Hypothesis

A structured, single‑variable self‑experiment that aligns timed carbohydrate restriction with nocturnal HRV peaks will reduce epigenetic age acceleration (GrimAge) in healthy adults over a 12‑week period.

Mechanistic Rationale

Circadian‑gated nutrient sensing modulates mTOR and AMPK activity, influencing mitochondrial ROS production and NAD+ levels. These metabolic shifts affect DNA‑methyltransferase activity, thereby altering the pace of epigenetic clocks. HRV reflects vagal tone, which inversely correlates with systemic inflammation; higher nocturnal HRV predicts lower IL‑6 and TNF‑α, creating a milieu that favors maintenance of youthful methylation patterns. By restricting carbohydrates to the early active phase and tracking glucose, sleep, and HRV, we create a closed loop where the dependent variable (epigenetic age) is driven by a causally linked upstream metabolic signal.

Methodology

1. Identify testable hypothesis – Carbohydrate intake confined to 08:00‑14:00 lowers GrimAge acceleration.
2. Baseline – Collect 2 weeks of glucose, sleep, HRV (wearable), and a blood sample for GrimAge.
3. Intervention – 12 weeks of time‑restricted feeding (TRF) with ≤30 g carbs outside the window, adhering to a sleep schedule ≥7 h.
4. Tracking – Continuous glucose monitor for post‑prandial peaks, nightly HRV average, sleep duration; log meals, stressors, light exposure.
5. Compliance – Defined as ≥90 % of days with carbs outside the window <10 % and nightly HRV ≥ baseline; deviations >20 % trigger a protocol review.
6. Follow‑up – After week 12, repeat GrimAge measurement and compare to baseline.
7. Analysis – Use a Bayesian change‑point model to estimate the posterior distribution of GrimAge shift; compute the probability that the change is ≤‑0.5 years (beneficial) and the region of practical equivalence (ROPE) set at [‑0.2, 0.2] years to assess trivial effects.

Predicted Outcomes & Falsifiability

• If the posterior probability of a ≥0.5‑year GrimAge reduction exceeds 0.8, the hypothesis is supported.
• If the 95 % credible interval includes zero or the ROPE probability >0.8, the hypothesis is falsified.

This design avoids common self‑tracking pitfalls by limiting variables, anchoring measurements to circadian context, and extending duration beyond the typical one‑month window, thereby moving from association to a testable causal claim within an n=1 framework.