Abstract
Animal models show a more rapid mammary gland response and more milk with subsequent lactations, as well as impairment of lactation performance by obesity. Whilst maternal obesity is linked to reduced breastfeeding initiation, breastfeeding confidence, and duration as well as early introduction of formula, maternal adiposity, breast anatomy and milk production (MP) have not been assessed in this population. Thirty-four lactating mothers 1–6 months postpartum and with BMI range of 17–35 kg/m2 participated in this study. We conducted ultrasound examination imaging to assess breast anatomy. The amount of glandular tissue (glandular tissue representation (GTR)) was classified as low, moderate, or high. Number and diameters of milk ducts as well as mammary blood flow (the resistive index) were measured. Maternal bra cup volume was calculated from current bra size. Maternal body composition was measured with bioimpedance spectroscopy. Mothers completed a questionnaire regarding their medical, obstetric and lactation history, and conducted a 24 h MP study to enable calculation of total volume, average and maximum feed volumes and breast storage capacity (24 h MP parameters). For statistical analysis, we used the correlation networks method (directions of multiple significant correlations are reported). Correlation networks show that pathways culminating in either high or low MP start as early as puberty. In this study, later menarche correlates with the absence of breast growth during both puberty and pregnancy, which further correlate with lower numbers of ducts and smaller diameters. Higher maternal adiposity correlates with larger bra cup volume (both correlate with absence of breast growth during pregnancy and low GTR) and lower 24 h MP parameters. Larger numbers of ducts and duct diameters correlate with higher parity and longer durations of previous lactations, and higher 24 h MP parameters. Mammary blood flow shows no correlations. Findings from this cross-sectional study corroborate animal studies showing that a number of modifiable and non-modifiable maternal factors may impact breast development and MP. Further research may inform interventions, such as maintaining healthy adiposity not only during pre-conception, pregnancy, and lactation, but as early as childhood and potentially infancy. Moreover, the results provide rationale for antenatal lactation assessment of women and intervention in high-risk mothers to ensure they reach their full lactation potential.
Author Contributions
Conceptualization, Z.G. and D.T.G.; methodology, D.T.G., C.T.L., A.R., D.W. and Z.G.; data collection, D.T.G. and Z.G.; formal analysis, Z.G., A.R. and D.W.; investigation, D.T.G. and Z.G.; resources, D.T.G.; data curation, D.T.G., J.L.M. and Z.G.; writing—original draft preparation, Z.G.; writing—review and editing, A.R., D.W., J.L.M., C.T.L., S.L.P. and D.T.G.; visualization, Z.G.; supervision, D.T.G.; project administration, J.L.M.; funding acquisition, D.T.G. All authors have read and agreed to the published version of the manuscript.
Funding
This research was funded by unrestricted research grant from Medela AG (Switzerland). The funder had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
Institutional Review Board Statement
The study was conducted in accordance with the Declaration of Helsinki. The study was approved by the Human Research Ethics Committee at The University of Western Australia (RA/4/20/6407) and conducted in accordance with the relevant guidelines and regulations.
Informed Consent Statement
Informed consent was obtained from all subjects involved in the study.
Data Availability Statement
Restrictions apply to the availability of some or all data generated or analyzed during this study. The corresponding author will on request detail the restrictions and any conditions under which access to some data may be provided.
Acknowledgments
We thank all our participants and their families for their time and help with this research.
Conflicts of Interest
D.T.G. declares participation in the Scientific Advisory Board of Medela AG. Z.G., J.L.M., C.T.L., S.L.P. and D.T.G. are/were supported by an unrestricted research grant from Medela AG, administered by The University of Western Australia. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results. All other authors declare no conflict of interest.
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