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Nutrition in early life and age-associated diseases.

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Tarry-Adkins, Jane L 
Ozanne, Susan E 


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.



Age-associated disease, Developmental programming, Mechanism, Oxidative stress, Sub-optimal nutrition, Aging, Animals, Cardiovascular Diseases, Cellular Senescence, Chronic Disease, Diabetes Mellitus, Type 2, Epigenesis, Genetic, Female, Humans, Models, Animal, Nutritional Status, Obesity, Pregnancy, Prenatal Exposure Delayed Effects

Journal Title

Ageing Res Rev

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Elsevier BV
Medical Research Council (MC_UU_12012/4)
British Heart Foundation (None)
British Heart Foundation (None)
Medical Research Council (MC_PC_12012)
British Heart Foundation [Grant IDs: PG/09/037/27387, FS/09/029/27902]; Medical Research Council [Grant ID: MC UU 12012/4]