I’m looking to sanity-check something I’ve been running into and would love input from anyone who’s dug into glycation physiology beyond surface-level HbA1c interpretation.
My HbA1c consistently comes back around ~5.3%, which on paper looks higher than expected. However, this conflicts with nearly every other metabolic signal I have:
CGM data over 2 weeks glucose 71mg/dl, low post-prandial excursions, blood work fasted insulin .4uIU/ml and 74mg/dl fasted.
Lipoprotein insulin sensitivity markers: small LDL-P low, favorable particle size
Body composition: lean, physically active, resistance + cardio trained
Diet: controlled calories, high protein, moderate carbs (primarily peri-workout), low sugar intake
Lifestyle: time-restricted feeding, consistent training, good cardiovascular markers
In short, nothing else suggests impaired glucose handling.
Question:
How much weight should HbA1c carry in isolation when red blood cell (RBC) lifespan, turnover rate, or glycation kinetics may differ from population averages?
Are there mechanistic or clinical arguments for longer RBC lifespan (or slower clearance of glycated hemoglobin) contributing to a falsely elevated A1c despite low ambient glucose exposure?
How often do you see discordance between A1c and CGM / insulin sensitivity markers in metabolically healthy, highly active individuals?
In these cases, what secondary markers do you personally trust more:
CGM averages & glucose
Fasting insulin
I’m not trying to “explain away” data. Just trying to figure out whether A1c is reflecting true glycemic exposure in my case, or whether RBC biology is skewing the signal.
Would love thoughts, papers, or real-world clinical experience where A1c didn’t tell the full story. Also for more context. I was using Mots-c 5mg 3 times a week, slupp-332 250mcg for 6 weeks. Also continues retatrutide 1mg once a week.