Cow milk consumption, insulin-like growth factor-I, and human biology: A life history approach

Human Biology Program and Department of Anthropology, Indiana University, Bloomington, Indiana 47405, USA.
American Journal of Human Biology (Impact Factor: 1.7). 03/2012; 24(2):130-8. DOI: 10.1002/ajhb.22201
Source: PubMed


To assess the life history consequences of cow milk consumption at different stages in early life (prenatal to adolescence), especially with regard to linear growth and age at menarche and the role of insulin-like growth factor I (IGF-I) in mediating a relationship among milk, growth and development, and long-term biological outcomes.
United States National Health and Nutrition Examination Survey (NHANES) data from 1999 to 2004 and review of existing literature.
The literature tends to support milk's role in enhancing growth early in life (prior to age 5 years), but there is less support for this relationship during middle childhood. Milk has been associated with early menarche and with acceleration of linear growth in adolescence. NHANES data show a positive relationship between milk intake and linear growth in early childhood and adolescence, but not middle childhood, a period of relatively slow growth. IGF-I is a candidate bioactive molecule linking milk consumption to more rapid growth and development, although the mechanism by which it may exert such effects is unknown.
Routine milk consumption is an evolutionarily novel dietary behavior that has the potential to alter human life history parameters, especially vis-à-vis linear growth, which in turn may have negative long-term biological consequences.

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Available from: Andrea S Wiley, Jan 30, 2014
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    • "It is thus not surprising that milk consumption during pregnancy increased fetal growth, infant size at birth and birth weight [130,131]. In terms of evolutionary biology, regular cow’s milk consumption is a very recent behavorial change, which may have adverse long-term health effects in humans [132]. During the last century, due to the implementation of widespread cooling technology milk and other dairy products became alvailable on a large scale and cow’s milk-based artificial infant feeding have been introduced into human biology. "
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    ABSTRACT: This article provides a new view of the cellular mechanisms that have been proposed to explain the links between infant formula feeding and the development of atopy and obesity. Epidemiological evidence points to an allergy- and obesity-preventive effect of breastfeeding. Both allergy and obesity development have been traced back to accelerated growth early in life. The nutrient-sensitive kinase mTORC1 is the master regulator of cell growth, which is predominantly activated by amino acids. In contrast to breastfeeding, artificial infant formula feeding bears the risk of uncontrolled excessive protein intake overactivating the infant's mTORC1 signalling pathways. Overactivated mTORC1 enhances S6K1-mediated adipocyte differentiation, but negatively regulates growth and differentiation of FoxP3(+) regulatory T-cells (Tregs), which are deficient in atopic individuals. Thus, the "early protein hypothesis" not only explains increased mTORC1-mediated infant growth but also the development of mTORC1-driven diseases such as allergy and obesity due to a postnatal deviation from the appropriate axis of mTORC1-driven metabolic and immunologic programming. Remarkably, intake of fresh unpasteurized cow's milk exhibits an allergy-preventive effect in farm children associated with increased FoxP3(+) Treg numbers. In contrast to unprocessed cow's milk, formula lacks bioactive immune-regulatory microRNAs, such as microRNA-155, which plays a major role in FoxP3 expression. Uncontrolled excessive protein supply by formula feeding associated with the absence of bioactive microRNAs and bifidobacteria in formula apparently in a synergistic way result in insufficient Treg maturation. Treg deficiency allows Th2-cell differentiation promoting the development of allergic diseases. Formula-induced mTORC1 overactivation is thus the critical mechanism that explains accelerated postnatal growth, allergy and obesity development on one aberrant pathway.
    Allergy Asthma and Clinical Immunology 07/2014; 10(1):37. DOI:10.1186/1710-1492-10-37 · 2.03 Impact Factor
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    • "Even though several studies have shown positive associations between milk intake and height in prepubertal children[13-16], others have shown no such relationships[17,18]. A recent analysis reports that the biological sequalae of routine milk consumption, such as statural growth, are not well understood[19]. Even though the circulating levels of the growth promoting peptide, insulin-like growth factor-I (IGF-I), rises after milk consumption[20], it is unclear whether the rise in IGF-I levels is due to the IGF-I contained in milk or as a result of endogenous IGF-I production[20]. "
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    PLoS ONE 10/2013; 8(10):e78653. DOI:10.1371/journal.pone.0078653 · 3.23 Impact Factor
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    • "Milk ingestion is a novel human behaviour introduced by the Neolithic revolution, industrially maximized by widespread refrigeration technology [39]. The NHANES[40] and the Growing-Up Today Study[41] observed increased BMI in children and adolescents in association with increased milk consumption. "
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    ABSTRACT: Milk protein intake has recently been suggested to improve metabolic health. This Perspective provides evidence that metabolic effects of milk protein intake have to be regarded in the context of the individual's pre-existing metabolic and exercise status. Milk proteins provide abundant branched-chain amino acids (BCAAs) and glutamine. Plasma BCAAs and glutamine are increased in obesity and insulin resistance, but decrease after gastric bypass surgery resulting in weight loss and improved insulin sensitivity. Milk protein consumption results in postprandial hyperinsulinemia in obese subjects, increases body weight of overweight adolescents and may thus deteriorate pre-existing metabolic disturbances of obese, insulin resistant individuals.
    Nutrition & Metabolism 10/2013; 10(1):60. DOI:10.1186/1743-7075-10-60 · 3.26 Impact Factor
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