The markers in the cardiovascular panel carry strong evidence. Lipoprotein(a) is a genetically determined, causal risk factor for atherosclerotic disease and aortic stenosis that a standard lipid panel does not measure, and the European Atherosclerosis Society recommends measuring it at least once in every adult (Kronenberg et al., Eur Heart J, 2022). C-reactive protein concentration is associated with coronary heart disease, stroke and vascular mortality independently of conventional risk factors in a meta-analysis of individual data from 54 cohorts (Emerging Risk Factors Collaboration, Lancet, 2010). Ultrasound assessment of carotid plaque predicts future coronary events more accurately than intima-media thickness alone, which is why the carotid examination looks for plaque and not only for wall thickness (Inaba et al., Atherosclerosis, 2012). Fasting insulin and glucose give the HOMA index of insulin resistance, a model in use since 1985 (Matthews et al., Diabetologia, 1985). The omega-3 index, the share of EPA and DHA in red cell membranes, was proposed as a risk factor for death from coronary heart disease on the basis of cohort and trial data (Harris et al., Prev Med, 2004).
The immune and aging markers carry moderate to emerging evidence. In a Japanese general-population cohort followed for eleven years, medium and high natural killer cell cytotoxic activity was associated with lower cancer incidence and low activity with higher incidence (Imai et al., Lancet, 2000). DNA methylation clocks estimate age across tissues with high accuracy (Horvath, Genome Biol, 2013) and are the basis of the biological age markers in the Longevity Deep Dive.
What the evidence does not show: no trial has demonstrated that lowering an epigenetic clock value, or raising NK cell activity, reduces disease incidence, so these results are reported as markers and the plan rests on the cardiovascular, metabolic and immune findings with established treatment paths.