Paul Peppard
· Professor of Population Health SciencesVerifiedUniversity of Wisconsin-Madison · Community and Environmental Health Sciences
Active 1995–2025
About
Paul Peppard is a Professor of Population Health Sciences at the University of Wisconsin–Madison, having joined the faculty in 2008. He holds MS degrees in Preventive Medicine and Statistics, as well as a PhD in Epidemiology from UW-Madison. His research focuses on epidemiologic investigations into the causes and consequences of sleep disorders, with specific interests including the impact of the obesity epidemic on sleep apnea prevalence, behavioral and genetic predictors of sleep disorders, and the health outcomes associated with sleep disorders such as cognitive dysfunction, hypertension, and depression. Dr. Peppard is also Co-Director of the Survey of the Health of Wisconsin (SHOW), a statewide research study aimed at measuring a broad range of health conditions across Wisconsin. His academic contributions include teaching advanced epidemiology courses and modules on epidemiologic methods, measurement error, and Mendelian randomization. His work emphasizes health disparities, population health monitoring, and the broader understanding of sleep health within public health.
Research topics
- Medicine
- Gerontology
- Environmental health
- Internal medicine
- Computer Science
- Microbiology
- Biology
- Psychiatry
- Geography
- Psychology
- Social psychology
- Ophthalmology
- Data science
Selected publications
npj Aging · 2025-06-18 · 3 citations
articleOpen accessThis study investigated the role of food insecurity as an effect modifier between the gut microbiome, including groups of microbes (cliques), and risk of cognitive impairment (RCI). The analytical sample (n = 360) included adult participants of the Survey of the Health of Wisconsin with complete data on food insecurity, RCI, and 16S rRNA sequencing from stool samples. Microbial cliques associated with RCI were identified using an interpretable machine-learning-based algorithm. All analyses were stratified by food insecurity level, and adjusted for relevant confounders. We identified two cliques whose associations with RCI were modified by food insecurity status. The presence of the clique with either Eisenbergiella or Eubacterium was more strongly associated with RCI for the food-insecure group (β = 0.29, p < 0.0001). A clique representing the presence of Ruminococcus torques, Bacteroides, CAG-352F, and/or Eubacterium had a stronger association with RCI for the food-secure group (β = 0.1, p < 0.0001). Findings suggest food security be considered in RCI etiology.
Physical activity and mental health in patients with multimorbidity
Mental health and physical activity · 2025-01-27
articleMedicine & Science in Sports & Exercise · 2025-09-16
articleAlthough the FDA have not determined safe levels of caffeine for children and adolescents, the American Academy of Pediatrics strongly discourages caffeine consumption for young children and recommends that adolescents aged 12 - 17 should limit their caffeine intake (CAFF) to less than 100 mg per day. While studies have examined the association between CAFF and sedentary behavior in children and adolescents, the potential moderating effects of age and sex on this relationship have not yet been explored. PURPOSE: To determine the potential moderating effect of age and sex on the association between excessive CAFF and sedentary behavior. METHODS: Data on 1286 adolescents (ages 14 - 17 years, 50.3% female) from the National Health and Nutrition Examination Survey conducted between 2015 - 2018. Self-report sedentary behavior was determined by time spent watching TV and computer use (≥2 (excessive) vs. <2 hours/day). CAFF was assessed using 2-day dietary recall and categorized as number of days with >100 mg (0, 1, or 2 days). Logistic regression for complex survey data was used to analyze the data. The fully conditional specification method was used to handle missing data. RESULTS: 48% and 36% reported CAFF exceeding 100 mg/day on one or two days, respectively. Overall, 44% and 47% reported spending 2+ hours watching TV and computer use, respectively. CAFF was not associated with excessive TV watching and age and sex were not significant moderators. However, age (p < .0001) and sex (p = .0105) were found to be significant moderators of the association between excessive CAFF and excessive computer use. This association was observed to be strongest for males and for those 16 years old (see Figure). CONCLUSION: Age and sex moderates the association between excessive CAFF and excessive computer time, suggesting that tailored interventions to reduce sedentary behavior may require simultaneous efforts to address excessive CAFF with careful consideration of the adolescent’s age and sex.
Projecting the 30-year burden of obstructive sleep apnoea in the USA: a prospective modelling study
The Lancet Respiratory Medicine · 2025-08-26 · 14 citations
article0214 Association Between Sleep Inertia and Cognitive Performance in the Wisconsin Sleep Cohort Study
SLEEP · 2025-05-01
articleOpen accessAbstract Introduction Sleep inertia is a transitional state between wake and sleep, resulting in disorientation or grogginess upon waking. Frequent symptoms of sleep inertia are reduced alertness and impaired performance. Although sleep inertia is common, its relationship with objective neurocognitive assessment is understudied and unclear. Thus, this investigation examined the association between subjective, typical sleep inertia severity and a standardized afternoon-assessed objective cognitive testing battery in a population sample of middle-aged and older adults. Methods Wisconsin Sleep Cohort participants (N = 462; average age = 74 ± 6.7 years) completed the validated Sleep Inertia Questionnaire (SIQ) and six cognitive tasks: Grooved Pegboard (PEGSUM), Symbol Digits Modalities Test (SDMT), Auditory Verbal Learning Test (AVLT), Oral Word Frequency (OWFRAW), Digit Cancellation Test (Digitcan), and Trail Making Test Part B (TMT-B). All tests were administered and coded by a trained technician following standardized protocols. Associations between total and subscale (physiological, responses to sleep inertia, emotional, and cognitive) SIQ scores with performance on the cognitive tasks (outcome) were assessed using linear regression modeling. All models were adjusted for age, sex, body mass index, education, caffeine use, apnea-hypopnea index, smoking, alcohol, and circadian preference (morning/evening). Results Mean SIQ score was 10.74 (SD: 9.54, range: 0 - 63). With every 1 unit increase in the SIQ score, there was an average 1.52-second increase in the time to complete PEGSUM (p &lt; 0.0001), a reduction in the average number of matches on SDMT by 0.11 (p = 0.011), and an increase of an average of 1.08 seconds to complete TMT-B (p &lt; 0.0001). SIQ subscale analysis demonstrated that performance on these tasks was associated with physiological, emotional, and cognitive SIQ subscale scores, but not responses to sleep inertia subscale score. Sensitivity analysis considering apolipoprotein E4 status (N = 391) did not substantially alter results. Conclusion These findings suggest sleep inertia may be an important consideration when objectively assessing neurocognitive performance. Future research that examines neurocognitive function among patients with excessive sleep inertia, and probes cause-effect relationships between sleep inertia and cognitive performance are indicated. Support (if any) US National Institutes of Health, National Institute on Aging grants R01AG079352 and R01AG058680.
SLEEP · 2025-05-01
articleOpen accessSenior authorAbstract Introduction Approximately 72% of high school students do not get enough sleep (8-10 hours) on school nights. Insufficient sleep is associated with obesity, diabetes, injuries, poor mental health, and problems with attention and behavior among adolescents. The reasons for sleep loss differs by sex. Screen time and daily caffeine intake has been found to be associated with sleep disturbance and daytime sleepiness. The American Academy of Pediatrics recommends that adolescents aged 12 – 17 should limit their caffeine intake to less than 100mg per day. However, the relationship between caffeine and sleep duration may be moderated by sex and excessive computer screen time. Methods Data on 640 adolescents (ages 16–17 years, 53% female) from the National Health and Nutrition Examination Survey conducted between 2015–2018. Screen time was determined by self-reported computer use during leisure time (≥2 (excessive) vs. &lt; 2 hours/day). Excessive caffeine intake was assessed using 2-day dietary recall and categorized as number of days (0, 1, or 2 days) with &gt;100mg. Self-reported sleep duration ranged 3 to 14 hours per school night. Linear regression for complex survey data was used to analyze the data. The fully conditional specification method was used to handle missing data. Results While excessive caffeine was positively associated with sleep duration, the strength of the relationship varied by sex (p=0.018) and excessive computer use (p=0.020), respectively. Specifically, females who consumed excessive caffeine for 1 or 2 days reported 0.57 hours (SE=0.24), and 0.59 hours (SE=0.25) longer average sleep duration, respectively. Furthermore, among adolescents with excessive computer/screen time, those who consumed excessive caffeine for 1 day and 2 days reported 0.51 (SE=0.19) and 0.86 hours (SE=0.25) longer sleep duration, respectively. No difference in the caffeine-sleep duration association was found amongst males and those reporting &lt; 2 hours of screen time. The longer sleep duration was due mainly to later wake-up time as bedtime were similar. Conclusion Sex and excessive screen time moderates the association between excessive caffeine intake and sleep duration. Longer self-reported sleep duration may not indicate restful sleep as caffeine has been shown to disrupt sleep and affect circadian rhythm. Support (if any) none.
SLEEP · 2025-05-01
articleOpen accessSenior authorAbstract Introduction Literature suggests associations of both sleep inertia and hypersomnia with cognitive function and social environment with cognition function. However, the social environment has not been investigated as a potential moderator of the association of sleep with cognition. We examined both sleep parameters as predictors of poorer cognitive function, with social environment variables as potential moderators, in the Wisconsin Sleep Cohort study. Methods Survey data was collected from the ongoing Wisconsin Sleep Cohort (n=505, 45% female, mean [SD] age 74 [6.7] years). The sleep measures were the Hypersomnia Severity Index (HSI) and the Sleep Inertia Questionnaire (SIQ). Cognition measures were assessed in a 30-45 minute battery of tests that included symbol digit modalities, trail making, a pegboard task, digit cancellation, the audio verbal learning test (AVLT), and oral word fluency. Separate multiple linear models were used for each cognitive measure. Measures of the social environment included support and strain scores for participants’ relationships with both friends and family. Both type and quality of relationships were evaluated to explore variations in moderating effects. Social environment questions came from the Midlife in the United States (MIDUS) study. Models were adjusted for age, race, sex, self-reported health status, and education and were fit using PROC GLMSELECT in SAS. Results Support in relationships with friends significantly (p=0.007) interacted with SIQ such that higher levels of friend support was associated with a mitigation of the reduction in pegboard task performance associated with greater sleep inertia. Borderline significance was found for family support and family strain as potential moderators of associations between SIQ and cognition. All other interactions between relationship factors, hypersomnia, and SIQ predicting cognitive function were not statistically significant. Conclusion Some social environment measures were associated with moderation of the relationship of SIQ and cognition. Subsequent research could explore potential underlying mechanisms and what specific aspects of these social environment scores are salient. Support (if any) This work was supported by the National Institute on Aging (R01AG058680) at the US National Institutes of Health.
Frontiers in Cellular and Infection Microbiology · 2024-06-13 · 2 citations
erratumOpen access[This corrects the article DOI: 10.3389/fcimb.2023.1165295.].
Alzheimer s & Dementia · 2024-12-01
articleOpen accessAbstract Background Obstructive sleep apnea (OSA) is associated with hypoxia‐induced neuronal impairment and dysfunction—key risk factors for the pathogeneses of age‐related neurodegenerative diseases such as Alzheimer‘s disease (AD). This study examined longitudinal associations between OSA severity and CSF biomarkers associated with AD, synaptic dysfunction, and neuroinflammation in a sample of late‐middle‐aged adults with increased risk for AD. Method N=25 cognitively unimpaired adults (64% female, mean age 65.8 ± 7.1 years, 42.3% APOE‐ε4 carriers) from the Wisconsin Alzheimer‘s Disease Research Center (ADRC) participated in overnight polysomnography, where the number of apneas, hypopneas, and respiratory effort related arousals (RERAs) per hour of sleep were recorded. OSA severity was estimated using the base 10 logarithm of the Respiratory Disturbance Index, or log 10 (RDI+1). Following sleep assessment, CSF samples were acquired via lumbar puncture over two subsequent study visits (mean 5.8 years between visits) and analyzed using the NeuroToolKit (NTK), a panel of robust prototype assays (Roche Diagnostics International Ltd), with measures including core AD biomakers—amyloid beta (Aβ) 42 , Aβ 42 :Aβ 40 , pTau 181 , pTau 181 :Aβ 42 , and tTau—as well as neurogranin, neurofilament light (NfL), α‐synuclein, glial fibrillary acidic protein (GFAP), chitinase‐3‐like protein 1 (YKL‐40), soluble triggering receptor expressed on myeloid cells 2 (sTREM2), neuronal pentraxin II (NPTX2), and synaptosome associated protein 25 (SNAP25). Linear mixed effects models (with random intercept and random slope) were assembled to test longitudinal associations, adjusting for age, sex, and APOE‐ε4 carriage. Result AD biomarker models indicated that RDI was associated with increased CSF levels of tTau (β=0.084, SE=0.013, p=0.014) and pTau 181 (β=0.022, SE=0.003, p=0.023), but neither outcome remained robust after Bonferroni correction for multiple comparisons (adjusted α=0.0039). In contrast, models of synaptic dysfunction and neuroinflammation surpassed Bonferroni correction, showing a significant association between RDI and levels of α‐synuclein (β=0.09, SE=0.013, p=0.002) and neurogranin (β=0.13, SE=0.03, p=0.002). Conclusion This work provides new evidence for the deleterious influence of OSA on biomarkers of synaptic dysfunction, neuroinflammation, and AD in a sample of late‐middle age to older adults enriched with risk for AD.
Research Square · 2024-11-25 · 1 citations
preprintOpen access
Recent grants
NIH · $2.5M · 2017
NIH · $15.0M · 2016
Frequent coauthors
- 100 shared
Erika W. Hagen
University of Wisconsin–Madison
- 92 shared
Terry Young
- 67 shared
Jodi H. Barnet
University of Wisconsin–Madison
- 61 shared
Kristen Malecki
Society of Environmental Toxicology and Chemistry
- 56 shared
Laurel Finn
University of Wisconsin–Madison
- 35 shared
Emmanuel Mignot
University of Copenhagen
- 26 shared
Poul Jennum
Rigshospitalet
- 26 shared
Laurel A. Ravelo
University of Wisconsin–Madison
Education
- 2000
Ph.D., Population Health Sciences
University of Wisconsin-Madison
- 1996
M.S., Population Health Sciences
University of Wisconsin-Madison
- 1993
B.A., Public Health
University of California, Berkeley
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