Carotenoids are important bioactive substances in breast milk, the profile of which is seldom studied. This study aimed to explore the profile of carotenoids in breast milk and maternal/cord plasma of healthy mother–neonate pairs in Shanghai, China, and their correlation with dietary intake. Maternal blood, umbilical cord blood and breast milk samples from five lactation stages (colostrum, transitional milk and early-, mid- and late-term mature milk) were collected. Carotenoid levels were analysed by HPLC. Carotenoid levels in breast milk changed as lactation progressed (P < 0·001). β-Carotene was the primary carotenoid in colostrum. Lutein accounted for approximately 50 % of total carotenoids in transitional milk, mature milk and cord blood. Positive correlations were observed between five carotenoids in umbilical cord blood and maternal blood (P all < 0·001). β-Carotene levels were also correlated between maternal plasma and three stages of breast milk (r = 0·605, P < 0·001; r = 0·456, P = 0·011, r = 0·446; P = 0·013, respectively). Dietary carotenoid intakes of lactating mothers also differed across lactation stages, although no correlation with breast milk concentrations was found. These findings suggest the importance of exploring the transport mechanism of carotenoids between mothers and infants and help guide the development of formulas for Chinese infants as well as the nutritional diets of lactating mothers.

Approximately one-in-ten reproductive age adults in the USA follow a plant-based diet, yet there is limited information on the influence of vegan and vegetarian diets on the mineral composition of breast milk. This study explored the major and trace mineral composition in breast milk and associations with maternal diet patterns. We used a cross-sectional design to collect a single sample of breast milk from individuals following vegan (n 23), vegetarian (n 19) and omnivore (n 21) diet patterns. Plant-based diet (n 42) was defined as following either vegan or vegetarian diets. Sixteen minerals were assessed using inductively coupled plasma mass spectrometry and inductively coupled plasma optical emission spectrometry. Data were evaluated using traditional statistical techniques and five different machine learning approaches. The distribution of Se (median; quartile 1 and 3) was significantly different between groups (vegetarians 21, 18–26 µg/l; vegans 19, 18–25 µg/l and omnivores 17, 14–20 µg/l; P = 0·007) using a Kruskal–Wallis test. Machine learning techniques also identified Se as a potential biomarker for differentiating breast milk by maternal diet pattern. Individuals following a plant-based diet generally had a lower BMI, higher breast milk Se and lower breast milk I and Fe concentrations compared with those following omnivore diets. This suggests that maternal dietary pattern (plant-based v. omnivore) may be helpful clinical information to consider when caring for the breast-feeding dyad, with the strongest evidence related to differences in Se concentration.

Growth patterns of breastfed infants show substantial inter-individual differences, partly influenced by breast milk (BM) nutritional composition. However, BM nutritional composition does not accurately indicate BM nutrient intakes. This study aimed to examine the associations between both BM intake volumes and macronutrient intakes with infant growth. Mother–infant dyads (n 94) were recruited into the Cambridge Baby Growth and Breastfeeding Study (CBGS-BF) from a single maternity hospital at birth; all infants received exclusive breast-feeding (EBF) for at least 6 weeks. Infant weight, length and skinfolds thicknesses (adiposity) were repeatedly measured from birth to 12 months. Post-feed BM samples were collected at 6 weeks to measure TAG (fat), lactose (carbohydrate) (both by 1H-NMR) and protein concentrations (Dumas method). BM intake volume was estimated from seventy infants between 4 and 6 weeks using dose-to-the-mother deuterium oxide (2H2O) turnover. In the full cohort and among sixty infants who received EBF for 3+ months, higher BM intake at 6 weeks was associated with initial faster growth between 0 and 6 weeks (β + se 3·58 + 0·47 for weight and 4·53 + 0·6 for adiposity gains, both P < 0·0001) but subsequent slower growth between 3 and 12 months (β + se − 2·27 + 0·7 for weight and −2·65 + 0·69 for adiposity gains, both P < 0·005). BM carbohydrate and protein intakes at 4–6 weeks were positively associated with early (0–6 weeks) but tended to be negatively related with later (3–12 months) adiposity gains, while BM fat intake showed no association, suggesting that carbohydrate and protein intakes may have more functional relevance to later infant growth and adiposity.

The nutrient composition of breast milk alters during lactation, and maternal BMI adds more intricacy into its complexity. We aimed to compare leptin, ghrelin, adiponectin and insulin-like growth factor-1 (IGF-1) levels of pre-feed and post-feed breast milk in mothers with obesity and normal weight, and tried to determine their effects on infants’ growth over weight for length z-score. Twenty obese and twenty normal weight mothers with 2-month-old infants were enrolled in this case–control study. Five millilitre pre-feed breast milk and 5 ml post-feed breast milk were collected. Breast milk leptin, ghrelin, adiponectin and IGF-1 were measured by commercial kits. The pre-feed breast milk of mothers with obesity had significantly higher levels of ghrelin than mothers with normal weight (P = 0·025), whereas the post-feed breast milk of mothers with normal weight had higher levels of adiponectin than the mothers with obesity (P = 0·010). No significant differences were observed in leptin and IGF-1 levels between the two groups. Post-feed breast milk IGF-1 levels of mothers with obesity were correlated with infant’s weight for length z-score at 2 months (r −0·476; P = 0·034). In linear regression models, parity affected the ghrelin in pre-feed breast milk (P = 0·025). Our results revealed that maternal pre-pregnancy BMI was associated with breast milk components.

Human breast milk (BM) is the best source of nutrition in early life, particularly during the first 6 months. Nevertheless, human BM composition is variable, and more insight in the exact factors contributing to this variability is warranted. In this review, we explored the impact of maternal dietary intake and nutritional status (e.g. anthropometric measures, BMI, bioimpedance) on human milk macronutrient composition. PubMed, Scopus and Cochrane were systematically searched till November 2019. In total, 4946 publications underwent title–abstract screening; 101 publications underwent full-text screening. Eventually, fifty publications were included in this review, investigating either associations between maternal dietary intake (n 29) and/or maternal nutritional status (n 29), and macronutrient composition of human BM. Reported energy composition ranged from 213 to 301 kJ/100 ml, and 67 % and 54 % of the studies reported associations between with maternal nutritional intake and status, respectively. Protein content ranged from 0·8 to 3·3 g/100 ml, and four studies suggested a negative association with nutritional status. Fat content ranged from 2·1 to 9·8 g/100 ml, and 68 % of the studies reported positive associations with nutritional status. Carbohydrate content ranged from 5·8 to 7·5 g/100 ml, and 67 % of the included studies did not report an association between intake and status. Literature investigating associations of maternal dietary intake and nutrition status with BM composition of macronutrients and energy content is diversified, both in terms of used methodology and results. Further studies using well-defined and standard parameters are essential to aid the formulation of scientific recommendations.

Despite evidence showing that the intake of ultra-processed food has a negative impact on health, diet quality and dietary vitamin E, its impact on vitamin E nutritional status and breast milk remains unknown. This study aimed to assess the influence of the consumption of ultra-processed foods on vitamin E biomarkers of lactating women. A cross-sectional study was performed with 294 lactating women. Food consumption was obtained by 24-h dietary recall, and foods were grouped according to the NOVA classification. Levels of α-tocopherol were analysed by HPLC. Breast milk vitamin E (BMVE) adequacy was based on the quantity of the vitamin in the estimated intake volume. The Kruskal–Wallis test was used to compare the tertiles and linear regression to association between ultra-processed food consumption and biomarkers. Ultra-processed foods accounted for 16 % of energy intake and vitamin E intakes by all women were considered low. Serum α-tocopherol was 26·55 (sd 7·98) µmol/l, 5 % (n 11) showed inadequate vitamin E (< 12 µmol/l) and 78 % had an inadequate BMVE content (< 4 mg/780 ml). The regression showed that a higher dietary share of ultra-processed foods was associated with lower concentrations of serum α-tocopherol (β = –0·168, 95 % CI –0·047, 0·010, P = 0·003) and inadequate BMVE content (β = –0·144, 95 % CI = –0·505, 0·063, P = 0·012) (adjustment for income and maternal age). Thus, higher dietary shares of ultra-processed foods had an impact on vitamin E biomarkers, suggesting that inadequate dietary intake practices during lactation may reduce the supply of vitamin E to women and breast milk.

Type of feeding during early life influences growth trajectory and metabolic risk at later ages. Modifications in infant formula composition have led to evaluate their effects on growth and energetic efficiency (EE) compared with breast-feeding. Main goal was to analyse type of feeding potential effects during first months of life, plus its EE, on growth patterns in healthy formula fed (standard infant formula (SF) vs. experimental infant formula enriched with bioactive nutrients (EF)) and breastfed (BF) infants participating in the COGNIS RCT (http://www.ClinicalTrials.gov, Identifier: NCT02094547) up to 18 months of age. Infants follow-up to 18 months of age (n 141) fed with a SF (n 48), EF(n 56), or BF (n 37), were assessed for growth parameters using WHO standards. Growth velocity (GV) and catch-up were calculated to identify growth patterns. EE of breast milk/infant formula was also estimated. Infants’ growth at 6 months showed higher length and lower head circumference gains in SF and EF infants than BF infants. Both weight-for-length and weight-for-age catch-up growth showed significant differences in formula fed groups compared with the BF. No significant differences in GV or catch-up were found at 6–12 and 12–18 months. Regarding EE, infant formula groups showed significantly lower weight and length gains/g of milk protein, and higher weight and length gains/g of milk lipids, than the BF infants. GV during first 6 months, which may be influenced by feeding, seems to be the main predictor of subsequent growth trajectory. Breast-feeding may have positive effects on growth programming due to its nutrients’ EE.

We aimed to investigate the trends of breast milk lutein concentrations at different times and their relationship with dietary lutein intake during the 12 weeks after delivery. Breast milk samples were collected from thirty-seven mothers at 4, 8 and 12 weeks postpartum. A HPLC detection method was used to measure breast milk lutein concentrations. Dietary intake was assessed using an FFQ, and then dietary lutein intake was calculated. The correlations between dietary lutein intake and breast milk lutein concentrations during lactation were investigated by Pearson’s correlation coefficient. General linear regression models were used to evaluate the optimal regression equation. The mean values of dietary lutein intake at 4, 8 and 12 weeks postpartum were 5·22 (sd 3·60), 7·28 (sd 4·30) and 7·33 (sd 4·24) mg/d, respectively. The mean values of breast milk lutein concentrations at 4, 8 and 12 weeks postpartum were as follows: 46·41 (sd 41·36), 57·96 (sd 40·00) and 62·33 (sd 30·10) μg/l, respectively. Breast milk lutein concentrations were positively associated with dietary lutein intake at 4 weeks postpartum (r 0·527, P < 0·05), which was consistent with the positive correlations observed at 8 and 12 weeks postpartum (r 0·444, P < 0·05; r 0·468, P < 0·05) by the sensitivity analysis. Increased dietary lutein intake can increase the concentration of lutein in the breast milk, and women are recommended to increase their dietary intake of green leafy vegetables and fruits that are rich in lutein during the pregnancy and postpartum periods.

Observational studies suggest that breast-feeding is associated with a more favourable BMI and cardio-metabolic markers, but potential underlying mechanisms are unclear. As serum adiponectin has an important function in adults for glucose and lipid metabolism, we assessed 251 participants of the Prevention and Incidence of Asthma and Mite Allergy birth cohort whether breast milk adiponectin is associated with childhood BMI and cardio-metabolic markers. We measured adiponectin levels in breast milk collected around 3 months after birth of the child and subsequently obtained weight and height repeatedly up to the age of 17 years. A medical examination (including blood pressure, glycated Hb and cholesterol) was performed at the age of 8, 12 and 16 years. We used multivariable mixed models to assess the association between breast milk adiponectin and BMI and cardio-metabolic markers at these ages. In models adjusted for exact age of breast milk collection, maternal age, presence of siblings, maternal BMI, pregnancy weight gain and child’s birth weight, each unit increase in log breast milk adiponectin (in ng/ml) was associated with a 0·28 lower BMI z score (95 % CI –0·56, 0·00) at 3 months. After the age of 1 year, there was a tendency towards a higher BMI z score with increased breast milk adiponectin at some ages, but this pattern was not consistent throughout childhood. There were no associations between breast milk adiponectin and any of the cardio-metabolic markers in childhood. We conclude that in our study with follow-up until 17 years of age, breast milk adiponectin has no long-term effect on BMI and cardio-metabolic health during childhood.

Pregnant and lactating women and breastfed infants are at risk of vitamin D deficiency. The supplemental vitamin D dose that optimises maternal vitamin D status and breast milk antirachitic activity (ARA) is unclear. Healthy pregnant women were randomised to 10 (n 10), 35 (n 11), 60 (n 11) and 85 (n 11) µg vitamin D3/d from 20 gestational weeks (GW) to 4 weeks postpartum (PP). The participants also received increasing dosages of fish oil supplements and a multivitamin. Treatment allocation was not blinded. Parent vitamin D and 25-hydroxyvitamin D (25(OH)D) were measured in maternal plasma at 20 GW, 36 GW and 4 weeks PP, and in milk at 4 weeks PP. Median 25(OH)D and parent vitamin D at 20 GW were 85 (range 25–131) nmol/l and ‘not detectable (nd)’ (range nd–40) nmol/l. Both increased, seemingly dose dependent, from 20 to 36 GW and decreased from 36 GW to 4 weeks PP. In all, 35 µg vitamin D/d was needed to increase 25(OH)D to adequacy (80–249 nmol/l) in >97·5 % of participants at 36 GW, while >85 µg/d was needed to reach this criterion at 4 weeks PP. The 25(OH)D increments from 20 to 36 GW and from 20 GW to 4 weeks PP diminished with supplemental dose and related inversely to 25(OH)D at 20 GW. Milk ARA related to vitamin D3 dose, but the infant adequate intake of 513 IU/l was not reached. Vitamin D3 dosages of 35 and >85 µg/d were needed to reach adequate maternal vitamin D status at 36 GW and 4 weeks PP, respectively.

Breast milk (BM) hormones have been hypothesised as a nutritional link between maternal and infant metabolic health. This study aimed to evaluate hormone concentrations in BM of women with and without gestational diabetes mellitus (GDM), and the relationship between maternal factors, BM hormones and infant growth. We studied ninety-six nulliparous women with (n 48) and without GDM and their exclusively breastfed term singletons. Women with GDM received dietary therapy or insulin injection for euglycaemia during pregnancy. Hormone concentrations in BM, maternal BMI and infant growth were longitudinally evaluated on postnatal days 3, 42 and 90. Mothers with GDM had decreased concentrations of adiponectin (Pcolostrum<0·001; Pmature-milk=0·009) and ghrelin (Pcolostrum=0·011; Pmature-milk<0·001) and increased concentration of insulin in BM (Pcolostrum=0·047; Pmature-milk=0·021). Maternal BMI was positively associated with adiponectin (β=0·06; 95 % CI 0·02, 0·1; P=0·001), leptin (β=0·16; 95 % CI 0·12, 0·2; P<0·001) and insulin concentrations (β=0·06; 95 % CI 0·02, 0·1; P<0·001), and inversely associated with ghrelin concentration in BM (β=–0·08; 95 % CI –0·1, –0·06; P<0·001). Among the four hormones, adiponectin was inversely associated with infant growth in both the GDM (βweight-for-height=–2·49; 95 % CI –3·83, –1·15; P<0·001; βhead-circumference=–0·39; 95 % CI –0·65, –0·13; P=0·003) and healthy groups (βweight-for-height=–1·42; 95 % CI –2·38, –0·46; P=0·003; βhead-circumference=–0·15; 95 % CI –0·27, –0·03; P=0·007). Maternal BMI and GDM are important determinants of BM hormone concentrations. Milk-borne adiponectin is determined by maternal metabolic status and plays an independent down-regulating role in early infant growth.

Adiponectin and leptin are involved in appetite control and body weight regulation. We aimed to evaluate the relationship between breast milk adipokine levels and short-term growth of preterm and term infants. Thirty-one preterm (median=35.3 weeks) and 34 term (median=38.7 weeks) infants were enrolled. Enzyme-linked immunosorbent assay was used to detect adipokines in mature milk. Infant growth was followed during the first 3 months. Although weight gain in the first month was insufficient, positive linear growth was observed in the following months for preterm infants, while term infants had positive steady linear growth. The median level of adipokines was found to be higher in preterm infants (P>0.05). Adiponectin showed significant negative correlations with some anthropometric measurements of term infants. However, in preterm infants, adiponectin was negatively correlated with length increment and positively correlated with body mass index (BMI) increment in the second–third month. In addition, leptin was negatively associated with the head circumference at birth in preterm infants and the triceps skinfold thickness increment in the first–second month term infants (P<0.05). In linear regression models, while gestational age, adiponectin and leptin were not related, maternal age and pre-pregnancy BMI had effects on body weight increment in 0–1 months (P<0.05). In conclusion, adiponectin may affect short-term growth, while leptin has no important effect. It would be beneficial to carry out longitudinal studies to evaluate the effects of these adipokines on the growth of infants.

At birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ+ cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ+ CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

Breast-fed infants are susceptible to vitamin D deficiency rickets. The current vitamin D ‘adequate intake’ (AI) for 0–6-month-old infants is 10 µg/d, corresponding with a human milk antirachitic activity (ARA) of 513 IU/l. We were particularly interested to see whether milk ARA of mothers with lifetime abundant sunlight exposure reaches the AI. We measured milk ARA of lactating mothers with different cultural backgrounds, living at different latitudes. Mature milk was derived from 181 lactating women in the Netherlands, Curaçao, Vietnam, Malaysia and Tanzania. Milk ARA and plasma 25-hydroxyvitamin D (25(OH)D) were analysed by liquid-chromatography-MS/MS; milk fatty acids were analysed by GC-flame ionisation detector (FID). None of the mothers reached the milk vitamin D AI. Milk ARA (n; median; range) were as follows: Netherlands (n 9; 46 IU/l; 3–51), Curaçao (n 10; 31 IU/l; 5–113), Vietnam: Halong Bay (n 20; 58 IU/l; 23–110), Phu Tho (n 22; 28 IU/l; 1–62), Tien Giang (n 20; 63 IU/l; 26–247), Ho-Chi-Minh-City (n 18; 49 IU/l; 24–116), Hanoi (n 21; 37 IU/l; 11–118), Malaysia–Kuala Lumpur (n 20; 14 IU/l; 1–46) and Tanzania-Ukerewe (n 21; 77 IU/l; 12–232) and Maasai (n 20; 88 IU/l; 43–189). We collected blood samples of these lactating women in Curaçao, Vietnam and from Tanzania–Ukerewe, and found that 33·3 % had plasma 25(OH)D levels between 80 and 249·9 nmol/l, 47·3 % between 50 and 79·9 nmol/l and 19·4 % between 25 and 49·9 nmol/l. Milk ARA correlated positively with maternal plasma 25(OH)D (range 27–132 nmol/l, r 0·40) and milk EPA+DHA (0·1–3·1 g%, r 0·20), and negatively with latitude (2°S-53°N, r −0·21). Milk ARA of mothers with lifetime abundant sunlight exposure is not even close to the vitamin D AI for 0–6-month-old infants. Our data may point at the importance of adequate fetal vitamin D stores.

Mandatory I fortification in bread was introduced in Australia in 2009 in response to the re-emergence of biochemical I deficiency based on median urinary I concentration (UIC)<100 µg/l. Data on the I status of lactating mothers and their infants in Australia are scarce. The primary aim of this study was to assess the I status, determined by UIC and breast milk I concentration (BMIC), of breast-feeding mothers in South Australia and UIC of their infants. The secondary aim was to assess the relationship between the I status of mothers and their infants. The median UIC of the mothers (n 686) was 125 (interquartile range (IQR) 76–200) µg/l and median BMIC (n 538) was 127 (IQR 84–184) µg/l. In all, 38 and 36 % of the mothers had a UIC and BMIC below 100 µg/l, respectively. The median UIC of infants (n 628) was 198 (IQR 121–296) µg/l, and 17 % had UIC<100 µg/l. Infant UIC was positively associated with maternal UIC (β 0·26; 95 % CI 0·14, 0·37, P<0·001) and BMIC (β 0·85; 95 % CI 0·66, 1·04, P<0·001) at 3 months postpartum after adjustment for gestational age, parity, maternal secondary and further education, BMI category and infant feeding mode. The adjusted OR for infant UIC<100 µg/l was 6·49 (95 % CI 3·80, 11·08, P<0·001) in mothers with BMIC<100 µg/l compared with those with BMIC≥100 µg/l. The I status of mothers and breast-fed infants in South Australia, following mandatory I fortification, is indicative of I sufficiency. BMIC<100 µg/l increased the risk of biochemical I deficiency in breast-fed infants.