Format

Send to

Choose Destination
See comment in PubMed Commons below
Nutr Res Rev. 2000 Jun;13(1):3-29. doi: 10.1079/095442200108728981.

Undernutrition, infection and immune function.

Author information

1
Institute of Human Nutrition, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. pcc@sotone.ac.uk

Abstract

Undernutrition and infection are the major causes of morbidity and mortality in the developing world. These two problems are interrelated. Undernutrition compromises barrier function, allowing easier access by pathogens, and compromises immune function, decreasing the ability of the host to eliminate pathogens once they enter the body. Thus, malnutrition predisposes to infections. Infections can alter nutritional status mediated by changes in dietary intake, absorption and nutrient requirements and losses of endogenous nutrients. Thus, the presence of infections can contribute to the malnourished state. The global burden of malnutrition and infectious disease is immense, especially amongst children. Childhood infections impair growth and development. There is a role for breast-feeding in protection against infections. Key nutrients required for an efficient immune response include vitamin A, Fe, Zn and Cu. There is some evidence that provision of the first three of these nutrients does improve immune function in undernourished children and can reduce the morbidity and mortality of some infectious diseases including measles, diarrhoeal disease and upper and lower respiratory tract infections. Not all studies, however, show benefit of single nutrient supplementation and this might be because the subjects studied have multiple nutrient deficiencies. The situation regarding Fe supplementation is particularly complex. In addition to immunization programmes and improvement of nutrient status, there are important roles for maternal education, improved hygiene and sanitation and increased supply of quality water in the eradication of infectious diseases.

PMID:
19087431
DOI:
10.1079/095442200108728981
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Cambridge University Press
    Loading ...
    Support Center