Jessica H. Baker, Ph.D. - US grants
Affiliations: | 2010 | Psychology | Virginia Commonwealth University, Richmond, VA, United States |
| 2010- | Psychiatry | University of North Carolina, Chapel Hill, Chapel Hill, NC |
Area:
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The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, Jessica H. Baker is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 2016 — 2019 | Baker, Jessica H | K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Biomarkers of Weight Change in Anorexia Nervosa @ Univ of North Carolina Chapel Hill ? DESCRIPTION (provided by applicant): I am an Assistant Professor with the Center of Excellence for Eating Disorders in the Department of Psychiatry at The University of North Carolina (UNC). I have training in behavior genetics and eating disorders, with a focus on bulimia nervosa (BN) and related symptomatology. I am seeking training in -omic sciences (i.e., genomics, transcriptomics), advanced genetic epidemiological methods, anorexia nervosa- related psychopathology, and longitudinal data analysis. Career Goals: I want to bring eating disorder outcome research to the next level by merging my specific interest in genetics with my emerging interest in anorexia nervosa (AN) treatment outcome, specifically relapse. Thus, my core career goal is to develop an understanding of biomarkers (-omic markers, biological markers) of AN treatment outcome. I will use this knowledge to develop integrated profiles of relapse risk, which will inform novel, biologically-informed, and effective treatment interventions Career Development: I plan to build my skills and expertise in five areas: 1. AN psychopathology, treatment approaches, and outcome; 3. Definitions of recovery in the eating disorders field; 3. Advanced -omic sciences and genetic epidemiological methods 4. Longitudinal data analyses including latent trajectory modeling. 5. The responsible conduct of research. Research Project: The proposed project leverages existing resources by using two ongoing longitudinal parent projects at UNC to identify biomarkers of relapse after inpatient treatment for AN. Parent projects include: 1) Biomarkers of Anorexia Nervosa (BAN)-100 women admitted for inpatient treatment for AN assessed at admission and discharge, and then 3, 7, and 12 months post-discharge. Assessments include biomarkers (cortisol, adrenocorticotropic hormone, norepinephrine, and gene expression) as well as psychological, behavioral, and cognitive symptomatology; and 2) Road to Recovery in Eating Disorders (RRED), a subsample of BAN participants (n=60) followed-up 1 and 2-years post-discharge. The definition of relapse used in this proposal is operationalized as weight change, or the amount of weight lost (or gained and maintained) since hospital discharge (follow-up weight minus discharge weight). First, I will examine gene expression change during therapeutic weight restoration using RNAseq. Second, I will examine the association between biomarkers (gene expression change and HPA-axis and adrenergic pathway activation) and psychological, behavioral, and cognitive factors and weight change at 3-time points within 1-year of discharge from treatment from a specialized eating disorder inpatient unit (BAN sample). These results will identify preliminary profiles of weight change. Third, using sophisticated longitudinal modeling strategies learned during the course of this award period, I will characterize the long-term pattern of weight maintenance/relapse from inpatient discharge to 2-years post-discharge in patients with AN (RRED sample). In future independent applications (R01s) these results will inform further exploration of the influence of -omic factors on treatment outcome-such as the development of a polygenic risk score and the impact of this score on relapse and provide biological targets for treatment and screening. Only through the understanding of biomarkers of theraputically restored weight loss in AN, can we fully identify those at risk for relapse in orderto develop effective treatment protocols-ultimately improving AN outcome. Environment: The research and training will take place in the Departments of Psychiatry and Genetics at UNC. Mentorship: The mentorship team includes lead mentor, Dr. Cynthia Bulik, a clinical psychologist, and internationally recognized expert in eating disorder research and whose funded interests range from genomics to treatment. Secondary mentors include: Dr. Patrick Sullivan, a psychiatrist and leading expert in psychiatric -omics; Dr. Kari North, a genetic epidemiologist who will provide expertise in longitudinal data analysis and methods and integrating genetic and nongenetic data into these analysis; Dr. Anna Bardone-Cone, a clinical psychologist and recognized expert in defining recovery in eating disorders; and Dr. Daniel Bauer, a quantitative psychologist and expert in longitudinal modeling. |
0.988 |
| 2020 | Baker, Jessica H | R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Ovarian Hormones, Reward Response, and Binge Eating in Bulimia Nervosa: An Experimental Design @ Univ of North Carolina Chapel Hill PROJECT SUMMARY Human observational studies suggest ovarian hormones are involved in the neurobiology of bulimia nervosa (BN), specifically the symptom of binge eating: cumulatively, it appears that low estradiol (E2) or progesterone (P4) antagonized E2 are associated with increased binge eating. Problematic however, is that the effect of ovarian hormones on BN symptoms in humans has been inferred from animal studies and from changes in behavior occurring with presumed and measured levels of hormones during the menstrual cycle. Such observational studies cannot conclude a causal, mechanistic link. Moreover, why ovarian hormones influence symptom onset or fluctuation is unknown. Given that ovarian hormones, specifically E2, have pronounced effects on reward processing and neuropathways and neurotransmitters (e.g., dopamine) involved in reward, E2 may influence binge eating through its effect on reward processes that are altered in BN. Thus, we hypothesize BN represents a hormone sensitive phenotype and this sensitivity is displayed as an impaired reward response (i.e., reward-related inhibitory control deficits, heightened reward sensitivity, impaired delay discounting) in the context of low E2. Because women with BN represent a subgroup of the population with reduced dopamine activity, which is enhanced by E2, low E2 may promote reward-motivated behaviors such as binge eating via dopamine withdrawal. We propose this proof-of-concept study to examine our overarching hypothesis. We will complete a 3-month longitudinal, within-person experimental design that parallels animal models to directly manipulate ovarian hormones in females with BN (N = 10): temporarily inducing hypogonadism using a GnRH agonist and then addback E2 and P4 independently in a double-blind cross-over manner. During each phase of the manipulation, subjects will complete symptom reports of binge eating and behavioral tasks and questionnaires of reward processing and reward response. We will complete the following aims: 1): Quantify the direct effect of E2 and P4 on binge eating in women with BN; 2): Determine the effect of E2 on reward response (e.g., delay discounting) and related correlates (e.g., behavioral inhibition); 3): Examine the association between reward response and binge eating before and after E2 addback. If BN truly represents a hormone sensitive phenotype, we will see direct change in binge eating during the hormone challenge. Based on our previous work, we expect to see a beneficial effect of E2 and an exacerbating effect of P4. An experimental design is the only way we can confidently explore the direct impact of ovarian hormones on BN. This high-risk proposal has significant potential for high-reward. Successful completion of the aims will provide guidance in regard to if (and how) E2 and P4 directly affect binge eating in BN. This will provide the empirical direction needed for the investigators to complete a larger, hypothesis-driven mechanistic trial, in turn, providing direction for future research addressing neuroendocrine, neurobiological, and brain activity and function in BN. |
0.988 |