Abstract

After birth, the body shifts from glucose as primary energy substrate to milk-derived fats, with sugars from lactose taking a secondary place. At weaning, glucose recovers its primogeniture and dietary fat role decreases. In spite of human temporary adaptation to a high-fat (and sugars and protein) diet during lactation, the ability to thrive on this type of diet is lost irreversibly after weaning. We could not revert too the lactating period metabolic setting because of different proportions of brain/muscle metabolism in the total energy budget, lower thermogenesis needs and capabilities, and absence of significant growth in adults. A key reason for change was the limited availability of foods with high energy content at weaning and during the whole adult life of our ancestors, which physiological adaptations remain practically unchanged in our present-day bodies. Humans have evolved to survive with relatively poor diets interspersed by bouts of scarcity and abundance. Today diets in many societies are largely made up from choice foods, responding to our deeply ingrained desire for fats, protein, sugars, salt etc. Consequently our diets are not well adjusted to our physiological needs/adaptations but mainly to our tastes (another adaptation to periodic scarcity), and thus are rich in energy roughly comparable to milk. However, most adult humans cannot process the food ingested in excess because our cortical-derived craving overrides the mechanisms controlling appetite. This is produced not because we lack the biochemical mechanisms to use this energy, but because we are unprepared for excess, and wholly adapted to survive scarcity. The thrifty mechanisms compound the effects of excess nutrients and damage the control of energy metabolism, developing a pathologic state. As a consequence, an overflow of energy is generated and the disease of plenty develops.

Highlights

  • Lactation and the dietary induction of the metabolic syndrome It seems crystal clear that the triggering factor of the metabolic syndrome and related diseases is our inability to process -for years- an excess of ingested energy, mainly lipid

  • In our food energy-handling metabolism, fats are practically absent in our life in utero but are a main source of energy during lactation because of Correspondence: malemany@ub.edu 1Department of Nutrition and Food Science, Faculty of Biology, University of Barcelona, Barcelona, Spain Full list of author information is available at the end of the article its substantial presence in milk, decreasing sharply after weaning

  • An excess of energy is generated and the disease of plenty develops. This is produced not because we lack the biochemical mechanisms to use this energy, but because we are unprepared for excess and wholly adapted to survive scarcity; these same mechanisms compound the effects of excess nutrients and damage our mechanisms of control of metabolism, developing pathologic states

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Summary

Background

The main role of lipids, from infancy and throughout all our adult life, is limited to constitute the mainstay of our own energy reserves. A few of the mechanisms used during our milk-only suckling period are put in action again (at least to a limited extent) in adult overfeeding: increased thermogenesis [60] and protein turnover [61], use of fatty acids as main energy substrate [62], preservation of glucose, essential amino acids and amino N [63], and enhancement of the independence and capabilities of the defense (immune) system [64]; but the rest of conditions are different: the brain is already fully functional, muscle is active, comparatively larger and mature, the importance of thermogenesis is limited [65], and -especially-, growth is arrested; the tolerance of brain to ketone bodies and acidosis is lower than during development, glucose homeostasis is more regulated, and brain cortical influences (i.e. over appetite and food selection) are again different (more focused and powerful), often overriding the automatic mechanisms controlling appetite and food intake [35]. We are illequipped for continued low-level stress, such as the universal worrying for economic and sentimental questions or the unnatural invasion of our personal space in public places [116]

Conclusions
16. Schutz Y
27. Himms-Hagen J
37. York DA: CRF and glucocorticoids
44. Scherer PE
46. Pond CM
48. Tilg H
54. Sheffield-Moore M
65. Norgan NG
68. Loos RJF
71. Groop LC
79. Prentice AM
90. Uauy R: Dietary fat quality for optimal health and well-being
Findings
94. Rogers AR
Full Text
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