The science of nutrition aims to define the overall quantity and individual nutritients required by the human population.

Humans deal uniformly badly with a deficiency of a nutrient whether this be the very short term (oxygen), the short term (water) or longer term (food ). Survival times depend upon body stores at the onset of deprivation. The consequence of a deficiency of single or several nutrients from the diet may be lethal over a period of time.

Modern western populations are faced with an excess of food. This may lead to an over-generous intake of nutrients. The manner in which each individual deals with this is in part dependent upon their genetic and isoenzymic constitution. The basal metabolic rate and level of physical activity are also important. The excess intake may be in all nutrients or be confined to a few specific nutrients. The stage of life and health status are also important.

Growth is frequently used as a non-specific term to describe the changes associated with the development of form and function. Growth may readily be measured as length, weight and chemical composition. By such measurements, normal and abnormal growth can be identified.

Growth requires nutrient utilisation to be directed to energy storage, cell multiplication and skeletal utilisation. These metabolic fuels are co-ordinated in their role in growth by systemic and local regulatory factors. Growth includes:

• whole body growth

• individual organ growth

• cellular growth and replication

• tissue turnover and repair

  • cell death ( apoptosis)

These overlap and are all involved in the achievement of functional maturity. The amount of dietary energy and protein necessary for growth varies between species, and is influenced by the time taken for the growth phase. Differences between species and the genetically determined rate of proliferation will influence cell number and body mass.

Hypertrophy is the reversible increase in the size of a cell through the accumulation of more structural components. Hyperplasia is an increase in the number of cells in a tissue or organ, and an increase in the organ size.

Maternal nutrient supply to the foetus in the latter part of gestation will affect the rate of growth and the composition of the infant. Hypertrophy becomes more significant in the more mature foetus, as does the differential growth of different cells, tissue and body protein mass and organs.

The increase in weight from birth to adult maturity is determined by the proportion of the life span spent in maturation and growth. The development of reproductive maturity usually means the end of growth. Humans are somewhat different from other mammals in that body weight increases 15-fold from the birth weight. Protein deposition continues for a quarter of the time between birth and death.

1. Growth is an increase in weight, height, and composition of body organs, cells and tissue repair. This requires appropriate nutrient intake of energy and protein.

2. Hypertrophy is a reversible increase in cell size. Hyperplasia is an increase in the number of cells. Organ growth is in three phases, the development of cell lines, differentiation and maturation to mature function.

3. Growth at cellular and organ level is a coordinated process, controlled by various specific signalling molecules, many of which are hormones. The growth process at maturity is in response to need. Disuse leads to atrophy.

4. Growth is only possible if energy intake exceeds expenditure. Height is dependent upon sex and ethnic, genetic, dietary and environmental factors

  1. Catch-up growth requires sufficient nutritional intake including high quality protein and energy content. This growth spurt is seen in children who, following failure to achieve their age growth norms and are subsequently well.
  2. A multicellular organism must balance cell generation and cell death to maintain a constant size. Senescent, damaged or abnormal cells are removed. Physiological cell death, apoptosis, is directed towards scattered individual cells rather than all the cells in a particular area.

Further Reading

Ashworth A, Millward DJ ( 1986) Catch up growth in children. Nutrition Reviews, 44, 157-63.
Burns, H.J.G. (1990) Growth promotors in humans. Proceedings of the Nutrition Society49, 467–72.
Carson, D.A. and Ribeiro, J.N. (1993) Apoptosis and disease. Lancet341, 1251–4.
Carter-Su, C., Schwarz, J. and Smit, L.S. (1996) Molecular mechanism of growth hormone action. Annual Review of Physiology57, 187–208.
Cole TJ ( 2000) Secular trends in growth. Proceedings of the Nutrition Society. 59, 317-324.
Cryer, A., Williams, S.E. and Cryer, J. (1992) Dietary and other factors involved in the proliferation, determination and differentiation of adipocyte precursor cells. Proceedings of the Nutrition Society, 51, 379–85.
Dauncey MJ, White P, Burton KA, Katsumata M ( 2001) Nutrition-hormone receptor –gene interactions: implications for development and disease. Proceedings of the Nutrition Society.. 60. 63-72.
Freeman M ( 2000) Feedback control of intercellular signalling in development Nature 408, 313-18.
Goss, R.J. (1990) Similarities and differences between mechanisms of organ and tissue growth regulation. Proceedings of the Nutrition Society49, 4372.
Jackson, A.A. (1990) Protein requirements for catch-up growth. Proceedings of the Nutrition Society49, 507–16.
Koletzko B, Aggett PJ, Bindels JG, Bung P, Ferre P, Gil P, Lentze MJ, Roberfroid M, Strodeo S.( 1998) Growth, development and differentiation: a functional food science approach. British Journal of Nutrition. 80, Suppl 1, S5-S45.
Loveridge, N., Farquharson, C. and Scheven, B.A.A. (1990) Endogenous mediators of growth. Proceedings of the Nutrition Society49, 443–50.
Mathers JC ( 1998) Nutrient regulation of intestinal proliferation and apoptosis. Proceedings of the Nutrition Society 57, 219-223.
Nicholson DW ( 2001)Baiting death inhibitors . Nature 410, 33-34.
Phillips, L.S., Harp, J.B., Goldstein, S., Klein, J. and Pao, C.-I. (1990) Regulation and action of insulin-like growth factors at the cellular level.Proceedings of the Nutrition Society49, 451–8.
Reeds, P .J. and Fiorotto, M.L. (1990) Growth in perspective. Proceedings of the Nutrition Society49, 411–20.
Renehan AG, Booth C, Potten CS ( 2001) What is apoptosis , and why is it important? British Medical Journal 322, 1536-8
Schott, G.D. (1992) The extent of man from Vitruvius to Marfan. Lancet340, 1518–20.
Shirin H, Moss SF ( 1998) Helicobacter pylori induced apoptosis . Gut 43, 592-594.
Strasser A, O’Connor L, Dixit VM ( 2000) Apoptosis signalling Annual Review Biochemistry 69, 217-45.
Symonds, M.E. (1996) Regulatory factor in the control of development and maturity. Proceedings of the Nutrition Society55, 519–70.
Thompson EB ed ( 1998) Apoptosis Annual Review Physiology 60, 525-666
Walker, A.R.P, Walker, B.E, Glatthaar, I.I. and Vorster, H.H. (1994) Maximum genetic potential for adult stature that is aimed as desirable.Nutrition Review52, 208–15.
Waterlow, J.C. (1961) The rate of recovery of malnourished infants in relation to the protein and calorie levels of the diet. Journal of Tropical Pediatrics7, 16–22.
Watson WH, Cai J. Jones DP ( 2000) Diet and apoptosis. 20 485-505
Whitfield J ( 2001) All creatures great and small. Nature 413, 342-44
Wright, N.A. (1992) in Oxford Textbook of Pathology (eds J.O’D. McGee, P .G. Isaacson and N.A. Wright), Oxford University Press, Oxford.


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