Tracking Biomarkers of Aging
by Mike Lustgarten, Ph.D. February 18, 2022
Aging and disease are biochemical processes that happen over many decades – if we track well established markers of organ and systemic function, can aging and disease risk be minimized, thereby extending lifespan? That’s the central premise of my approach for optimizing health and longevity.
The basics for tracking include blood biomarkers that have been studied for 50 – 100+ years, depending on the biomarker. Most of these biomarkers are commonly measured at a yearly physical, and are relatively cheap (< 35 $USD for the standard chemistry panel and complete blood count).
They include markers of kidney function (creatinine, BUN, uric acid), liver function (ALT, AST, albumin, alkaline phosphatase), red blood cells and their related measures (MCV, RDW), immune cells (neutrophils, lymphocytes, monocytes), the lipid panel (total cholesterol, triglycerides, HDL, LDL), glucose, and others as primary measures.
It’s well known how these biomarkers change during aging, and their association with all-cause mortality risk, but randomized controlled trials (RCTs) aimed optimizing them while young, and then doing that for as long as possible don’t yet exist as a strategy for optimizing health and potentially, longevity.
We don’t have to wait for RCTs to inform about whether this approach is beneficial or not. We can actively track and optimize these biomarkers now, as many companies exist that allow for both at-home and in-person testing at commercial labs (LabCorb and Quest as examples). Even better, a physician doesn’t need to sign off on these tests-they can be ordered online. In other words, we have access to the tools (blood biomarkers) that can be used to optimize our health.
The biggest issue is, how can one optimize each of these biomarkers simultaneously, and not just in isolation (i.e. only glucose or the lipid panel, while ignoring the data for the others). Note that when I say, “optimize”, that doesn’t mean to get one’s data to exist within the reference range, which is not listed on a lab report with the goal of optimizing health, but rather, it’s there as a signal for an increased risk of disease. More specifically, an optimal range that is more narrow than the reference range exists for each of these biomarkers, and I have many videos on my YouTube channel that present those data.
A combination of diet, exercise, and supplements can be used to optimize levels of these biomarkers. I carefully track each of these variables, using a food scale and an online nutrition-tracking app to quantify macronutrients, micronutrients, and individual foods, a fitness tracker to quantify cardiovascular fitness-related metrics, and I also quantify daily supplemental intake.
By recording these data over a long period of time in conjunction with many blood tests, one can optimize not only the blood biomarkers toward a profile of youth and decreased all-cause mortality risk, but in the process, can personalize their nutrition beyond a simple dietary ideology (i.e. vegan, vegetarian, carnivore, omnivore, etc.). Use of this approach allows for the identification of the diet composition that may be ideal at the individual level.
Similarly, tracking regular fitness metrics like heart rate variability (HRV) and the resting heart rate (RHR) with a fitness tracker can help optimize not only cardiovascular fitness, but one’s overall exercise program, including how often, for how long (i.e. workout duration), and the intensity of each workout.
Last, use of supplements is generally included in the anti-aging approach because they improved some health-related metric or longevity in animal models or RCTs, but by tracking daily supplemental intake, one can determine if the supplement has a net neutral, positive, or negative effect on the blood biomarkers.
For example, through rigorous tracking, after seeing that my blood homocysteine levels were higher than optimal, with use of this approach, I discovered that trimethylglycine, folate, and B6 were not significantly correlated, whereas methyl-B12 was significantly correlated with lower homocysteine. Accordingly, with the goal of reducing homocysteine, I stopped supplementing with trimethylglycine, folate, and B6, while including methyl-B12 in my approach.
If we’re chronologically old, but biologically young based on these (and other blood biomarkers), are we really our chronological age, or some younger age?
