Human growth and chronic disease: A memorial to Jim Tanner

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.

Keywords::

• Foetal programming, chronic disease, growth, maternal nutrition, placenta

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.