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.