The relationship between abdominal obesity and serum α-Klotho levels has gained increasing attention, particularly as it intersects with the systemic immune-inflammation index (SII), which could help explain the underlying mechanisms of aging.
Recent findings from researchers analyzing data from 6,997 middle-aged and elderly Americans participating in the National Health and Nutrition Examination Surveys (NHANES), conducted between 2011 and 2016, reveal significant correlations between abdominal obesity—measured through the weight-adjusted waist index (WWI)—and reduced serum α-Klotho levels. This transmembrane protein has been recognized as having anti-aging properties, but its interactions with obesity and inflammation needed more clarity.
Alpha-Klotho, encoded by the Klotho gene, plays various roles, including suppressing aging and protecting against age-related diseases. Studies indicate individuals with obesity tend to have lower serum α-Klotho concentrations. Yet inconsistencies exist, often tied to the methodologies used to assess obesity, leading researchers to seek more accurate measures like WWI.
WWI, which controls for weight to focus on central obesity, emerged as a more precise marker compared to traditional body mass index (BMI). The findings showed a substantial negative correlation: for each increase of 0.25-fold in WWI, participants experienced about a 7.79% decrease in α-Klotho levels.
Examining the role of inflammation, the study found SII, derived from blood components such as neutrophils and lymphocytes, to serve as a significant mediator of the relationship between abdominal obesity and Klotho levels. Notably, SII accounted for roughly 11.6% of the total effect of WWI on α-Klotho concentrations, with its effect more pronounced among participants aged 60 years or older, exhibiting mediation of 26.3% compared to just 4.2% for those under this age.
These insights point to systemic inflammation as central to how abdominal obesity might influence aging markers like α-Klotho, highlighting not just individual health but broader public health challenges linked to aging populations. The significant impact of obesity-driven inflammation on aging-related pathways posits a compelling rationale for interventions targeting weight and inflammatory markers to promote healthier aging.
While this research lays important groundwork, limitations remain, particularly around the cross-sectional nature of the data, which does not establish causality. Future studies will be necessary to ascertain these relationships and their broader applicability across diverse populations.
Overall, the evidence suggests strategies aimed at managing obesity and its inflammatory consequences may yield health benefits through the maintenance or elevation of α-Klotho levels, significantly for older adults.