Susan Malone

Faculty

Susan Malone headshot

Susan Kohl Malone

PhD RN

Assistant Professor

1 212 992 7047

433 First Ave
New York, NY 10010
United States

Accepting PhD students

Susan Kohl Malone, PhD, RN, is an Assistant Professor at NYU Rory Meyers College of Nursing. Her research focuses on understanding how sleep patterns and circadian rhythms impact metabolic health, with particular emphasis on preventing type 2 diabetes through personalized sleep interventions. She investigates how improving sleep health can reverse metabolic syndrome in diverse populations and addresses critical health disparities in sleep and cardiometabolic outcomes. Prof. Malone also teaches courses on lifestyle approaches to wellness and mentors doctoral students in sleep health research.

Malone has led multiple NIH-funded research projects, and is currently investigating metabolically-relevant hormonal rhythms in adults with prediabetes and short sleep duration, as well as multimodal dynamic biosensing for quantifying long COVID symptom progression. Her work combines nursing science, behavioral science, and circadian biology to develop evidence-based interventions that improve health outcomes across the lifespan.

Prior to joining the faculty at NYU Meyers, Malone served as a Senior Research Scientist at the college and completed postdoctoral training at the University of Pennsylvania's Center for Sleep and Circadian Neurobiology. She brings extensive clinical experience as a certified school nurse and diabetes educator, having worked in various healthcare settings including diabetes treatment centers and school health programs. This clinical background informs her translational research approach to making sleep science accessible and applicable to real-world health challenges.

Among her many honors, Malone had the unique honor of having the annual Susan Kohl Award established in her name at Georgetown University.

She completed postdoctoral training as a Senior Research Scientist at New York University Rory Meyers College of Nursing and as a Postdoctoral Fellow at the University of Pennsylvania Perelman School of Medicine's Center for Sleep and Circadian Neurobiology, where she developed expertise in sleep and circadian health research. Her doctoral dissertation examined whether chronotype modifies the relationship between sleep duration and body mass index in adolescents, establishing her foundation in sleep health across the lifespan.

PhD in Nursing, University of Pennsylvania School of Nursing
MSN in Nursing, University of Pennsylvania School of Nursing
BSN in Nursing, Georgetown University School of Nursing

Cardiometabolic Health
Circadian Rhythms
Diabetes Prevention
Health Disparities
School Health
Sleep Research

American Academy of Nursing
Eastern Nursing Research Society
International Association of Circadian Health Clinics
Sigma Theta Tau Nursing Honor Society
Sleep Research Society
Society for Research in Biological Rhythms
Society of Behavioral Medicine

Marion R. Gregory Award for distinguished completed doctoral dissertation, University of Pennsylvania School of Nursing (2015)
Heilbrunn Nurse Scholar Award, Rockefeller University (2014)
Research Poster Winner, National Association of School Nurses Annual Conference (2013)
Leadership Identification Scholarship, University of Pennsylvania School of Nursing (1985)
Susan Kohl Award, Georgetown University (1985)
Sigma Theta Tau, Nursing Honor Society (1984)

Association between Time-of-Day for Eating, Exercise, and Sleep with Blood Pressure in Adults with Elevated Blood Pressure or Hypertension: A Systematic Review 

Keiser, T., Katz, S., Robson, S., Greaney, J., Malone, S. K., Farrahi, V., & Patterson, F. (2024).
Abstract
Abstract
~

Feasibility, Acceptability, and Preliminary Effectiveness of a Sleep Intervention in Adults at Risk for Metabolic Syndrome With Short Sleep Duration

Malone, S. K., Patterson, F., Grunin, L., Yu, G., Dickson, V. V., & Melkus, G. D. (2024). (Vols. 73, Issue 1, pp. 72-80). 10.1097/NNR.0000000000000693
Abstract
Abstract
Background: The prevalence of short sleep duration is rising and is linked to chronic comorbidities, such as metabolic syndrome (MetS). Sleep extension interventions in adults with MetS comorbidities and short sleep duration are limited and vary widely in terms of approach and duration. Objectives: This pilot study aimed to test the feasibility and acceptability of a personalized 12-week systematic sleep time extension intervention on post-intervention sleep outcomes in middle-aged adults at risk forMetSwith actigraphy-estimated short sleep duration. Methods: A single-arm, 12-week, 12-session systematic sleep time extension intervention was delivered weekly via videoconferencing. Feasibility and acceptability were assessed using retention rates and mean sleep diary completions. Sleep was estimated for 14 consecutive days prior to and immediately following the 12-week intervention using wrist actigraphy. Daytime sleepiness was assessed using the Epworth Sleepiness Scale. Paired sample t-tests modeled changes in study outcomes. Results: Study participants (N = 41) had a mean age of 52 years and were mostly female and White; 86% attended >80% of sessions, and mean sleep diary completion was 6.7 diaries/week. Significant improvements in sleep from pre- to post-intervention included increased total sleep time, earlier sleep onsets, more regular sleep onsets, a higher sleep regularity index, and reduced daytime sleepiness. Extending sleep, as well as improving sleep timing and regularity in middle-aged adults with actigraphy-estimated short sleep duration and at risk for MetS, is feasible and acceptable. Discussion: Behavioral sleep characteristics may be modifiable and present a novel behavioral paradigm for mitigating MetS risk. This pilot study provides a proof of concept for the feasibility, acceptability, and preliminary effectiveness of a systematic sleep time extension for middle-aged adults at risk for MetS with actigraphy-estimated short sleep duration.

Racial Differences in Treatment Response to a Sleep Extension Intervention

Malone, S. K., Patterson, F., Grunin, L., Goyal, C., Hu, J., Perez, N. B., Kaitlyn, M., Victoria, D., & Gail, M. D. (2024).
Abstract
Abstract
~

Associations of social isolation and loneliness with the onset of insomnia symptoms among middle-aged and older adults in the United States : A population-based cohort study

Qi, X., Malone, S. K., Pei, Y., Zhu, Z., & Wu, B. (2023). (Vols. 325). 10.1016/j.psychres.2023.115266
Abstract
Abstract
There is an inconsistent conclusion regarding the relationship of social isolation and loneliness with poor sleep. We investigated the associations of social isolation and loneliness with new-onset insomnia symptoms in a nationally-representative sample of 9,430 adults aged ≥50 who were free of any insomnia symptoms/sleep disorders at baseline (wave 12/13) and followed up to 4 years from the Health and Retirement Study. Social isolation was measured by Steptoe's Social Isolation Index. Loneliness was measured by the revised 3-item UCLA-Loneliness Scale. Insomnia symptoms were quantified using the modified Jenkins Sleep Questionnaire. During a mean follow-up of 3.52 years, 1,522 (16.1%) participants developed at least one insomnia symptom. Cox models showed that loneliness was associated with the onset of difficulties initiating or maintaining sleep, early-morning awakening, nonrestorative sleep, and at least one of these symptoms after adjusting for potential covariates; while social isolation was not associated with the onset of difficulties maintaining sleep, early-morning awakening, or at least one insomnia symptom after adjusting for health indicators. These results are consistent in sensitivity analyses and stratified analyses by age, sex, race/ethnicity, and obesity. Public health interventions aimed at fostering close emotional relationships may reduce the burden of poor sleep among middle-aged and older adults.

Associations of Social Isolation and Loneliness with the Onset of Insomnia Symptoms among Middle-Aged and Older Adults in the United States: A Population-Based Cohort Study

Qi, X., Malone, S. K., Pei, Y., & Wu, B. (2023). (Vols. 325).
Abstract
Abstract
~

Automated Insulin Delivery for Hypoglycemia Avoidance and Glucose Counterregulation in Long-Standing Type 1 Diabetes with Hypoglycemia Unawareness

Flatt, A. J., Peleckis, A. J., Dalton-Bakes, C., Nguyen, H. L., Ilany, S., Matus, A., Malone, S. K., Goel, N., Jang, S., Weimer, J., Lee, I., & Rickels, M. R. (2023). (Vols. 25, Issues 5, pp. 302-314). 10.1089/dia.2022.0506
Abstract
Abstract
Objective: Automated insulin delivery (AID) may benefit individuals with long-standing type 1 diabetes where frequent exposure to hypoglycemia impairs counterregulatory responses. This study assessed the effect of 18 months AID on hypoglycemia avoidance and glucose counterregulatory responses to insulin-induced hypoglycemia in long-standing type 1 diabetes complicated by impaired awareness of hypoglycemia. Methods: Ten participants mean ± standard deviation age 49 ± 16 and diabetes duration 34 ± 16 years were initiated on AID. Continuous glucose monitoring was paired with actigraphy to assess awake- and sleep-associated hypoglycemia exposure every 3 months. Hyperinsulinemic hypoglycemic clamp experiments were performed at baseline, 6, and 18 months postintervention. Hypoglycemia exposure was reduced by 3 months, especially during sleep, with effects sustained through 18 months (P ≤ 0.001) together with reduced glucose variability (P < 0.01). Results: Hypoglycemia awareness and severity scores improved (P < 0.01) with severe hypoglycemia events reduced from median (interquartile range) 3 (3-10) at baseline to 0 (0-1) events/person·year postintervention (P = 0.005). During the hypoglycemic clamp experiments, no change was seen in the endogenous glucose production (EGP) response, however, peripheral glucose utilization during hypoglycemia was reduced following intervention [pre: 4.6 ± 0.4, 6 months: 3.8 ± 0.5, 18 months: 3.4 ± 0.3 mg/(kg·min), P < 0.05]. There were increases over time in pancreatic polypeptide (Pre:62 ± 29, 6 months:127 ± 44, 18 months:176 ± 58 pmol/L, P < 0.01), epinephrine (Pre: 199 ± 53, 6 months: 332 ± 91, 18 months: 386 ± 95 pg/mL, P = 0.001), and autonomic symptom (Pre: 6 ± 2, 6 months: 6 ± 2, 18 months: 10 ± 2, P < 0.05) responses. Conclusions: AID led to a sustained reduction of hypoglycemia exposure. EGP in response to insulin-induced hypoglycemia remained defective, however, partial recovery of glucose counterregulation was evidenced by a reduction in peripheral glucose utilization likely mediated by increased epinephrine secretion and, together with improved autonomic symptoms, may contribute to the observed clinical reduction in hypoglycemia.

Automated insulin delivery for hypoglycemia avoidance and glucose counterregulation in long-standing type 1 diabetes with hypoglycemia unawareness

Flatt, A., Peleckis, A., Dalton-Bakes, C., Nguyen, H., Ilany, S., Matus, A., Malone, S. K., Goel, N., Jang, S., Weimer, J., Lee, I., & Rickels, M. (2023).
Abstract
Abstract
~

Prolonged Use of an Automated Insulin Delivery System Improves Sleep in Long-Standing Type 1 Diabetes Complicated by Impaired Awareness of Hypoglycemia

Malone, S. K., Matus, A. M., Flatt, A. J., Peleckis, A. J., Grunin, L., Yu, G., Jang, S., Weimer, J., Lee, I., Rickels, M. R., & Goel, N. (2023). 10.1177/19322968231182406
Abstract
Abstract
Background: This study assessed changes in actigraphy-estimated sleep and glycemic outcomes after initiating automated insulin delivery (AID). Methods: Ten adults with long-standing type 1 diabetes and impaired awareness of hypoglycemia (IAH) participated in an 18-month clinical trial assessing an AID intervention on hypoglycemia and counter-regulatory mechanisms. Data from eight participants (median age = 58 years) with concurrent wrist actigraph and continuous glucose monitoring (CGM) data were used in the present analyses. Actigraphs and CGM measured sleep and glycemic control at baseline (one week) and months 3, 6, 9, 12, 15, and 18 (three weeks) following AID initiation. HypoCount software integrated actigraphy with CGM data to separate wake and sleep-associated glycemic measures. Paired sample t-tests and Cohen’s d effect sizes modeled changes and their magnitude in sleep, glycemic control, IAH (Clarke score), hypoglycemia severity (HYPO score), hypoglycemia exposure (CGM), and glycemic variability (lability index [LI]; CGM coefficient-of-variation [CV]) from baseline to 18 months. Results: Sleep improved from baseline to 18 months (shorter sleep latency [P

Sleep Variability, Eating Timing Variability, and Carotid Intima-Media Thickness in Early Adulthood

Hoopes, E. K., Witman, M. A., D'Agata, M. N., Brewer, B., Edwards, D. G., Robson, S. M., Malone, S. K., Keiser, T., & Patterson, F. (2023). (Vols. 12, Issues 19, p. e029662). 10.1161/JAHA.123.029662
Abstract
Abstract
Background Day-to-day variability in sleep patterns and eating timing may disrupt circadian rhythms and has been linked with various adverse cardiometabolic outcomes. However, the extent to which variability in sleep patterns and eating timing relate to atherosclerotic development in subclinical stages remains unclear. Methods and Results Generally healthy adults (N=62, 29.3±7.3 years, 66% female) completed 14 days of sleep and dietary assessments via wrist accelerometry and photo-assisted diet records, respectively. Variability in sleep duration, sleep onset, eating onset (time of first caloric consumption), eating offset (time of last caloric consumption), and caloric midpoint (time at which 50% of total daily calories are consumed) were operationalized as the SD across 14 days for each variable. Separate regression models evaluated the cross-sectional associations between sleep and eating variability metrics with end-diastolic carotid intima-media thickness (CIMT) measured via ultrasonography. Models adjusted for age, sex, systolic blood pressure, sleep duration, and total energy intake. Each 60-minute increase in sleep duration SD and sleep onset SD were associated with a 0.049±0.016 mm (P=0.003) and 0.048±0.017 mm (P=0.007) greater CIMT, respectively. Variability in eating onset and offset were not associated with CIMT; however, each 60-minute increase in caloric midpoint SD was associated with a 0.033±0.015 mm greater CIMT (P=0.029). Exploratory post hoc analyses suggested that sleep duration SD and sleep onset SD were stronger correlates of CIMT than caloric midpoint SD. Conclusions Variability in sleep patterns and eating timing are positively associated with clinically relevant increases in CIMT, a biomarker of subclinical atherosclerosis, in early adulthood.

Sleep Variability, Eating Timing Variability, and Carotid Intima-Media Thickness in Early Adulthood

Malone, S. K., Wittman, M. A., D’Agata, M. N., Edwards, D. G., Robson, S. M., Malone, S. K., Keiser, T., & Patterson, F. (2023).
Abstract
Abstract
~