We have spent thousands of hours across aging research, clinical literature, and expert interviews. This is the distilled version: the markers that actually matter, the context standard care never provides, and the evidence-backed changes that move the needle on how well you age.
Start here: three free things you can do today
- Build cardiorespiratory fitness three times a week. Low fitness is a stronger predictor of all-cause mortality than smoking, hypertension, or diabetes in the largest study to test it.
- Eat enough protein, 1.2 to 2g per kg of body weight, unless you have kidney disease. It is the most consistent dietary association with preserved muscle mass after 50.
- Eat inside an 8 to 10 hour window. Associated with lower fasting insulin and reduced inflammatory signaling, and longer windows activate autophagy.
A few choices a day, most at no cost. The full 90-day plan below turns these into a routine you can keep.
Source: Mayo Clinic and CDC
Why this matters
Standard care measures whether you have developed a disease yet. Longevity research measures something different: how fast you are aging, across which systems, and why. Chronological age is your birthday. Biological age is what your cells, markers, and systems reflect about how quickly you are aging. Two people who are both 50 can have markers that look 10 years apart.
James Fries introduced the compression of morbidity hypothesis in 1980: the objective is to compress the period of decline into as short a window as possible at the end of a long life. Forty years of research since have built a measurable framework around that idea. The 2013 Lopez-Otin paper named nine hallmarks of aging, from genomic instability and telomere attrition to deregulated nutrient sensing and cellular senescence, and gave the field a mechanistic map of what is actually changing under the surface.
The markers that matter
ApoBOptimal below 60 mg/dL · Standard below 100 mg/dL
In plain English. Apolipoprotein B, the protein that coats every atherogenic particle, a direct measure of cardiovascular risk.
Apolipoprotein B is the protein that coats every atherogenic particle, so it counts particles rather than estimating cholesterol mass the way LDL does. That makes it a more direct measure of cardiovascular longevity risk. The gap between "not at clinical risk" and longevity-optimal is 40 points on this marker. In the longevity research framework, each 30 mg/dL reduction in ApoB is associated with a meaningful reduction in cardiovascular event risk. Atherosclerosis is one of the four horsemen of aging, and ApoB is the marker that tracks it earliest.
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Your whole body, on one timeline.
Every lab, every wearable, every check-in, tracked over the years and read as a system.

