Estimated Average Glucose (eAG)
Glucose Metabolism marker
Estimated Average Glucose
Estimated Average Glucose (eAG)
Average blood glucose over the preceding 2-3 months, calculated directly from HbA1c. Expresses long-term control in the same units as a finger-prick reading rather than as a percentage.
PED Notes
Not an independent measurement. eAG is derived arithmetically from HbA1c (eAG in mmol/L = 1.59 x HbA1c% - 2.59), so it carries every limitation HbA1c has and adds none of its own information. That matters for enhanced athletes because AAS-driven erythrocytosis, frequent blood donation, and shortened red cell survival all falsely lower HbA1c and therefore falsely lower eAG. Growth hormone, MK-677, and high-dose insulin users can show a deceptively reassuring eAG while running genuinely high post-meal glucose. If insulin resistance is the question, fasting insulin, HOMA-IR, or a CGM will tell you far more than eAG will.
When high
Raised eAG (corresponding to HbA1c above 5.7%):
- Confirm HbA1c is trustworthy first -- recent blood donation, therapeutic phlebotomy for high haematocrit, or any haemolysis makes both HbA1c and eAG read falsely low, so a raised value despite those factors is more concerning, not less
- Add fasting insulin and HOMA-IR -- these detect insulin resistance months to years before HbA1c moves
- Consider a CGM for 2 weeks -- the single most informative step, showing post-meal excursions that an averaged value hides
Compound-related contributors:
- Growth hormone and MK-677 -- both reliably induce insulin resistance; MK-677 in particular raises fasting glucose within weeks. Reduce dose, shift GH to a lower daily dose, or cycle off
- Exogenous insulin misuse -- paradoxically worsens control through weight gain and receptor downregulation
- Oral AAS -- worsen insulin sensitivity more than injectables at equivalent doses
Supplements:
- Berberine -- 500mg 2-3x/day with meals; comparable to metformin in several head-to-head trials
- Myo-inositol -- 2-4g/day; improves insulin signalling
- Magnesium -- 300-400mg/day; deficiency impairs insulin sensitivity
- Chromium picolinate -- 200-400mcg/day; modest effect, strongest where intake is deficient
Pharmacological options (physician-supervised):
- Metformin -- 500-2000mg/day; first-line, reduces hepatic glucose output; the standard choice for GH-induced insulin resistance
- GLP-1 agonists (semaglutide, tirzepatide) -- powerful glycaemic and weight effects; increasingly used alongside GH protocols
- Acarbose -- 50-100mg with meals; blunts post-meal spikes specifically
Non-pharmacological:
- Post-meal walking -- 10-15 minutes after eating meaningfully blunts glucose excursions
- Resistance training -- increases GLUT4-mediated glucose disposal independent of insulin
When low
Low eAG:
- Usually reflects a low HbA1c rather than genuine hypoglycaemia. In enhanced athletes the common causes are shortened red cell survival from erythrocytosis, recent blood donation, or therapeutic phlebotomy, all of which make HbA1c and eAG read artificially low.
- If you use exogenous insulin, a genuinely low average with hypoglycaemic episodes is dangerous. Reassess dosing with a physician and use a CGM.
- Check for haemolysis and iron status -- haemolytic anaemia and recent transfusion both distort the result.
Interpretation:
- eAG of 6.5 mmol/L corresponds to HbA1c 5.7%, the threshold for prediabetes.
- eAG of 7.8 mmol/L corresponds to HbA1c 6.5%, the diagnostic threshold for diabetes.
- Because eAG is a direct transformation of HbA1c, do not treat agreement between the two as independent confirmation of anything.
History Chart
Reading History
Frequently Asked Questions
Reference Ranges
Standard Range
VitalMetrics Range