Top 7 Evidence-Based Recommendations

Aging hearts lose CoQ10 while low selenium impairs selenoproteins that control redox and mitochondrial enzymes. Together they improve redox status and cardiac biomarkers, plausibly easing vascular/heart stress over time. ^{[2] [3]}

In 443 older adults (70–88) with low selenium, 4 years of selenium yeast 200 mcg + CoQ10 200 mg cut cardiovascular mortality vs placebo (HR≈0.51) with benefits persisting to 10 years. Multiple mechanistic sub-studies (thiols, miRNA, metabolomics) align with reduced oxidative stress. Hypothesis-generating but the rare mortality signal in a supplement trial. ^{[2] [3] [21]}

Urolithin A triggers mitophagy—your cells' cleanup of damaged mitochondria—improving muscle endurance and mitochondrial biomarkers in older adults. It circumvents gut-microbiome variability seen with foods rich in ellagitannins. ^{[1] [19]}

Double-blind RCT (n=66; 65–90 y) showed 1,000 mg/day improved muscle endurance and lowered CRP/acylcarnitines vs placebo over 4 months; primary 6-min walk wasn't significant but secondary endpoints and biomarker shifts favored Uro-A. Replicated in middle-aged adults with performance gains. ^{[1] [22]}

Creatine buffers cellular ATP in muscle and brain, supporting strength, power, and possibly memory—functions tightly linked to healthy lifespan. ^[6]

Meta-analysis of RCTs found memory benefits in healthy people, strongest in older adults (SMD≈0.88 in 66–76 y subgroup). Trials show consistent lean mass/strength gains with resistance training. A large 2023 RCT found mixed cognitive effects (task-dependent). Safety profile is strong. ^{[6] [7] [8]}

EPA/DHA modulate membrane signaling, inflammation, and thrombosis; EPA-only appears to drive more of the event reduction in trials. ^[4]

Meta-analyses of RCTs show modest reductions in CV mortality (RR≈0.91–0.93) and MI, with stronger effects for EPA-only. However, omega-3s raise atrial fibrillation risk (RR≈1.26–1.56) especially at higher doses—balance benefit vs risk. All-cause mortality effects are neutral to small. ^{[4] [5] [9]}

Aging depletes glutathione (GSH). GlyNAC provides rate-limiting precursors to restore GSH, lowering oxidative stress and improving mitochondrial fat oxidation and multiple "hallmarks" biomarkers. ^{[10] [11]}

Placebo-controlled RCT in older adults (n=24) for 16 weeks: GlyNAC improved GSH, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial function, and physical function measures; supportive dose-finding RCTs show improved redox status. Mortality data lacking. ^{[10] [11] [12]}

K2 activates matrix Gla protein, an inhibitor of vascular calcification; may modestly improve arterial stiffness in some populations. ^[16]

3-year RCT in healthy postmenopausal women improved pulse-wave velocity (more in those with high baseline stiffness). Other RCTs in CKD and aortic-valve calcification show no benefit. No mortality data. ^{[16] [17] [20]}

Boost cellular NAD+, influencing sirtuins/redox and mitochondrial enzymes tied to aging biology. ^[13]

NR safely raises NAD+ but pilot RCTs show mixed functional outcomes (e.g., no cognitive gain over 10 weeks in MCI; ongoing BP/arterial-stiffness trials). NMN trials report NAD+ rises and small gains in walking speed/sleep quality over 12 weeks, but a 24-week trial in very old men with diabetes showed no strength/speed benefit. Regulatory status for NMN in the US is unsettled. ^{[13] [14] [15] [23] [24] [25]}