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Breastfeeding is internationally recognized as the recommended standard for infant nutrition, informed by evidence of its multiple benefits for both mother and baby. In the context of common metabolic conditions such as polycystic ovary syndrome, diabetes (type 1, type 2, and gestational), and obesity, breastfeeding may be particularly beneficial for both mother and infant. However, there is evidence of delayed lactogenesis and reduced breastfeeding rates and duration in women with these conditions, and the effects of altered maternal metabolic environments on breastmilk composition (and potentially infant outcomes) are incompletely understood. In this review, we explore the relationships between maternal metabolic conditions, lactogenesis, breastfeeding, and breastmilk composition. We examine relevant potential mechanisms, including the central role of insulin both in lactogenesis and as a milk-borne hormone. We also describe the bioactive and hormonal components of breastmilk and how these may link maternal and infant health.

Gestational diabetes mellitus (GDM) is the fastest growing type of diabetes, affecting between 2 to 38% of pregnancies worldwide, varying considerably depending on diagnostic criteria used and sample population studied. Adverse obstetric outcomes include an increased risk of macrosomia, and higher rates of stillbirth, instrumental delivery, and birth trauma. Metabolomics, which is a platform used to analyse and characterise a large number of metabolites, is increasingly used to explore the pathophysiology of cardiometabolic conditions such as GDM. This review aims to summarise metabolomics studies in GDM (from inception to January 2021) in order to highlight prospective biomarkers for diagnosis, and to better understand the dysfunctional metabolic pathways underlying the condition. We found that the most commonly deranged pathways in GDM include amino acids (glutathione, alanine, valine, and serine), carbohydrates (2-hydroxybutyrate and 1,5-anhydroglucitol), and lipids (phosphatidylcholines and lysophosphatidylcholines). We also highlight the possibility of using certain metabolites as predictive markers for developing GDM, with the use of highly stratified modelling techniques. Limitations for metabolomic research are evaluated, and future directions for the field are suggested to aid in the integration of these findings into clinical practice.

Ectopic prolactin production from a malignancy is infrequently reported. We report here a 60-year-old gentleman who presented with hyperprolactinaemia (9100 mIU/L) causing expressible galactorrhoea, decreased libido and fatigue thought to be due to ectopic prolactin secretion from a metastatic melanoma. Upon initiation of pembrolizumab, the patient's symptoms resolved and he became normoprolactinaemic. This corresponded with a partial response on radiological imaging. Although the core biopsy of the metastatic melanoma did not exhibit immunostaining for prolactin, we believe that only a subset of the tumour cells possesses prolactin-secreting capacity. This case illustrates the need to consider ectopic prolactin production for a solid malignant tumour as a rare cause of hyperprolactinaemia in patients with a normal pituitary MRI, in the absence of other causes.

Adults with hypophosphatasia (HPP) may suffer femoral fractures resembling the atypical femoral fractures that can occur with long‐term bisphosphonate treatment, and there is an emerging consensus that bisphosphonates should not be used in adults with HPP and low bone mass. However, the spectrum of HPP in adults is wide: ranging from the severely affected—who commonly have osteomalacia—through to the minimally affected. The former typically have biallelic and the latter, heterozygous ALPL mutations. We have reviewed reports of fractures in adults with genetically proven HPP which suggest that the risk of fracture is at least 200‐fold greater in those with biallelic mutations. We also discuss two cases of postmenopausal women with heterozygous ALPL mutations. One had fractures and severe osteoporosis, but histology revealed no evidence of osteomalacia. The second had taken alendronate for 8 years, but despite profound suppression of bone turnover, histology again revealed no evidence of osteomalacia. The management of adults with HPP who have coexisting osteoporosis is challenging. More data are clearly needed, but we suggest that the risks of bisphosphonate therapy may be relatively low in patients who have heterozygous mutations and no histological evidence of osteomalacia. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.