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Abstract
Context: Memorial to Jim Tanner.
Objective: To examine the links between early growth and chronic disease in later life.
Methods: Literature review.
Results: There is now a developmental model for the origins of chronic disease in which the causes to be identified are linked to normal variations in feto-placental, infant and childhood growth and development. These variations lead to variations in the supply of nutrients to the baby that permanently alters gene expression, a process known as ‘programming’.
Conclusions: Variations in the processes of development programme the function of a few key systems that are linked to chronic disease—the immune system, anti-oxidant defences, inflammatory responses, the number and quality of stem cells, neuro-endocrine settings and the balance of the autonomic nervous system. There is not a separate cause for each different disease. Which chronic disease originates during development may depend more on timing than on qualitative differences in exposures to external influences.
Acknowledgements
The writing of this lecture has been greatly helped by discussions with Professors Kent Thornburg, Oregon Health & Science University, and Michelle Lampl, Emory University, and my colleagues in the MRC Lifecourse Epidemiology Unit, University of Southampton.
Declaration of interest : The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.