Impact of Maternal Hypertension on Human Milk Mitochondrial DNA and Oxidative Stress

Background: Human milk, the optimal nutritional source for infants, contains several cell types capable of crossing the infant's gastrointestinal tract and integrating into developing organ systems. Mitochondria within these cells, key regulators of energy production and oxidative stress, may play an important role in infant development and susceptibility to chronic disease. Although maternal health is known to influence human milk content, its impact on human milk mitochondrial function has not been investigated. The aim of this study is to evaluate the influence of maternal health on mitochondrial homeostasis in the human milk of hypertensive (Hyp) and non-hypertensive (non-Hyp) mothers. Methods: Human milk samples (n= 40 from 20 mothers) collected longitudinally at 2, 6 and 12 weeks postpartum from overweight and obese Hyp and non-Hyp mothers (BMI: 32 ± 5.5 kg/m 2 ; age: 33 ± 5.1 years) from an existing dataset (R01HD098186) were used in this study. Levels of 8-isoprostane (oxidative stress marker), total protein, mitochondrial DNA (mtDNA) integrity, and mtDNA copy number (mtDNA-CN) were quantified using ELISA and real-time PCR. Differences between groups and longitudinal changes were assessed. Human milk biochemical parameters were associated with maternal age, BMI, and gestational weight gain. Results: Human milk mtDNA-CN was approximately 60% lower, while reactive 8-isoprostane levels were 30% higher in Hyp compared with non-Hyp mothers (p = 0.044 and p = 0.049, respectively). No group differences were observed in total protein or mtDNA integrity. Within subjects, human milk collected at 6 weeks postpartum showed higher mtDNA-CN compared with samples collected at 2 weeks (p = 0.033). No associations were found between variables. Conclusion: These innovative findings suggest that maternal cardiovascular health status affects mitochondrial function, leading to an increase in oxidative stress in human milk. Understanding these relationships may open new avenues for early-life interventions aimed at improving long-term infant health. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.