#1

and more useful on that regard. it is also WAY more useful as an indicator of change in “good or bad” after intervention (whether dietary or through lots of taurine/carnosine/metformin). Kind of like oxidized LDL in this regard [also an indicator of recent change over the past few weeks], and can be reduced via taurine

Mine was:

  • FRUCTOSAMINE

(umol/L)

    • 268

Jun 2024

  • Range: 205-285

==
But this is really sad and high because it’s still unusually high even though I was frequently taking canagliflozin the week before and mostly stuck to beans and tomatoes (only healthy foods), albeit still a lot of carbs. and my weight has consistently been 95 (lower than it usually is) so my net calorie intake has been lower.
[i havent been boiling very many vegetables though even though i should]. primarilyi’ve been eating canned tomatoes and beans, and not so much real vegetables… Maybe I should switch more [I havent even used this instant pot yet

My average glucose has been 97 but fructosamine of 268 implies much much higher… (There is very high variation in the .4 correlation). But if I’m having nonenzymatic glycation at higher values…

Even the aginGSOS panel showed a lot of glycosylation in a background of otherwise super healthy values

I’m swapping out garbanzo for kidney beans and probably upping fat intake and will retake

3 Likes
#2

It sounds like you are getting some glucose spikes, even though your 97 gm/dL is decent.

Thoroughly cooking starchy veggies will increase digestion rate and increase average blood glucose, so for those veggies that can be eaten raw or undercooked, that’s better. Of course there can be anti-nutrient issues more often when you eat raw; sometimes it’s a can’t-win situation.

#3

Yeah I’ll have to get 1,6 AG

I have really really bad spikes in response to berries, contrary to everyone else. It sucks. I’ll have to replace them with peaches

Screenshot_20240613_183628_YouTube
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#4

I might test this next time, Fructosamine | Ulta Lab Tests

#5

Do you know where we can get glycated albumin tested?

#6
#7

Great, thanks a lot Alex.

#8

god i meant 1,5-Anhydroglucitol (1,5-AG)

1 Like
#9

tested again, 252 now

[this time i ate fewer berries/fruits]

====
On 10/22/2020 I got…

8 Glycated serum proteins (GSP) 273.0 µmol/L 100.0 - 260.0 µM

So this has always been an issue for me, borderline high issue…

These are the same units as fructosamine it makes me wonder if they’re almost the same, or if one explains more than 50% of the variance of the other. [looks like they might just be the SAME]…

#10

AGEs are formed by the degradation of fructosamine adducts, such as Nε-fructosyl-lysine (FL), of glucose-modified proteins and by the direct modification of proteins by reactive dicarbonyl metabolites, such as methylglyoxal. Examples of major AGEs quantitatively found in the clinical setting are: hydroimidazolone, MG-H1—formed by modification of arginine residues with methylglyoxal; and Nε-carboxymethyl-lysine (CML) – formed mainly by the oxidative degradation of FL residues. There is also a minor, trace level AGE protein crosslink with intense fluorescence called pentosidine, formed by the reaction of pentose metabolites with spatially close arginine and lysine residues. Protein glycation adducts exist in mainly two forms: glycation adduct residues of proteins – sometimes called “protein-bound” glycation adducts, and glycation free adducts or glycated amino acids. Glycation free adducts are formed mostly from proteolysis of endogenous glycated proteins with also a contribution from digestion of glycated proteins in food – as recently reviewed7. AGEs have long been considered as risk predictors of diabetic nephropathy and other microvascular complications of diabetes8. Analysis of skin collagen in patients with T1DM showed that a combination of AGEs and the FL-linked analyte, furosine, was linked to risk of progression of diabetic nephropathy9. A blood and/or urine-based biomarker would provide more convenient clinical sampling for risk prediction of nephropathy progression. Exploring this, plasma protein content of CML was examined and found to be not linked to the risk of developing diabetic nephropathy10. In patients with T1DM and normoalbuminuria (NA), plasma MG-H1 free adduct concentration was an independent risk predictor for increased thickening of glomerular basement membrane measured in renal biopsies, linked to early stage development of diabetes nephropathy11. Oxidative stress has also been implicated in the development of diabetic nephropathy through increased oxidative damage to renal proteins, including formation of the protein nitration adduct, 3-nitrotyrosine (3-NT)12. Protein glycation and oxidative damage of multiple chemically-defined types may be quantified robustly and concurrently by stable isotopic dilution analysis liquid chromatography-tandem mass spectrometry (LC–MS/MS)13. In a previous study of patients with T1DM, we found changes in serum protein glycation adducts, related serum free adducts and also protein oxidation and nitration adduct levels between patients with NA and new onset microalbuminuria (MA) but no difference between patients with MA with later stable or declining renal function14.