Carogero Caruso, Professor of Biopathology and Biomedicine at the University of Palermo in Italy, has found a link between high levels of anti-inflammatory cytokine InterLeukin-10 (IL-10) and longevity.

Professor Caruso, whose research is published in this month's Journal of Medical Genetics, said: "Longevity is definitely more easily controlled by those who can counter inflammatory disease."

Long term low grade inflammation has has been linked to the development of a large assortment of degenerative and chronic illnesses. Anti-inflammatory drugs have been found to decrease the incidence of heart disease, cancer (both breast cancer and colon cancer), and other illnesses. Therefore it is not too surprising to find that people who live longer have more anti-inflammatory IL-10 and less inflammation promoting hormone TNFa.

To investigate this further, the research team examined the frequency of genes coding for IL-10 and TNFa in 72 men and 102 women, all of whom had reached the age of 100. Similar DNA testing was also carried out in 115 men and 112 women aged between 22 and 60.

The results showed that significantly more centenarian men expressed genes encoding for high levels of the anti-inflammatory IL-10 than did younger men, although there were no differences in the levels of the pro-inflammatory TNFa among the various age groups.

And significantly more centenarian men expressed genes for the combination of high IL-10 and low TNFa production than did their younger peers. There were no differences in levels of the cytokines, either separately or in combination, among the women.

This latest work builds on previous work by Caruso's group showing that there is a genotypic variation that increases IL-10 production and is associated with longevity.

The presence of -1082GG genotype, suggested to be associated with high IL-10 production, significantly increases the possibility to reach the extreme limit of human lifespan in men. Together with previous data on other polymorphic loci (Tyrosine Hydroxylase, mitochondrial DNA, IL-6, haemochromatosis, IFN-), this finding points out that gender is a major variable in the genetics of longevity, suggesting that men and women follow different strategies to reach longevity. Concerning the biological significance of this association, we have not searched for functional proves that IL-10 is involved. Thus, we should conclude that our data only suggest that a marker on 1q32 genomic region may be involved in successful ageing in man. However, recent data on IL-6 and IFN- genes suggest that longevity is negatively associated with genotypes coding for a pro-inflammatory profile. Thus, it is intriguing that the possession of -1082G genotype, suggested to be associated with IL-10 high production, is significantly increased in centenarians.

This latest result is another example of how inflammation response affects longevity. Yet another example is the recently discovered link between Parkinson's Disease and COX-2 enzyme levels. Many of the newer non-steroidal anti-inflammatory drugs (NSAIDs), such as Celebrex and Vioxx, work by blocking just the COX-2 enzyme while the older generation NSAIDs inhibit both COX-1 and COX-2 enzymes. It is possible that COX-2 inhibitors may delay the development of Parkinson's Disease. More generally, expect to see a continued stream of reports on the results of studies that investigate how anti-inflammatory hormones and drugs slow or prevent a number of diseases of old age.