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Background Organization of the sleep states and a normal sleep pattern in the neonatal period and early infancy is essential for brain development and plasticity. The establishment of a consolidated circadian sleep-wake cycle occurs between 1 and 4 months of life in term infants. This period may be even longer for preterm infants who are exposed to relentless interventions in neonatal intensive care units. The sleep should be respected and protected. Objective and methods Human milk (HM) contains bioactive sleep-promoting components, and recent evidence shows that some of these components show circadian oscillations. This article reviews the existing evidence regarding the role of these HM components on sleep. This topic is prefaced with a brief information about the basic concepts concerning sleep. Consecutively, chronobiotic and chrononutrition concepts are introduced. Results Melatonin, tryptophan, nucleosides/nucleotides, and vitamin B12 are components of HM that have sleep-promoting characteristics. The sleep-inducing effects of these components are well-established in animal and adult human studies. Interestingly, melatonin, tryptophan, and 5′-adenosine monophosphate and 5′-guanosine monophosphate nucleotides in HM have been shown to exhibit also circadian oscillations. Although 5′-uridine monophosphate does not have a circadian rhythm, its levels increase during the night. Conclusion HM has a potential to function as a “synchronizer,” helping the infant to consolidate a circadian sleep-wake cycle, thanks to its several bioactive components with chronobiotic characteristics. Research is warranted to address gaps in this field, such as the association between the circadian oscillations of the sleep-promoting factors in HM and the quantity/quality of infant sleep.

Preterm infants fed fortified human milk (HM) in standard (STD) fashion grow slower than preterm formula fed infants. Recently, low protein intake has been proven to be the primary limiting factor responsible for this growth failure. The main reason of protein undernutrition despite fortification is that STD fortification is based on the customary assumptions about the composition of HM. However, the protein concentration of preterm HM is variable and decreases with the duration of lactation. Also, the protein concentration of banked donor milk, which is most often provided by mothers of term infants, is likely to be lower. Hence, most of the HM fed to preterm infants during the fortification period is likely to have an inadequately low protein concentration. This hypothesis has been confirmed very recently by comparing the assumed and actual protein intakes in preterm infants fed fortified HM. Novel fortification models have been devised to deal with the problem of ongoing protein undernutrition. Individualized fortification is the recommended method to optimize HM fortification. There are two models of individualization: ‘‘adjustable fortification’’ and ‘‘targeted fortification’’. Both ways are feasible and effective in improving protein intakes and growth. Adjustable fortification has the advantage of being practical and avoids excessive protein intakes.

In preterm infants, feeding with human milk (HM) is a very effective intervention for the prevention of infections and necrotizing enterocolitis (NEC), and for potentially improved neurocognitive and cardiovascular outcomes in the long-term. Hospitals and physicians are advised to recommend HM for preterm and other high-risk infants either by direct breastfeeding and/or using the mother's own expressed milk. Donor HM is the preferred feeding when the mother's own milk is not available in sufficient quantity. While in some countries donor HM has been considered an effective tool in the delivery of health care to infants, skepticism regarding its nutritional and immunological quality has limited its distribution in other countries. The purpose of this paper is to summarize the clinical benefits of donor HM in preterm infants, and to discuss common concerns limiting its distribution as standard care. Clinically, the use of donor HM has been shown to prevent NEC, reduce feeding intolerance and improve long-term outcomes in premature infants. Common concerns, such as slow growth and loss of important biological components of donor HM due to storage and pasteurization, should not be a reason for denial of donor milk. Optimization of banking procedures and of HM fortification is available and should be applied. Banked donor milk should be promoted as standard component of health care for premature infants.

Fluorescence polarization of the amniotic fluid from 39 high risk pregnancies requiring preterm delivery was measured in order to assess the maturity of the fetal lung. The study population included 15 cases of intrauterine growth retardation, ten maternal hypertension, five maternal Hodgkin's disease, three placenta previa, two fetal malformation, two polyamnios, one untreated diabetes, one maternal nephropathy. All patients underwent a single amniocentesis before deciding whether to deliver a preterm baby and FP of the amniotic fluid was done within two hours from amniocentesis. In five cases this was > 0.311, the cut-off limit taken as an indicator of fetal pulmonary status, and three of these developed respiratory distress syndrome. In 34 cases FP values were < or = 0.311; in spite of the apparent lung maturity two of these newborns developed respiratory distress syndrome. On the basis of these results the FP sensitivity was calculated as 60%, specificity 94% and the overall accuracy 90%.