Externalizing (EXT) and Internalizing (INT) symptoms, and if EXT and INT symptoms in turn influenced change in distress tolerance. Finally, we examined if any of these trends differed by gender. Results indicated that distress tolerance is temporally stable, with little mean- or individual-level change. Latent growth models reported that level of distress tolerance is cross-sectionally associated with both EXT and INT symptoms, yet longitudinally, only associated with EXT symptoms. These results suggest that distress tolerance should be a focus of research on etiology and intervention.

Understanding the relative contributions of direct environmental effects and passive genotype–environment correlations in the association between familial risk factors and child disruptive behavior disorders

Abstract: Current research has established a number of robust predictors of child disruptive behavior disorder (DBD) symptoms. These include maladaptive, inconsistent, harsh, punitive, or abusive parenting; marital conflict among parents; divorce; and parental antisocial behavior. Across both clinical and community samples, maladaptive parental disciplinary practices are linked with offspring attention-deficit hyperactivity disorder (ADHD), oppositional-defiant disorder (ODD) , and conduct disorder (CD) symptoms (Loeber & Stouthamer-Loeber, 1986; Burt et al. 2003; Caspi et al. 2004; Stormshak et al. 2000; Stanger et al. 2004). Similarly, divorce and marital discord are significantly related to DBD symptoms (Gartstein & Fagot, 2003; Burt et al. 2008). Finally, one of the strongest predictors of child conduct problems is parental antisocial behavior (Herndon & Iacono, 2005), as it is consistently associated with offspring DBD symptoms, delinquency, and criminal acts. Arguably, these studies put forth familial factors as environmental risk factors contributing directly to child DBD symptoms. Indeed, a recent meta-analysis of twin studies reported that shared environmental factors (i.e., factors common to both members of a sibling pair that make them similar) accounted for 10%–15% of the variance in child DBD symptoms and diagnoses (Burt, 2009). Other studies indicate familial risk factors are associated with child DBD symptoms in large part through shared environmental mechanisms (McGue et al. 1996; Pike et al. 1996; Burt et al. 2003; Burt et al. 2007;). However, additional research on the link between familial risk factors and child DBD symptoms suggests alternative explanations which implicate genetic influences. One key finding largely supporting this is that parental antisociality is highly heritable. In a review of studies on the etiology of child antisociality, Rhee and Waldman (2002) found genes influenced 32% of the variance in child antisociality, and shared environmental factors influenced 16%. Previous studies (Bornovalova. 2010) indicate parental externalizing psychopathology (including adult antisociality) influences child DBD symptoms through transmitting a common genetic vulnerability. Likewise, multiple studies report genetic influences on marital relationships (Reiss et al. 2000; Spotts et al. 2004; Spotts et al. 2006), divorce (McGue & Lykken, 1992), and maladaptive parenting (Jaffee & Price, 2008; see Kendler & Baker, 2007 for a review). Collectively, this research suggests patterns of influence generally attributed to the familial environment are in part genetically mediated. Putative environmental factors may be indirectly related to offspring DBD symptoms through the mechanism of passive gene-environment correlation (rGE). Passive rGE occurs when parents provide both the genes and environment that lead to a certain child outcome. As applied to the current topic, a heritable propensity toward impulsive and disinhibitory behavior may increase likelihood of exhibiting high antisocial traits, especially while being reared in an environment characterized by marital conflict, divorce, and maladaptive parenting. The combination of genetic and environmental risk in turn increases likely manifestation of child DBD symptoms in the offspring (Bornovalova, 2010; Silberg et al. 2012). Unfortunately, neither studies of biological families nor typical twin designs are able to disentangle environmental sources of influence from passive rGE because parents provide both genes and environment for their biological children. And, in classic twin designs, passive rGE can mimic shared environmental influences when the origins are, in fact, a function of common parent– child genes. An elegant method of disentangling environmental influences from passive rGE involves comparing the effects of putative environmental variables in genetically unrelated families (adoptive families) and genetically related families (biological families). The logic of this design is as follows: In families where the biological parents are rearing their own offspring, parents provide both the child’s environment and his/her genes. Thus, any association between parenting and child DBD symptoms could be due to genetically mediated influences, purely environmental influences, or any combination of the two. In contrast, in an adoptive family, the child’s adoptive parents provide the environment, but the child’s birth parents provide his/her genetic makeup and typically do not provide environmental influences after the child was adopted. As such, the possibility of passive rGE is eliminated (provided children are not selectively placed into adoptive homes). If the magnitude of association between familial factors and child DBD symptoms is significantly greater in biological families than in adoptive families, then some degree of passive rGE is indicated because the association between family environment and biological offspring outcomes depends on both genetic and shared environmental factors. Conversely, if the magnitude of the familial factors-child DBD symptoms association is comparable in biological and adoptive families, then passive rGE effects are ruled out and environmental risk processes are implicated (Plomin, 1994). Six previous studies (Dunn et al. 1985; Dunn & Plomin, 1986; Dunn et al. 1986; Rende et al. 1992; Braungartrieker et al. 1995; O'Connor et al. 2000) used this design to examine contribution of passive rGE in the association between familial risk factors and DBD symptoms. Findings generally indicated, with the exception of divorce (which consistently shows solely a direct environmental effect), a mix of direct environmental effects and passive rGE effects. Using a very different method (the Extended Children of Twins Design, a design incorporating children of twins and their cousins capitalizing on a large range of genetic relatedness in immediate and extended family), at least four other studies (Neiderhiser et al. 2004; Harden et al. 2007; Neiderhiser et al. 2007; Narusyte et al. 2011; Silberg et al. 2012) found similar effects. Collectively, these studies suggest both passive rGE and direct environmental effects account for the relationship between family conflict, parenting behavior, and parental antisociality and child DBD symptoms. Although these studies contribute importantly to understanding the relative influence of environmental effects and rGE, each examined one or two selected contextual risk factors making it difficult to evaluate the relative contribution of each. Moreover, previous work suggests the importance of examining maternal and paternal parenting factors separately (Rothbaum & Weisz, 1994; Denham et al. 2000; Johnson et al. 2001) but only a few studies (Neiderhiser et al. 2004; Neiderhiser et al. 2007) have investigated possible differences between fathering and mothering in the interplay between genetic and environmental factors. This last point is quite important, as the effects of maternal versus paternal parenting effects may differ in (a) strength of effect, and (b) underlying mechanism of transmission (Rothbaum & Weisz, 1994; Denham et al. 2000; Johnson et al. 2001; Neiderhiser et al. 2004; Neiderhiser et al. 2007). Additionally, among these studies there is large variability in offspring age (ranging from toddlers to adolescents). It is important to extend these studies by examining the effects of multiple familial risk factors on child DBD symptoms late enough in development to allow manifestation of such symptoms. Finally, it is especially worthwhile to attempt to replicate and extend findings from multiple studies using widely different methods (e.g., adoptive designs; Extended Children of Twins Designs), since confidence in the veracity of an effect increases if the same results are found using multiple methodological approaches.

The temporal "pulse" of drinking: Tracking 5 years of binge drinking in emerging adults.

Abstract: Binge drinking is associated with clinically significant individual-level and public health consequences. The topography of binge drinking may influence the emergence of consequences, but studies of topography require a higher level of temporal resolution than is typically available in epidemiological research. To address topography across the 5 "peak" years of binge drinking (18 to 23 years), we assessed daily binge drinking via successive 90-day timeline follow-back interviews of 645 young adults (resulting in almost 700,000 data points). RESULTS showed a weekend "pulse" of binge drinking that remained consistent across the entire 5 year span, with occasional holiday-based perturbations. Two-part latent growth curve modeling applied to this dataset showed that the often-observed decrease in drinking associated with "maturing out" was due more to decreased participation in binge drinking occasions, rather than to amounts consumed when drinking (intensity). Similarly, the number of binge drinkers varied by day of the week, but the intensity of binge drinking, for those drinking, varied little by day of the week. This approach also showed distinctive predictors for participation and intensity; baseline expectancies and sociability accounted for individual differences in participation, whereas impulsivity-sensation seeking predicted intensity. Individual patterns of binge drinking participation and intensity also predicted drinking consequences over the 5 years of the study. Given these results, binge drinking patterns may serve as a useful phenotype for future research on pathological drinking. (PsycINFO Database Record Language: en

Did That Brownie Do Its Job? Stress, Eating, and the Biobehavioral Effects of Comfort Food

Abstract: Comfort eating is a widespread behavior, but does it actually work? The purpose of this review is to provide a summary of the existing research on the potentially comforting effects of comfort food. We begin by summarizing the existing nonhuman animal research in this area, and then summarize the human research. On the basis of this foundational research, we provide a conceptual model of comfort eating that can be used as a hypothesis-generating tool to guide future research. Finally, we highlight what we consider to be the most exciting future directions in comfort eating. These include (i) determining whether comfort eating is trait-like or state-like, (ii) understanding the antecedents and sequelae of comfort eating, (iii) elucidating the types of food implicated in comfort eating, (iv) creating linkages between comfort eating and comfort drinking, (v) incorporating measures of the autonomic nervous and immune systems in addition to the current focus on the hypothalamic-pituitary-adrenocortical axis, (vi) studying both short-term and long-term effects, and (vii) testing the biological and psychological mechanisms of comfort eating. Given that comfort eating has been practiced for centuries, we conclude that the time is ripe to advance the science of comfort eating. Keywords: comfort eating; stress eating; emotional eating; HPA axis; cortisol; stress-response dampening; food; alcohol

Anxiety, depression, and cigarette smoking: a transdiagnostic vulnerability framework to understanding emotion-smoking comorbidity.

Abstract: Research into the comorbidity between emotional psychopathology and cigarette smoking has often focused upon anxiety and depression's manifest symptoms and syndromes, with limited theoretical and clinical advancement. This article presents a novel framework to understanding emotion-smoking comorbidity. We propose that transdiagnostic emotional vulnerabilities-core biobehavioral traits reflecting maladaptive responses to emotional states that underpin multiple types of emotional psychopathology-link various anxiety and depressive psychopathologies to smoking. This framework is applied in a review and synthesis of the empirical literature on 3 transdiagnostic emotional vulnerabilities implicated in smoking: (a) anhedonia (Anh; diminished pleasure/interest in response to rewards), (b) anxiety sensitivity (AS; fear of anxiety-related sensations), and (c) distress tolerance (DT; ability to withstand distressing states). We conclude that Anh, AS, and DT collectively (a) underpin multiple emotional psychopathologies, (b) amplify smoking's anticipated and actual affect-enhancing properties and other mechanisms underlying smoking, (c) promote progression across the smoking trajectory (i.e., initiation, escalation/progression, maintenance, cessation/relapse), and (d) are promising targets for smoking intervention. After existing gaps are identified, an integrative model of transdiagnostic processes linking emotional psychopathology to smoking is proposed. The model's key premise is that Anh amplifies smoking's anticipated and actual pleasure-enhancing effects, AS amplifies smoking's anxiolytic effects, and poor DT amplifies smoking's distress terminating effects. Collectively, these processes augment the reinforcing properties of smoking for individuals with emotional psychopathology to heighten risk of smoking initiation, progression, maintenance, cessation avoidance, and relapse. We conclude by drawing clinical and scientific implications from this framework that may generalize to other comorbidities.

Parsing the heterogeneity of impulsivity: A meta-analytic review of the behavioral implications of the UPPS for psychopathology.

Abstract: The construct of impulsivity is implicated in a wide variety of psychopathology. However, the heterogeneous factors or subcomponents that differentially predict outcomes are still in the process of being parsed. The present review and meta-analysis focuses on the psychopathological correlates of the Negative Urgency, (lack of) Premeditation, (lack of) perseverance, Sensation Seeking, and Positive Urgency (UPPS/UPPS-P; Whiteside & Lynam, 2001). which provides a relatively new model of impulsivity that posits 5 potentially overlapping pathways to impulsive action. The present meta-analysis included 115 studies that used the UPPS, with a total of 40,432 participants. Findings suggested that the Negative Urgency pathway to impulsivity demonstrated the greatest correlational effect sizes across all forms of psychopathology, with the Positive Urgency pathway demonstrating a pattern of correlations similar to that of Negative Urgency. These findings raise questions regarding the conceptual and practical separability of these pathways. Lack of Premeditation and Lack of Perseverance also demonstrated similar correlational patterns, suggesting that further investigation of the distinctiveness of these pathways is warranted.

Feeding Infants and Toddlers Study: What Foods are Infants and Toddlers Eating?

Abstract: Infants as young as 7 months of age showed food patterns that have been observed in older children and adults. From 18% to 33% of infants and toddlers between ages 7 and 24 months consumed no discrete servings of vegetables, and 23% to 33% consumed no fruits.