Nutrition in early life and age-associated diseases

Abstract

The prevalence of age-associated disease is increasing at a striking rate globally. It is known that a strong association exists between a suboptimal maternal and/or early-life environment and increased propensity of developing age-associated disease, including cardiovascular disease (CVD), type-2 diabetes (T2D) and obesity. The dissection of underlying molecular mechanisms to explain this phenomenon, which is known as 'developmental programming' is still emerging; however three common mechanisms have emerged in many models of developmental programming. These mechanisms are (a) changes in tissue structure, (b) epigenetic regulation and (c) accelerated cellular ageing. This review will examine the epidemiological evidence and the animal models of suboptimal maternal environments, focusing upon these molecular mechanisms and will discuss the progress being made in the development of safe and effective intervention strategies which ultimately could target those 'programmed' individuals who are known to be at-risk of age-associated disease.

Effect of maternal baboon (Papio sp.) dietary mismatch in pregnancy and lactation on post‐natal offspring early life phenotype

“…Strikingly, by age 3 years, MM of both sexes had surpassed controls in nearly every measure of body size. Human and animal studies have shown that rapid post‐natal catch‐up growth following poor intrauterine growth increases risk of age‐associated diseases . In humans, studies have documented that catch‐up growth is associated with early indicators of type 2 diabetes and obesity, endothelial dysfunction, hypertension, cardiovascular disease, and non‐alcoholic fatty liver disease .…”

“…Mismatch intrauterine growth increases risk of age-associated diseases. 24 In humans, studies have documented that catch-up growth is associated with early indicators of type 2 diabetes and obesity, 25,26 endothelial dysfunction, 27 hypertension, 28 cardiovascular disease, 29 and non-alcoholic fatty liver disease. 30 Similarly, experimental studies with rodents that were protein or calorie restricted in utero and TA B L E 5 Offspring morphometrics at birth in males and females then received obesogenic diets post-natally have shown reduced longevity, 31,32 obesity, 33,34 fatty livers, 35 insulin resistance, 36 hyperleptinaemia, 34 and hepatic fibrosis and inflammation.…”

Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence

“…If these adaptive modifications persist, or are more readily inducible later in life, they have the potential to promote energy absorption beyond metabolic capability when energy supplies increase, thereby causing insulin resistance, obesity and T2D in adulthood [9]. Among the factors affecting the risk of metabolic dysfunctions, including T2D, in adulthood, the prenatal and early postnatal malnutrition (both under- and overnutrition) is currently believed to be most important [10,11]. It should be noted that in this review only one aspect of malnutrition i.e., undernutrition but not overnutrition will be discussed.…”

A suboptimal maternal diet combined with accelerated postnatal growth results in an altered aging profile in the thymus of male rats

“…This can occur through the ‘sparing’ of certain vital organs, especially the brain, at the expense of other organs, including the heart, pancreas, kidney and skeletal muscle, resulting in compromised structure and function of these organs. Furthermore, if the suboptimal maternal environment is combined with a mismatched postnatal milieu, this can further exacerbate the increased risk of the development of a wide range of age-associated diseases in the offspring later in life (2). Despite decline in immune function being known to play an important role in the development of many age-associated diseases, it has been poorly studied in the context of developmental programming.…”