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Metabolic estimate: method & sources

This page explains where Stay at Zero’s soft phases and orienting fat / ketones / glycogen bars come from. The model is informed by human fasting physiology in the literature, but it remains a product estimator — not a lab measurement and not medical advice.

Model limits

Explicitly:

  • We do not measure blood glucose, blood ketones, or liver glycogen.
  • We do not diagnose clinical ketosis, diabetes, or any disease.
  • Phase labels (e.g. Fat Burning, Ketosis) are soft UI labels tied to scores — not biological switches “after X hours”.
  • Glycogen in the UI is relative (dimensionless), not mmol/L.
  • Output depends on the fasting/eating history in the app; missing accurate carbohydrate and activity inputs increases uncertainty.

What the literature supports (orientation)

These human-study observations motivate a soft model rather than a rigid hourly clock:

  • The “metabolic switch” — a shift from glycogen-based energy toward fatty acids and ketones — is typically described in intermittent-fasting reviews after liver glycogen is depleted, often around ~12 hours and beyond, with large person-to-person spread. [1]
  • Even in the first day of fasting, gluconeogenesis already contributes a large share of glucose production; hepatic glycogenolysis does not cover the whole need. After ~22 hours, gluconeogenesis can account for most glucose production. [2]
  • Adipose triglyceride mobilization rises markedly between ~18 and 24 hours of fasting in healthy men — which is why the UI emphasizes rising fat utilization in that window without promising “100% fat burning”. [3]
  • In prolonged fasting, the body relies increasingly on ketone bodies as fuel (including for the brain) — classical starvation physiology, not a marketing shortcut of “ketosis after 16h”. [4][5]

Method in Stay at Zero (v1)

The scorer does not map `fasting_hours → phase`. It builds soft states from in-app fasting activity history:

  1. Inputs (v1): fasting duration, ~48 h rolling fast/eat history, optionally body mass and activity signals when available; per–eating-segment carbohydrate is planned expansion.
  2. Intermediate state: a relative liver-glycogen estimator (dimensionless), with older events decaying inside the window.
  3. Outputs: 0–100 scores (fat utilization, ketosis likelihood, glycogen) plus soft timer phase labels coupled to those scores and the fast goal.
  4. Snapshot: when a fast closes, the app freezes phase segments plus the scorer version for statistics.

Scorer math is an internal product specification; this page states assumptions and sources, not a claim of clinical accuracy.

How to read the UI

Intent mapping (not diagnostics):

UI signal Meaning
Fat (high) Rising likelihood that fat oxidation dominates — especially around 18–24 h in short-term fasting studies [3].
Ketones (high) Rising likelihood of ketogenesis as the fast deepens [1][4][5] — not a ketone-strip reading.
Glycogen (low) Relative depletion of the model glycogen store; in studies hepatic glycogen falls during fasting but with wide between-person range [2].
Phase labels Anabolic → Catabolic → Fat Burning → Ketosis → Deep Ketosis as soft UI, clipped to the goal — not fixed hour wedges.

References

Primary sources (DOI). Numbers in the text match the list below.

  1. Anton SD, et al. Flipping the Metabolic Switch: Understanding and Applying the Health Benefits of Fasting. Obesity (Silver Spring). 2018;26(2):254–268. DOI · PubMed
  2. Rothman DL, Magnusson I, Katz LD, Shulman RG, Shulman GI. Quantitation of hepatic glycogenolysis and gluconeogenesis in fasting humans with 13C NMR. Science. 1991;254(5031):573–576. DOI · PubMed
  3. Klein S, Sakurai Y, Romijn JA, Carroll RM. Progressive alterations in lipid and glucose metabolism during short-term fasting in young adult men. Am J Physiol. 1993;265(5 Pt 1):E801–E806. DOI · PubMed
  4. Cahill GF Jr. Fuel metabolism in starvation. Annu Rev Nutr. 2006;26:1–22. DOI · PubMed
  5. Owen OE, Felig P, Morgan AP, Wahren J, Cahill GF Jr. Liver and kidney metabolism during prolonged starvation. J Clin Invest. 1969;48(3):574–583. DOI · PubMed

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