This gets cited here weekly, usually second-hand, so it is worth setting out what it does and does not establish.
HbA1c reflects roughly three months of average glycaemia weighted toward the most recent weeks, which is why repeating it at six weeks tells you very little. The improvement on this class comes from two directions — direct glucose-dependent insulin secretion and glucagon suppression, plus the indirect effect of weight loss on insulin sensitivity — and the second continues after the first has plateaued.
Where I think it is weakest: the completion rate deserves as much attention as the headline, because a large effect among those who finished is a different claim from a large effect among those enrolled.
So the question, as narrowly as I can put it: why A1C lags the way it does, and what to look at in the meantime if you want to know sooner. Not looking for reassurance. Looking for the part I have got wrong.
Figures above are from the primary publication rather than the press summary. If a number here disagrees with one you have, post yours and we will work out which of us is reading a secondary source.
JessicaH_TX said:HbA1c reflects roughly three months of average glycaemia weighted toward the most recent weeks, which is why repeating it at six weeks tells you very…
Fasting insulin is the lab my functional medicine doctor cares about most for glycaemic control: it's a much earlier marker of metabolic dysfunction than glucose or A1C.
My fasting insulin: 30 → 12 → 7 uIU/mL over 9 months. Target is <7. By the time your fasting glucose is elevated, your insulin has been elevated for YEARS trying to compensate.
Ask your doctor to include fasting insulin in your bloodwork panel. It's cheap (~$20) and incredibly informative.
JessicaH_TX said:HbA1c reflects roughly three months of average glycaemia weighted toward the most recent weeks, which is why repeating it at six weeks tells you very…
Glycemic variability as the key metric for glycaemic control success: my coefficient of variation (CV) on CGM dropped from 37% to 21%. Target is <36%, with <30% being ideal.
Why this matters more than average glucose: large glucose swings cause oxidative stress, endothelial damage, and promote advanced glycation end-products (AGEs). A flat glucose line at 95 mg/dL is metabolically healthier than oscillating between 60 and 160, even if the average is the same.
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Shop Reference StandardsHPLC_Greg said:Glycemic variability as the key metric for glycaemic control success: my coefficient of variation (CV) on CGM dropped from 37% to 21%.
PCOS success story with glycaemic control: as someone with polycystic ovary syndrome, this medication has been transformative beyond weight loss.
After 12 months: periods became regular for the first time in ever, testosterone levels normalized, acne cleared significantly, and — unexpectedly — my hormonal symptoms have almost completely resolved.
GLP-1 agonists address the insulin resistance at the root of PCOS. For PCOS patients, this isn't "just" a weight loss drug — it's treating our underlying metabolic dysfunction.
LipidDoc_ATL said:Fasting insulin is the lab my functional medicine doctor cares about most for glycaemic control: it's a much earlier marker of metabolic dysfunction…
Mine went the same way, slower. I had assumed I was the exception until I read this.