Abstract:The window of lactation is a critical period during which nutritional and environmental exposures impact lifelong metabolic disease risk. Significant organ and tissue development, organ expansion and maturation of cellular functions occur during the lactation period, making this a vulnerable time during which transient insults can have lasting effects. This review will cover current literature on factors influencing lactational programming such as milk composition, maternal health status and environmental endo… Show more
“…There is, however, evidence that human milk exhibits substantial individual variation in the concentration of appetite‐regulating hormones, cytokine levels, fatty acid profiles, and other factors . As reviewed by Ellsworth et al , animal models have provided intriguing evidence that maternal obesity may alter milk leptin, insulin, and other bioactive elements, which in turn are associated with diabetes, obesity, and hepatic steatosis in the adulthood offspring . As animal models do not always translate well into human studies because of species differences in growth rate, mammary gland physiology, and critical windows of development , more human research is needed to test the “lactational programming” hypothesis; that is, the variation in levels of hormones, cytokines, and other bioactive compounds present in breast milk may have sustained effects on the offspring’s appetite and metabolic rate.…”
Section: Introductionmentioning
confidence: 99%
“…As reviewed by Ellsworth et al , animal models have provided intriguing evidence that maternal obesity may alter milk leptin, insulin, and other bioactive elements, which in turn are associated with diabetes, obesity, and hepatic steatosis in the adulthood offspring . As animal models do not always translate well into human studies because of species differences in growth rate, mammary gland physiology, and critical windows of development , more human research is needed to test the “lactational programming” hypothesis; that is, the variation in levels of hormones, cytokines, and other bioactive compounds present in breast milk may have sustained effects on the offspring’s appetite and metabolic rate. Although 25% of women in the United States have BMI in the obese range prior to pregnancy , increasing the risk of obesity in the offspring by two‐ to threefold , the role of human milk composition in the transmission of obesity risk from mother to child has only recently been examined as a potential mechanism.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, studies of milk hormone variation to date have not taken account of maternal metabolic status at different critical developmental windows. Growing evidence has suggested that fetal, infant, and childhood adiposity and obesity risk are modified by pregnancy glucose dysregulation, gestational weight gain (GWG), and postpartum weight loss (PPWL), independent of prepregnancy BMI , and also that metabolic status during these periods could be involved in mammary gland development and lactogenesis I and II . This is important because GWG, PPWL, and subclinical glucose dysregulation may be more easily modifiable aspects of maternal metabolic status than current or prepregnancy BMI.…”
Objective
The aim of this study was to test associations of prepregnancy BMI, gestational weight gain, oral glucose challenge test results, and postpartum weight loss as predictors of breast milk leptin, insulin, and adiponectin concentrations and whether these relationships vary over time.
Methods
Milk was collected at 1 and 3 months from 135 exclusively breastfeeding women from the longitudinal Mothers and Infants Linked for Healthy Growth (MILk) study. Hormones were assayed in skimmed samples using ELISA. Mixed‐effects linear regression models were employed to assess main effects and effect‐by‐time interactions on hormone concentrations.
Results
In adjusted models, BMI was positively associated with milk leptin (P < 0.001) and insulin (P = 0.03) and negatively associated with milk adiponectin (P = 0.02); however, the association was stronger with insulin and weaker with adiponectin at 3 months than at 1 month (time interaction P = 0.017 for insulin and P = 0.045 for adiponectin). Gestational weight gain was positively associated and postpartum weight loss was negatively associated with milk leptin (both P < 0.001), independent of BMI. Oral glucose challenge test results were not associated with these milk hormone concentrations.
Conclusions
Maternal weight status before, during, and after pregnancy contributes to interindividual variation in human milk composition. Continuing work will assess the role of these and other milk bioactive factors in altering infant metabolic outcomes.
“…There is, however, evidence that human milk exhibits substantial individual variation in the concentration of appetite‐regulating hormones, cytokine levels, fatty acid profiles, and other factors . As reviewed by Ellsworth et al , animal models have provided intriguing evidence that maternal obesity may alter milk leptin, insulin, and other bioactive elements, which in turn are associated with diabetes, obesity, and hepatic steatosis in the adulthood offspring . As animal models do not always translate well into human studies because of species differences in growth rate, mammary gland physiology, and critical windows of development , more human research is needed to test the “lactational programming” hypothesis; that is, the variation in levels of hormones, cytokines, and other bioactive compounds present in breast milk may have sustained effects on the offspring’s appetite and metabolic rate.…”
Section: Introductionmentioning
confidence: 99%
“…As reviewed by Ellsworth et al , animal models have provided intriguing evidence that maternal obesity may alter milk leptin, insulin, and other bioactive elements, which in turn are associated with diabetes, obesity, and hepatic steatosis in the adulthood offspring . As animal models do not always translate well into human studies because of species differences in growth rate, mammary gland physiology, and critical windows of development , more human research is needed to test the “lactational programming” hypothesis; that is, the variation in levels of hormones, cytokines, and other bioactive compounds present in breast milk may have sustained effects on the offspring’s appetite and metabolic rate. Although 25% of women in the United States have BMI in the obese range prior to pregnancy , increasing the risk of obesity in the offspring by two‐ to threefold , the role of human milk composition in the transmission of obesity risk from mother to child has only recently been examined as a potential mechanism.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, studies of milk hormone variation to date have not taken account of maternal metabolic status at different critical developmental windows. Growing evidence has suggested that fetal, infant, and childhood adiposity and obesity risk are modified by pregnancy glucose dysregulation, gestational weight gain (GWG), and postpartum weight loss (PPWL), independent of prepregnancy BMI , and also that metabolic status during these periods could be involved in mammary gland development and lactogenesis I and II . This is important because GWG, PPWL, and subclinical glucose dysregulation may be more easily modifiable aspects of maternal metabolic status than current or prepregnancy BMI.…”
Objective
The aim of this study was to test associations of prepregnancy BMI, gestational weight gain, oral glucose challenge test results, and postpartum weight loss as predictors of breast milk leptin, insulin, and adiponectin concentrations and whether these relationships vary over time.
Methods
Milk was collected at 1 and 3 months from 135 exclusively breastfeeding women from the longitudinal Mothers and Infants Linked for Healthy Growth (MILk) study. Hormones were assayed in skimmed samples using ELISA. Mixed‐effects linear regression models were employed to assess main effects and effect‐by‐time interactions on hormone concentrations.
Results
In adjusted models, BMI was positively associated with milk leptin (P < 0.001) and insulin (P = 0.03) and negatively associated with milk adiponectin (P = 0.02); however, the association was stronger with insulin and weaker with adiponectin at 3 months than at 1 month (time interaction P = 0.017 for insulin and P = 0.045 for adiponectin). Gestational weight gain was positively associated and postpartum weight loss was negatively associated with milk leptin (both P < 0.001), independent of BMI. Oral glucose challenge test results were not associated with these milk hormone concentrations.
Conclusions
Maternal weight status before, during, and after pregnancy contributes to interindividual variation in human milk composition. Continuing work will assess the role of these and other milk bioactive factors in altering infant metabolic outcomes.
“…However, the early postnatal period, especially lactation, is sometimes more crucial in increasing the susceptibility to maladaptive metabolic programming. 14,15 Rodent models as a useful tool for studying developmental programming…”
Obesity and its complications occur at alarming rates worldwide. Epidemiological data have associated perinatal conditions, such as malnutrition, with the development of some disorders, such as obesity, dyslipidemia, diabetes, and cardiovascular diseases, in childhood and adulthood. Exclusive breastfeeding has been associated with protection against long-term chronic diseases. However, in humans, the interruption of breastfeeding before the recommended period of 6 months is a common practice and can increase the risk of several metabolic disturbances. Nutritional and environmental changes within a critical window of development, such as pregnancy and breastfeeding, can induce permanent changes in metabolism through epigenetic mechanisms, leading to diseases later in life via a phenomenon known as programming or developmental plasticity. However, little is known regarding the underlying mechanisms by which precocious weaning can result in adipose tissue dysfunction and endocrine profile alterations. Here, the authors give a comprehensive report of the different animal models of early weaning and programming that can result in the development of metabolic syndrome. In rats, for example, pharmacological and nonpharmacological early weaning models are associated with the development of overweight and visceral fat accumulation, leptin and insulin resistance, and neuroendocrine and hepatic changes in adult progeny. Sex-related differences seem to influence this phenotype. Therefore, precocious weaning seems to be obesogenic for offspring. A better understanding of this condition seems essential to reducing the risk for diseases. Additionally, this knowledge can generate new insights into therapeutic strategies for obesity management, improving health outcomes.
“…Формирование циркадианного ритма продукции эпифизарного мелатонина в норме продолжается ускоренными темпами в первые дни и недели жизни, а материнское влияние на этот процесс осуществляется через грудное вскармливание. Известно, что в грудном молоке содержится более 60 биологически актив ных факторов, причем концентрация соматотропного гормона, пролактина, ИФр-1, инсулина, лептина, релаксина, эпидермального фактора роста в грудном молоке выше, чем в периферической крови матери [61][62][63][64]. У здоровых матерей в грудном молоке, особенно в молозиве, выявлены высокие уровни триптофана и мелатонина, подверженные циркадным изменениям [65,66].…”
The review presents the results of experimental and clinical studies, according to which the absence of circadian melatonin production in pregnant women associated with the pathologies they have (obesity, diabetes mellitus, metabolic syndrome, pregnancy complicated by gestosis and chronic placental insufficiency, etc.) disrupts the genetic process of organizing the rhythmic activity of genes of the suprachiasmatic nuclei of the hypothalamus and melatonin production in the pineal gland of the fetus, leading to dysregulation of metabolic processes in the childs body after birth and programming pathology in following life. The significance of this factor in the pathophysiological mechanisms of catch-up growth during the first months of life determines a new approach to assessing the risk of obesity and necessitates learning the consequences of impaired development of the brain and other functional systems in fetuses that are born earlier than the 26th week of pregnancy and are thereby deprived of maternal melatonin, a key signaling molecule that directs and coordinates the genetic development process, during the most critical period of early ontogenesis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.