Leptin intake during lactation prevents obesity and affects food intake and food preferences in later life

Abstract

Breast milk is practically the only food ingested during the first months of life in fully breastfed infants and it is assumed to match the infant's nutritional needs. Epidemiological data suggest that breastfeeding compared with infant formula feeding confers protection against several chronic diseases later on in life and, particularly, against obesity and related medical complications. However, causality has not been related to any specific compound of breast milk. Recent data in our laboratory have identified leptin as the specific compound that is responsible for some of these beneficial effects of breastfeeding. The hormone leptin was identified as a key candidate because it is present in breast milk, but is not present in infant formula, and when ingested during the suckling period can be absorbed by the immature stomach exerting biological effects. Evidence of the beneficial effects of breast milk leptin was obtained from human studies, showing that milk-borne maternal leptin appeared to give moderate protection to infants from excess weight gain. Direct cause-effect evidence was obtained in rats, where oral leptin supplementation during the suckling period resulted in a decrease in food intake, affected food preferences in favour of carbohydrates versus fat, and protected against overweight in adulthood, with an improvement of related parameters such as leptin and insulin sensitivity. These findings open a new area of research on the use of leptin in the design of more appropriate infant formula, which is significant considering the increasing incidence of obesity and its associated medical complications.

Introduction

Obesity and overweight are the most frequent disorders in children and teenagers in industrialised countries, and there is a continuous increase in their prevalence (Freedman, Srinivasan, Valdez, Williamson, & Berenson, 1997). Moreover, numerous studies show an association between being overweight as a child and being overweight in adulthood (Power, Lake, & Cole, 1997) with the risk of associated health complications such as cardiovascular disease and diabetes (Freedman, Dietz, Srinivasan, & Berenson, 1999; Power et al., 1997). Given that obesity is associated with considerable morbidity, is increasing in prevalence, and is often recalcitrant to therapy (Must, Jacques, Dallal, Bajema, & Dietz, 1992), the identification of strategies for its prevention, and particularly during the early stages of life, becomes particularly imperative.

In this sense, the view that nutrition and environmental factors during the early phases of human development can predispose or programme individuals to adult disease is not new but has awoken considerable interest particularly since the last decades. Barker and colleagues in their hypothesis on the “developmental origins of health and disease” proposed that adverse environmental factors in early life can cause disruption of normal growth and development that predicts future propensity to obesity and other related diseases (Barker, Eriksson, Forsen, & Osmond, 2002). There is considerable evidence supporting this proposal, such as the representative example of the Dutch famine which ravished the western part of Holland during the last 6 months of World War II (Ravelli, Stein, & Susser, 1976), in which males born to women exposed to poor nutrition in the first and second terms of their pregnancies were more likely to be obese than their peers, whose mothers did not experience poor nutrition.