About

Jeffrey C. Johnson, Ph.D., is a Professor of Anthropology at the University of Florida. He earned his B.A. in Anthropology from the University of California, Irvine in 1975 and his Ph.D. in Social Science from the same institution in 1981. Johnson has been active in research projects funded by Sea Grant and the National Oceanic and Atmospheric Administration for over thirty years. His extensive long-term research includes comparative studies of group dynamics of over-wintering crews at the American South Pole Station and other Antarctic stations operated by Poland, Russia, China, and India. He is interested in network models of complex biological systems and has worked on applying continuous time Markov chain and exponential random graph models to the study of trophic dynamics in food webs. His recent work, funded by the Office of Naval Research, involves developing methods for reliable tagging, coding, and network modeling of large corpora of related texts. Johnson has published extensively across multiple scientific disciplines, including anthropology, sociology, biology, and marine science. He was the founding editor of the Journal of Quantitative Anthropology and co-editor of Human Organization. Currently, he serves as an associate editor for the Journal of Social Structure and Social Networks. Johnson is also the Director of the Summer Institute for Research Design in Cultural Anthropology, funded by the National Science Foundation, and is the author of 'Selecting Ethnographic Informants' (Sage, 1990) and co-author of 'Analyzing Social Networks' (Sage, 2013). His professional career includes various positions and memberships, reflecting his active engagement in research and academic service.

Research topics

• Medicine
• Internal medicine
• Computer Science
• Cardiology
• Genetics
• Medical physics
• Pharmacology
• Environmental health
• Political Science
• Biology
• Bioinformatics
• Family medicine
• Psychiatry
• Gerontology
• Emergency medicine
• Chemistry
• Demography
• Pathology
• Immunology
• Gastroenterology

Selected publications

• Accelerating real‐world prediction and research in Alzheimer's: The M3AD study

  Alzheimer s & Dementia · 2026-03-01

  articleOpen access

  Chronic diseases, including Alzheimer's disease (AD) and related dementia (ADRD), do not exist solely as isolated entities. Instead, they weave concomitant trajectories of multiple diseases, conditions, behaviors, and risks, mutually influencing each other's course and natural history, in ways yet unexplored. Electronic health records (EHRs) provide us with a unique opportunity to look at related and unrelated clinical trajectories over time, thus potentially providing insight into unrecognized prodromes, while incorporating the complexities of patients' lives. We harmonize and federate a three-city EHR metaplatform of nearly 10 million patients (∼60,000 with AD/ADRD), which we further embed within census tracts, to contextualize these health trajectories. Our multidisciplinary approach ambitions a unique dynamic platform to inform strategies to tailor risk prediction, complex clinical management, and real-world evaluation of future treatments of AD/ADRD. We present the rationale for and design of the Multimorbidity Three-City Alzheimer's Disease EHR (M3AD) Study and real-world data metaplatform, progress and demonstration of feasibility, its expected singular and complementary contributions to the field. HIGHLIGHTS: Our success in living longer lives often brings chronic conditions and multimorbidity. Alzheimer's research should comprise life trajectories' complexity in multimorbidity. New real-world analytical approaches allow integrated prediction of Alzheimer's disease. We are building a three-city electronic health record (EHR) metaplatform for prediction, prevention, and impact We further embed EHR within census tracts to contextualize Alzheimer's trajectories.

  PublisherDOI

• The Future of Clinical Translational Pharmacology

  Clinical Pharmacology & Therapeutics · 2026-04-14

  article

  Will clinical translational pharmacology (CTP) seize the opportunity to become a leadership discipline driving the next era of patient-centered therapeutics? This white paper, based on input and discussion from the ASCPT Summit on the Future of Clinical Translational Pharmacology, issues a bold call to action for CTP to define itself as a discipline that embraces its multidisciplinary breadth, demanding a radical shift that visibly inhabits the full scope of its multitudinous identity. We propose a five-priority roadmap-Foundational Principles, Workforce and Leadership, Innovation and Technology, Health Equity and Global Health, and Public Visibility and Scientific Trust-to transform CTP into an engine of therapeutic advancement and optimization. The future of medicine depends on CTP's ability to lead, adapt, influence, and unify across silos, ensuring that scientific breakthroughs translate into real-world benefit for every patient, everywhere. The next decade demands urgency, unity, and unapologetic ambition to move beyond incremental change.

  PublisherDOI

• Genotype-Guided Antidepressant Prescribing for Patients With Depression

  JAMA Network Open · 2026-05-06

  articleOpen access

  Importance: The effectiveness of pharmacogenetics to guide prescribing of selective serotonin reuptake inhibitors (SSRIs) for depression remains unclear, despite the well-established association between SSRI pharmacokinetics and genetic variation. Objective: To determine whether pharmacogenetic-guided prescribing of SSRIs improves treatment response in patients with depression. Design, Setting, and Participants: The ADOPT PGx (A Depression and Opioid Pragmatic Trial in Pharmacogenetics) Depression pragmatic randomized clinical trial was conducted from August 10, 2021, through April 27, 2024, at primary care, psychiatry, or family medicine clinics at enrolling sites throughout the US. Patients were aged 8 years or older and had experienced depression for 3 months or longer. Intervention: Patients were randomized to genotype-guided SSRI prescribing (intervention group) or usual care (control group). Actionable drug metabolism phenotypes were defined as those for which pharmacogenetic clinical guidelines recommend alternative medication selection or dose adjustment. Main Outcomes and Measures: The primary outcome was change in Patient-Reported Outcomes Measurement Information System (PROMIS) depression T scores at 3 months among patients with the actionable phenotype. Secondary end points included adverse effect severity of SSRIs at 3 months and depression remission (measured with PROMIS depression scores and Patient Health Questionnaire-8 [PHQ-8] scores) at 6 months. Results: This study of 1460 patients included 1239 adults (84.9%) (mean [SD] age, 40.6 [16.7] years) and 221 children (15.1%) (mean [SD] age, 14.6 [1.8] years). Most patients were female (1096 [75.1%]). A total of 692 patients (47.4%) had an actionable phenotype; 351 (50.7%) were assigned to the intervention, and 341 (49.3%) were assigned to usual care. At baseline, 463 of the 692 patients (66.9%) reported having depressive symptoms for more than 2 years, 603 (87.1%) were receiving pharmacologic treatment, and 354 (51.2%) were receiving nonpharmacologic treatment. At 3 months, no significant differences were observed between the intervention and usual care groups in change in PROMIS depression T scores (mean [SD] change, -4.3 [8.4] vs -4.0 [8.1]; P = .68), medication adverse effect burden (mean [SD] change, 8.2 [4.3] vs 7.8 [4.5]; P = .37), or Patient Health Questionnaire-8 score change (mean [SD] change, -3.3 [5.2] vs -2.7 [4.8]; P = .13). However, at 6 months, the PROMIS depression T-score remission rate (score ≤16) was higher in the intervention group compared with the usual care group (153 of 317 patients [48.3%] vs 122 of 310 patients [39.4%]; P = .02). Conclusions and Relevance: In this randomized clinical trial, genotype-guided prescribing of SSRIs did not improve control of depression symptoms at 3 months compared with usual care but was associated with higher depression remission rates at 6 months. These findings suggest a possible longer-term clinical benefit and indicate that future studies should focus on the durability and long-term impact of genotype-guided prescribing in the management of depressive symptoms. Trial Registration: ClinicalTrials.gov Identifiers: NCT04445792 (Master Protocol Research Program platform trial) and NCT05966155 (ADOPT PGx Depression trial).

  PublisherDOI

• In vitro comparative analysis of metabolic capabilities and inhibitory profiles of selected CYP2D6 alleles on tramadol metabolism

  Clinical and Translational Science · 2025-01-27 · 2 citations

  articleOpen accessSenior authorCorresponding

  Abstract Tramadol, the 41st most prescribed drug in the United States in 2021 is a prodrug activated by CYP2D6, which is highly polymorphic. Previous studies showed enzyme‐inhibitor affinity varied between different CYP2D6 allelic variants with dextromethorphan and atomoxetine metabolism. However, no study has compared tramadol metabolism in different CYP2D6 alleles with different CYP2D6 inhibitors. We hypothesize that the inhibitory effects of CYP2D6 inhibitors on CYP2D6‐mediated tramadol metabolism are inhibitor‐ and CYP2D6 ‐allele‐specific. We performed comparative analyses of CYP2D6*1, CYP2D6*2, CYP2D6*10, and CYP2D6*17 using recombinant enzymes to metabolize tramadol to O ‐desmethyltramadol, measured via UPLC‐MS/MS. The Michaelis constant (K m ) and maximum velocity (V max ) for each CYP2D6 allele, and IC 50 values for different inhibitors were determined by nonlinear regression analysis. Intrinsic clearance was calculated as V max /K m . The intrinsic clearance of tramadol was almost double for CYP2D6*2 (180%) but was much lower for CYP2D6*10 and *17 (20% and 10%, respectively) compared to CYP2D6*1. The inhibitor potencies (defined by Ki) for the various inhibitors for the CYP2D6*1 allele were quinidine > terbinafine > paroxetine ≈ duloxetine >>bupropion. CYP2D6*2 showed the next greatest inhibition, with Ki ratios compared to CYP2D6*1 ranging from 0.96 to 3.87. For each inhibitor tested, CYP2D6*10 and CYP2D6*17 were more resistant to inhibition than CYP2D6*1 or CYP2D6*2, with most Ki ratios in the 3–9 range. Three common CYP2D6 allelic variants showed different metabolic capacities toward tramadol and genotype‐dependent inhibition compared to CYP2D6*1. Further studies are warranted to understand the clinical consequences of inhibitor and CYP2D6 genotype‐dependent drug–drug interactions on tramadol bioactivation.

  PublisherOA PDFDOI

• Local ancestry-informed GWAS of warfarin dose requirement in African Americans identifies a CYP2C19 splicing QTL

  The American Journal of Human Genetics · 2025-09-29 · 1 citations

  article
  PublisherDOI

• Local ancestry informed GWAS of warfarin dose requirement in African Americans identifies a novel CYP2C19 splice QTL

  medRxiv · 2025-03-05

  preprintOpen access

  Abstract African Americans (AAs) are underrepresented in pharmacogenomics which has led to a significant gap in knowledge. AAs are admixed and can inherit specific loci from either their African or European ancestor, known as local ancestry (LA). A previous study in AAs identified single nucleotide polymorphisms (SNPs) located in the CYP2C cluster that are associated with warfarin dose. However, LA was not considered in this study. An IWPC cohort (N=340) was used to determine the LA-adjusted association with warfarin dose. Ancestry-specific GWAS’s were conducted with TRACTOR and ancestry tracts were meta-analyzed using METAL. We replicated top associations in the independent ACCOuNT cohort of AAs (N=309) and validated associations in a warfarin pharmacokinetic study in AAs. To elucidate functional roles of top associations, we performed short-read RNA-sequencing from AA hepatocytes carrying each genotype for expression of CYP2C9 and CYP2C19 . We identified 6 novel genome-wide significant SNPs (P<5E-8) in the CYP2C locus (lead SNP, rs7906871 (P=3.14E-8)). These associations were replicated (P≤2.76E-5) and validated with a pharmacokinetic association for S-Warfarin concentration in plasma (P=0.048). rs7906871 explains 6.0% of the variability in warfarin dose in AAs. Multivariate regression including rs7906871, previously associated SNPs, clinical and demographic factors explain 37% of dose variability, greater than previously reported studies in AAs. RNA-seq data in AA hepatocytes identified a significant alternate exon inclusion event between exons 6 and 7 in CYP2C19 for carriers of rs7906871. In conclusion, we have found and replicated a novel CYP2C variant associated with warfarin dose requirement and potential functional consequences to C YP2C19 .

  PublisherOA PDFDOI

• Scoping review of associations between cytochrome P450 3A4/5 single nucleotide polymorphisms and risk factors for fentanyl overdose

  Pharmacogenomics · 2025-08-13 · 1 citations

  review

  INTRODUCTION: Fentanyl overdose is a public health crisis in the United States, as fentanyl was implicated in nearly 70% of drug overdose deaths in 2023. To provide insight into genetic factors that may influence risk of fentanyl overdose, we conducted a scoping review of associations between cytochrome P450 3A4 (CYP3A4) and 3A5 (CYP3A5) genetic variants and relevant phenotypes. AREAS COVERED: . We considered a diverse range of phenotypes relevant to fentanyl overdose, including opioid overdose, fentanyl pharmacokinetics and pharmacodynamics, opioid use (disorder), and pharmacotherapy response. EXPERT OPINION AND COMMENTARY: variants (e.g. rs2242480). Future research should prioritize prospective genotyping of at-risk populations, development of models that integrate pharmacogenetics with psychiatric genetics, and large-scale harmonization of relevant datasets.

  PublisherDOI

• Evaluation of Potential Racial Disparities in CYP2C19‐Guided P2Y12 Inhibitor Prescribing After Percutaneous Coronary Intervention

  UNC Libraries · 2025-05-01

  articleOpen access

  Black patients suffer worse outcomes after percutaneous coronary intervention (PCI) than White patients. Inequities in antiplatelet prescribing may contribute to this health disparity. We compared P2Y₁₂ inhibitor prescribing by race following CYP2C19 genotyping to guide antiplatelet therapy selection after PCI. Patients from 9 sites that performed clinical CYP2C19 genotyping after PCI were included. Alternative therapy (e.g., prasugrel or ticagrelor) was recommended for CYP2C19 no-function allele carriers, in whom clopidogrel is predicted to be less effective. The primary outcome was choice of P2Y₁₂ inhibitor (clopidogrel vs. alternative therapy) based on genotype. Of 3,342 patients included, 2,448 (73%) were White, and 659 (20%) were Black. More Black than White patients had a no-function allele (34.3% vs. 29.7%, P = 0.024). At hospital discharge following PCI, 44.2% of Black and 44.0% of White no-function allele carriers were prescribed alternative therapy. At the time of the last follow-up within 12 months, numerically fewer Black (51.8%) than White (56.7%) no-function allele carriers were prescribed alternative therapy (P = 0.190). However, the difference was not significant after accounting for other factors associated with P2Y₁₂ inhibitor selection (odds ratio 0.79, 95% confidence interval 0.58-1.08). Alternative therapy use did not differ between Black (14.3%) and White (16.7%) patients without a no-function allele (P = 0.232). Among real-world patients who received CYP2C19 testing after PCI, P2Y₁₂ inhibitor prescribing rates did not differ between Black and White patients. Our data suggest an absence of racial disparity in genotype-guided antiplatelet prescribing among patients receiving CYP2C19 testing.

  PublisherDOI

• Understanding synthetic data: artificial datasets for real-world evidence

  BMJ evidence-based medicine · 2025-07-02 · 5 citations

  article
  PublisherDOI

• <i>CYP2D6</i> Phenotypes and Emergency Department Visits Among Patients Receiving Opioid Treatment

  JAMA Network Open · 2025-07-28 · 4 citations

  articleOpen accessSenior authorCorresponding

  Importance: Cytochrome P450 2D6 (CYP2D6) bioactivates hydrocodone, tramadol, codeine, and oxycodone to active metabolites that primarily provide analgesic activity. Reduced CYP2D6 activity may be associated with poor pain control. Objective: To evaluate associations of impaired CYP2D6 activity based on genotype or CYP2D6 inhibitors, alone and together, with analgesic activity of CYP2D6-metabolized opioids among patients with pain. Design, Setting, and Participants: This retrospective national, community-based cohort study used electronic health records and genetics data from the All of Us Research Program. Participants included adults prescribed at least 1 CYP2D6-metabolized opioid for more than 7 days between January 1, 2014, and December 31, 2022, with whole-genome sequencing data available. Analysis groups were defined by CYP2D6 phenotype, which was determined based on CYP2D6 genotype or CYP2D6 inhibitor-mediated phenoconversion. Statistical analysis was performed from July 1, 2023, to January 15, 2025. Exposures: CYP2D6-metabolized opioids, with or without concomitant CYP2D6 inhibitor exposure, based on prescription records and overlap with opioids. Main Outcomes and Measures: The primary outcome was occurrence of any pain-related emergency department (ED) visits during opioid treatment, up to 60 days after opioid initiation. The association between ED visits and CYP2D6 phenotype was assessed using inverse probability treatment weighting-adjusted logistic regression. Additional analyses were conducted by drug and isolating CYP2D6 genotype and inhibitors. Results: Among 31 669 patients (mean [SD] age, 51.2 [15.4] years; 66.5% women) prescribed CYP2D6-metabolized opioids, 15 960 had reduced CYP2D6 activity, and 15 709 had normal or high CYP2D6 activity based on genotype and inhibitors. A higher percentage of patients with reduced CYP2D6 activity (hereafter referred to as phenotypic intermediate metabolizers [pIMs] or phenotypic poor metabolizers [pPMs]) had experienced pain-related ED visits compared with patients with normal or high CYP2D6 activity (phenotypic normal metabolizers [pNMs] and phenotypic ultrarapid metabolizers [pUMs]) (2.1% vs 1.8%; inverse probability-weighted odds ratio, 1.19; 95% CI, 1.06-1.33). There were no significant differences in ED visits among CYP2D6 genotypic IMs or PMs vs NMs or UMs when testing all 4 drugs together. Among genotypic NMs, ED visits were more frequent among the individuals prescribed CYP2D6 inhibitors (inverse probability-weighted odds ratio, 1.49; 95% CI, 1.32-1.68). In analyses by medication, drug interactions were important for all 4 medications, while genotype associations were significant only for hydrocodone, tramadol, and codeine. Conclusions and Relevance: In this cohort study, reduced CYP2D6 activity was associated with increased ED visits among individuals treated with CYP2D6-metabolized opioids. This finding suggests that incorporating data on CYP2D6 genotype and accounting for drug interactions in opioid prescribing may improve pain management and reduce ED visits.

  PublisherOA PDFDOI

Recent grants

• Training Program for Applied Research and Development in Genomic Medicine

  NIH · $3.2M · 2018–2028

• NIH Grant M01RR000082

  NIH · $30.1M · 2011

• NIH Grant R01NS073346

  NIH · $2.0M · 2016

• NIH Grant R03HL065729

  NIH · $145k · 2003

• NIH Grant R01HL064691

  NIH · $723k · 2005

Frequent coauthors

• Braxton D. Mitchell

  1437 shared

• Alan R. Shuldiner

  Regeneron (United States)

  1425 shared

• Vincent Thijs

  University of Melbourne

  1363 shared

• Daniel Woo

  University of Cincinnati

  1352 shared

• Hakan Ay

  Biomedical Research Institute

  1340 shared

• Pankaj Sharma

  ARC Centre of Excellence in Future Low-Energy Electronics Technologies

  1340 shared

• Hugh S. Markus

  University of Cambridge

  1340 shared

• Martin Dichgans

  German Center for Neurodegenerative Diseases

  1333 shared