Inflammatory response in the elderly.

PURPOSE OF REVIEW

During ageing there may be the onset of a chronic inflammatory state. This review examines the underlying causes of this phenomenon and the role that genotype plays in its intensity.

RECENT FINDINGS

There are predisposing factors for the chronic inflammation that occurs during ageing. These include increased oxidative stress, a decrease in ovarian function, a decrease in stress-induced glucocorticoid sensitivity of pro-inflammatory cytokine production in men, and an increased incidence of asymptomatic bacteriuria. Obesity induces chronic inflammation. Inflammation is a key factor in the progressive loss of lean tissue and impaired immune function observed in ageing. Polymorphisms in the promoter regions of pro- and anti-inflammatory cytokine genes influence the level of cytokine production and the ageing process. Thus, a genotype for high pro-inflammatory cytokine production results in high cytokine production and may accelerate the rate of tissue loss. Conversely, polymorphisms in the genes for anti-inflammatory cytokines may result in a slowing of tissue loss. In the healthy aged male population, the former polymorphisms are under-represented and the latter over-represented, indicating a genetically determined survival advantage in maintaining inflammation at a low level. Nutrients with anti-inflammatory properties, such as vitamin E and n-3 polyunsaturated fatty acid, may reduce the level of chronic inflammation and thereby ameliorate tissue and functional loss during ageing. New evidence suggests that, for the latter nutrient, gene-nutrient interactions occur that alter the effectiveness of dietary therapy.

SUMMARY

Ageing is associated with increased levels of chronic inflammation. This plays a major role in the decline in immune function and lean body mass. Anti-inflammatory nutrient therapy may slow the rate of decline. The pro- and anti-inflammatory cytokine genotype is linked negatively and positively, respectively, with life-span, because of its influence on inflammation.