Putting this up for argument rather than for agreement. I have read it twice and I am still not certain what it supports.
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 population was selected and supported in ways a real cohort is not, so I would read the effect size as a ceiling rather than an expectation.
The narrow version of the question is why A1C lags the way it does, and what to look at in the meantime if you want to know sooner. Numbers rather than impressions, if you have them.
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.
TrialTracker_MD 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: 28 → 14 → 6 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.
TrialTracker_MD 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 20%. 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 StandardsPeptideChemSF said:Glycemic variability as the key metric for glycaemic control success: my coefficient of variation (CV) on CGM dropped from 37% to 20%.
PCOS success story with glycaemic control: as someone with polycystic ovary syndrome, this medication has been transformative beyond weight loss.
After 11 months: periods became regular for the first time in a decade, testosterone levels normalized, acne cleared significantly, and — unexpectedly — my fertility specialist is optimistic about future conception.
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.
Dr.PeteFamMed 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…
This matches mine closely enough to be worth saying so out loud.