4. Discussion
inflammation, heart failure, death, fibrosis
ISCHAEMIC HEART DISEASE, INFLAMMATION, FIBROSIS, HEART FAILURE, ADHESION, INFLAMMATION, PATHOLOGICAL PROCESSES, OXIDATIVE STRESS, ENDOTHELIAL DYSFUNCTION
In this study, using data at inclusion, we examined the relationship to age of five biomarkers, all with an alleged involvement in the ageing process. While only ICAM-1 and adiponectin were significantly related to age, the biomarkers were differently related to other biomarkers of pathological processes, such as oxidative stress, fibrosis, inflammation and endothelial dysfunction. In order to seek alternative evaluation paths, we also applied SEM analysis to the five evaluated biomarkers. Our research group has used SEM modelling in previous publications [Hence, our results support the notion that no single biomarker mirrored the biological age, but the biomarkers were differently associated with pathological processes related to ageing, as summarised in the SEM analysis. Inflammation, which is an important aspect of ageing [ICAM-1 was also significantly reduced in the active treatment group and significantly changed relative to the placebo group. This may indicate a protective effect of the intervention on pro-inflammatory processes mediated via inflammation and oxidative stress and potentially also ageing. Several reports also indicate a broader influence of ICAM-1. It has also been shown that there is an association between the concentration of ICAM-1 in young individuals and cardiac function later in life [The adiponectin levels increased during the four years of the intervention, especially in the placebo group. Our results fit with a study by Beatty et al., reporting that in patients with ischaemic heart disease, those with a higher concentration of adiponectin suffered a significantly higher risk of developing heart failure and death, compared to those with a lower concentration [The leptin concentration was significantly lower in the active treatment group compared to the placebo group, indicating protective mechanisms of the intervention, potentially mediated via its anti-oxidative properties, as also observed by others [SCF, which is a growth factor for haemopoietic progenitor cells, regulates mast cell differentiation and B-cell growth and modulates cell adhesion [It has also been reported that the overexpression of microRNA-122 leads to cardiac fibrosis, among other effects through increased inflammation and fibrosis [From these results, it is an attractive hypothesis that the supplementation might also slow down the ageing process, even if this is not shown per se. However, the previously reported effects on IGFBP-1 by our group [As discussed above, inflammation is one of the major components of the ageing process. Our group has previously reported a significant reduction in six inflammatory biomarkers following supplementation with selenium and coenzyme QAnother aspect of the ageing process in the CV system is increased fibrosis [We recently published results from evaluations of SIRT1, which is a member of the sirtuin family. SIRT1 has been shown to possess anti-inflammatory and anti-oxidative properties, and it also influences genome stability [Finally, in the literature, much attention has been paid to the length of telomeres and their relation to biological age, even though other factors also influence their rate of attrition [We revealed a significant correlation between all but one of the selected biomarkers and age. In contrast to other reports from the literature, leptin did not present a statistical relation to age in this evaluation. This might be a result of the narrow age span (17 years) in our population. Despite this, the other four biomarkers presented significant associations.In summary, this and previous studies might indicate that individuals with low selenium status are at risk of an accelerated ageing process, i.a., due to an inflammatory state and oxidative stress. With selenium and coenzyme Q