I am a board-certified gastroenterologist and physician-scientist with a broad research background in neuroimmunology. I am currently applying my knowledge of neuroimmunology and inflammation to advancing our understanding of gastroparesis and other functional motility disorders. Through translational clinical trials and laboratory research, my long-term career goal is to understand the neuroimmune basis of functional motility gut disorders and provide improved diagnostics and treatments to patients.

Clinical Focus

  • Gastroparesis
  • Neurogastroenterology and Motility Disorders
  • Gastroenterology

Academic Appointments

Boards, Advisory Committees, Professional Organizations

  • Member, American Neurogastroenterology & Motility Society (2016 - Present)
  • Member, American Gastroenterology Association (AGA) (2015 - Present)

Professional Education

  • Board Certification: American Board of Internal Medicine, Gastroenterology (2019)
  • Fellowship: Stanford University Gastroenterology Fellowship (2018) CA
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2017)
  • Residency: New York Presbyterian Cornell Campus Internal Medicine Residency (2015) NY
  • Medical Education: Weill Cornell Medical College (2013) NY
  • PhD, The Rockefeller University, NY, NY, Neuroimmunology and Neuroendocrinology (2007)

Clinical Trials

  • GI-Challenge Study for Gastroparesis Patients and Healthy Controls Recruiting

    Gastroparesis Patients and Healthy Controls ages 20-49 will be asked to participate in an observational study measuring vagal activity following food ingestion in order to establish parameters of autonomic nerve/vagal function in healthy human subjects compared to those with gastroparesis. Information generated from this study may be used in the future to establish what is normal and abnormal enteric vagal tone and how much vagal nerve stimulation treatment may be required to help patients with gastroparesis.

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  • Vagal Nerve Stimulation for Gastroparesis Not Recruiting

    This study is investigating a new form of treatment for a digestive disorder called gastroparesis. Gastroparesis is thought to be caused by a mix of inflammation and neural dysfunction. The vagal nerve is a large nerve originating from the brain that regulates digestive function. Patients with gastroparesis have what is a called a low vagal tone which results in gastrointestinal motility problems and inflammation; therefore, investigators hypothesize that increasing vagal tone through a hand-held vagal nerve simulator will reduce inflammation and gastrointestinal motility problems in gastroparesis patients. Investigators will evaluate this hypothesis through the use of upper endoscopy testing, breath testing, and blood, stool, urine, heart rate variability, and saliva testing before and after 4 weeks of vagal nerve stimulation (VNS) treatment. There are 6 research visits Visit 1 and visit 2 may take up to 8 weeks (screening/baseline) Visit 3 and visit 4 will take 4 weeks (VNS treatment) visit 5 and 6 will take approximately 4 weeks (VNS followup/washout) Consequently, it is possible that if a patient were to be at the farthest ends of visit windows, they could potentially be in the study for approx 16 weeks. Visit 1 and 2 may be less than 8 weeks which would shorten the patient's overall involvement in the study. The treatment phase of the study will always be 4 weeks with an additional 4 week washout phase. Use of the VNS device takes 4 weeks. Endoscopy and blood work are taken before and after the treatment period.

    Stanford is currently not accepting patients for this trial. For more information, please contact Brandon Lam, BS, 650-725-0226.

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All Publications

  • MiR-10b-5p Rescues Diabetes and Gastrointestinal Dysmotility. Gastroenterology Singh, R., Ha, S. E., Wei, L., Jin, B., Zogg, H., Poudrier, S. M., Jorgensen, B. G., Park, C., Ronkon, C. F., Bartlett, A., Cho, S., Morales, A., Chung, Y. H., Lee, M. Y., Park, J. K., Gottfried-Blackmore, A., Nguyen, L., Sanders, K. M., Ro, S. 2021


    BACKGROUND & AIMS: Interstitial cells of Cajal (ICCs) and pancreatic beta cells require receptor tyrosine kinase (KIT) to develop and function properly. Degeneration of ICCs is linked to diabetic gastroparesis. The mechanisms linking diabetes and gastroparesis are unclear, but may involve miRNA mediated post-transcriptional gene silencing in KIT+ cells.METHODS: We performed miRNA-seq analysis from isolated ICCs in diabetic mice and plasma from patients with idiopathic and diabetic gastroparesis. miR-10b-5p target genes were identified and validated in mouse and human cell lines. For loss-of-function studies, we used KIT+ cell-restricted mir-10b knockout mice and KIT+ cell depletion mice. For gain-of-function studies, a synthetic miR-10b-5p mimic was injected in multiple diabetic mouse models. We compared the efficacy of miR-10b-5p mimic treatment vs. antidiabetic and prokinetic medicines.RESULTS: miR-10b-5p is highly expressed in ICCs from healthy mice, but drastically depleted in ICCs from diabetic mice. A conditional knockout of mir-10b in KIT+-cells or depletion of KIT+-cells in mice leads to degeneration of beta cells and ICCs, resulting in diabetes and gastroparesis. miR-10b-5p targets the transcription factor Kruppel-like factor 11 (KLF11), which negatively regulates KIT expression. The miR-10b-5p mimic or Klf11 siRNAs injected into mir-10b knockout mice, diet-induced diabetic mice, and TALLYHO polygenic diabetic mice rescues the diabetes and gastroparesis phenotype for an extended period of time. Furthermore, the miR-10b-5p mimic is more effective in improving glucose homoeostasis and GI motility as compared with common antidiabetic and prokinetic medications.CONCLUSIONS: miR-10b-5p is a key regulator in diabetes and gastrointestinal dysmotility via the KLF11-KIT pathway. Restoration of miR-10b-5p may provide therapeutic benefits for these disorders.

    View details for DOI 10.1053/j.gastro.2020.12.062

    View details for PubMedID 33421511

  • Serotonin is elevated in COVID-19-associated diarrhoea. Gut Ha, S., Jin, B., Clemmensen, B., Park, P., Mahboob, S., Gladwill, V., Lovely, F. M., Gottfried-Blackmore, A., Habtezion, A., Verma, S., Ro, S. 2021

    View details for DOI 10.1136/gutjnl-2020-323542

    View details for PubMedID 33402416

  • Serotonin Deficiency is Associated with Delayed Gastric Emptying. Gastroenterology Wei, L. n., Singh, R. n., Ha, S. E., Martin, A. M., Jones, L. n., Jin, B. n., Jorgenson, B. G., Zogg, H. n., Chervo, T. n., Gottfried-Blackmore, A. n., Nguyen, L. n., Habtezion, A. n., Spencer, N. J., Keating, D. J., Sanders, K. M., Ro, S. n. 2021


    Gastrointestinal (GI) motility is regulated by serotonin (5-hydroxytryptamine, 5-HT), which is primarily produced by enterochromaffin (EC) cells in the GI tract. However, the precise roles of EC cell-derived 5-HT in regulating gastric motility remain a major point of conjecture. Using a novel transgenic mouse line, we investigated the distribution of EC cells and the pathophysiological roles of 5-HT deficiency in gastric motility in mice and humans.We developed an inducible, EC cell-specific Tph1CreERT2/+ mouse, which was used to generate a reporter mouse line, Tph1-tdTom, and an EC cell-depleted line, Tph1-DTA. We examined EC cell distribution, morphology, and subpopulations in reporter mice. GI motility was measured in vivo and ex vivo in EC cell-depleted mice. Additionally, we evaluated 5-HT content in biopsy and plasma specimens from patients with idiopathic gastroparesis (IG).Tph1-tdTom mice revealed EC cells were heterogeneously distributed throughout the GI tract with the greatest abundance in the antrum and proximal colon. Two subpopulations of EC cells were identified in the gut: self-renewal cells located at the base of the crypt and mature cells observed in the villi. Tph1-DTA mice displayed delayed gastric emptying, total GI transit, and colonic transit. These gut motility alterations were reversed by exogenous provision of 5-HT. Patients with IG had a significant reduction of antral EC cell numbers and 5-HT content, which negatively correlated with gastric emptying rate.The Tph1CreERT2/+ mouse provides a powerful tool to study the functional roles of EC cells in the GI tract. Our findings suggest a new pathophysiological mechanism of 5-HT deficiency in IG.

    View details for DOI 10.1053/j.gastro.2021.02.060

    View details for PubMedID 33662386

  • Gastric Mucosal Immune Profiling and Dysregulation in Idiopathic Gastroparesis. Clinical and translational gastroenterology Gottfried-Blackmore, A. n., Namkoong, H. n., Adler, E. n., Martin, B. n., Gubatan, J. n., Fernandez-Becker, N. n., Clarke, J. O., Idoyaga, J. n., Nguyen, L. n., Habtezion, A. n. 2021; 12 (5): e00349


    It is unclear how immune perturbations may influence the pathogenesis of idiopathic gastroparesis, a prevalent functional disorder of the stomach which lacks animal models. Several studies have noted altered immune characteristics in the deep gastric muscle layer associated with gastroparesis, but data are lacking for the mucosal layer, which is endoscopically accessible. We hypothesized that immune dysregulation is present in the gastroduodenal mucosa in idiopathic gastroparesis and that specific immune profiles are associated with gastroparesis clinical parameters.In this cross-sectional prospective case-control study, routine endoscopic biopsies were used for comprehensive immune profiling by flow cytometry, multicytokine array, and gene expression in 3 segments of the stomach and the duodenal bulb. Associations of immune endpoints with clinical parameters of gastroparesis were also explored.The gastric mucosa displayed large regional variation of distinct immune profiles. Furthermore, several-fold increases in innate and adaptive immune cells were found in gastroparesis. Various immune cell types showed positive correlations with duration of disease, proton pump inhibitor dosing, and delayed gastric emptying.This initial observational study showed immune compartmentalization of the human stomach mucosa and significant immune dysregulation at the level of leukocyte infiltration in idiopathic gastroparesis patients that extends to the duodenum. Select immune cells, such as macrophages, may correlate with clinicopathological traits of gastroparesis. This work supports further mucosal studies to advance our understanding of gastroparesis pathophysiology.

    View details for DOI 10.14309/ctg.0000000000000349

    View details for PubMedID 33979305

  • Effects of processing conditions on stability of immune analytes in human blood. Scientific reports Gottfried-Blackmore, A., Rubin, S. J., Bai, L., Aluko, S., Yang, Y., Park, W., Habtezion, A. 2020; 10 (1): 17328


    Minimizing variability in collection and processing of human blood samples for research remains a challenge. Delaying plasma or serum isolation after phlebotomy (processing delay) can cause perturbations of numerous analytes. Thus, a comprehensive understanding of how processing delay affects major endpoints used in human immunology research is necessary. Therefore, we studied how processing delay affects commonly measured cytokines and immune cell populations. We hypothesized that short-term time delays inherent to human research in serum and plasma processing impact commonly studied immunological analytes. Blood from healthy donors was subjected to processing delays commonly encountered in sample collection, and then assayed by 62-plex Luminex panel, 40-parameter mass cytometry panel, and 540,000 transcript expression microarray. Variance for immunological analytes was estimated using each individual's baseline as a control. In general, short-term processing delay led to small changes in plasma and serum cytokines (range-10.8 to 43.5%), markers and frequencies of peripheral blood mononuclear cell phenotypes (range 0.19 to 3.54 fold), and whole blood gene expression (stable for>20K genes)-with several exceptions described herein. Importantly, we built an open-access web application allowing investigators to estimate the degree of variance expected from processing delay for measurements of interest based on the data reported here.

    View details for DOI 10.1038/s41598-020-74274-8

    View details for PubMedID 33060628

  • Noninvasive vagal nerve stimulation for gastroenterology pain disorders. Pain management Gottfried-Blackmore, A. n., Habtezion, A. n., Nguyen, L. n. 2020


    Abdominal pain continues to be a major challenge and unmet need in clinical practice. Normalization of bidirectional gut-brain signaling has generated much interest as a therapeutic approach to treat chronic abdominal pain. Vagal nerve stimulation (VNS) is emerging as a potential non-pharmacologic strategy for the treatment of abdominal pain. In this review paper, we will summarize the etiologies of chronic pain in gastrointestinal disorders and discuss the rational for VNS as a therapeutic approach to chronic abdominal pain, with particular emphasis in the gammaCore stimulator which allows for noninvasive VNS.

    View details for DOI 10.2217/pmt-2020-0067

    View details for PubMedID 33111642

  • Open-label pilot study: Non-invasive vagal nerve stimulation improves symptoms and gastric emptying in patients with idiopathic gastroparesis. Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society Gottfried-Blackmore, A., Adler, E. P., Fernandez-Becker, N., Clarke, J., Habtezion, A., Nguyen, L. 2019: e13769


    BACKGROUND: Gastroparesis, a chronic motility disorder characterized by delayed gastric emptying, abdominal pain, nausea, and vomiting, remains largely unexplained. Medical therapy is limited, reflecting the complex physiology of gastric sensorimotor function. Vagus nerve stimulation is an attractive therapeutic modality for gastroparesis, but prior methods required invasive surgery. In this open-label pilot study, we aimed to assess the benefit of non-invasive vagal nerve stimulation in patients with mild to moderate idiopathic gastroparesis.METHODS: Patients self-administered the gammaCore vagal nerve stimulator for 4weeks. The gastroparesis cardinal symptom index daily diary (GCSI-dd) was assessed during a two-week run-in period, ≥4weeks of therapy, and 4weeks after therapy was completed. Gastric emptying and autonomic function testing were also performed. The primary endpoint was an absolute reduction in CGSI-dd of 0.75 after nVNS.RESULTS: There was a total improvement in symptom scores (2.56±0.76 to 1.87±1.05; P=.01), with 6/15 (40%) participants meeting our primary endpoint. Therapy was associated with a reduction in gastric emptying (T1/2 155 vs 129minutes; P=.053, CI -0.4 to 45). Therapy did not correct autonomic function abnormalities, but was associated with modulation of reflex parasympathetic activity.CONCLUSIONS: Short-term non-invasive vagal nerve stimulation led to improved cardinal symptoms and accelerated gastric emptying in a subset of patients with idiopathic gastroparesis. Responders had more severe gastric delay at baseline and clinical improvement correlated with duration of therapy, but not with improvements in gastric emptying. Larger randomized sham-controlled trials of greater duration are needed to confirm the results of this pilot study.

    View details for DOI 10.1111/nmo.13769

    View details for PubMedID 31802596