True. I always go the same lab to reduce the chances of results varying from lab to lab. I expect that each lab test can vary in accuracy at the same lab, so I don’t want to add more variables than I need to.
Mine is 0.5% higher than my CGM data. Doctor Irl Hirsch calls us “high glycators.” It’s not a good thing but shows the imprecision of using an A1c number to equate it to a specific average blood glucose. This is a mistake.
An A1c of 6.0% is often translated to mean an average blood glucose of 126 mg/dL. In reality, the average blood glucose of people with an A1c of 6.0% ranges from 100-152 mg/dL. 126 mg/dL is simply the median value of that range.
The A1c is a sloppy statistic parading as precise with its decimal point resolution. If you use a CGM, time in range or TIR gives a much better representation of your glycemic exposure. It doesn’t obscure highs, lows, and large variability like the A1c does.
Finally, the A1c number sows misunderstanding between the patient and his/her doctor. The Doc is freaked out about hypoglycemia risk based on an A1c number alone. A patient with a good A1c and great time in range will be hard-pressed to ease the doctor’s fears without a good TIR report like the Dexcom Clarity 14-day Ambulatory Glucose Profile or AGP report.
While I don’t value the A1c number, I am always curious to see it.
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For me, A1C was always more of a barometer for my doctor(s) than for my management. Since getting pump+CGM 4 years ago, it has lost its relevance. I now consider staying in range (56-125) with low standard deviations to be the key to good control with the aim to minimize or eliminate future complications.
Thank goodness for tech and apps.
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… in populations, not so much individuals.
As I said… every study is on a population level.
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Yes… and populations are made of individuals…
I think framing A1C as a meaningless number misses the point… all of these other metrics are being used to ensure an A1C that isn’t elevated. You can’t gave a good average number, a good SD, a good time in range, and a high A1C… but of all those numbers the A1C is the only one that is actually an indication of what is actually happening to your blood cells as a result of all the other things…
And again, none of the other measures are known to be positively correlated with risks the way a1c is… the other measures are management tools, a1c is the result of ones efforts
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I am always in trouble with my doctor because of the number of lows I have. I can not feel a Hypo if I am working until I reach 50 BUT this level has not changed in 10 years since I was diagnosed. I have always been able to self treat a Hypo and I have never gone into a coma.
I also know a type 1 who is in her eighties. She experiences comas but still has all her marbles.
It is encouraging to hear from you Marilyn6 that you too suffer from this problem and have no bad side effects.
I know rapid fluctuating BGL has caused problems with my feet in the past but a change of insulin to Ryzodeg is stabilizing the hyper peaks.
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I was sitting in the exam room with my wife when we both went to a particular endo many years ago. Both of us were irritated that he complained about her low A1c. Not only did he complain to her about it (he expressed disapproval of having a 4.7), but he did so, knowing that she doesn’t have hardly any bad lows. I could understand him chiding her if she was making a concerted effort to keep her bg’s too low for her to be safe, but that’s not what she was doing.
So when I saw you wrote “in trouble with my doctor” I would suggest you not be intimidated. He (or she) WORKS FOR YOU–not the other way around.
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This 2016 diaTribe column has influenced my thinking about the relative merits of the A1c number. It’s well worth the read.
https://diatribe.org/BeyondA1c
This graphic from that article makes obvious the weakness of using the A1c to assess glycemic exposure.
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I get it. I run low. But, I would be super surprised by a 4.7. Thats an unusual #. Good if your not having lots of lows. But, kinda off the charts. Suspicious. I bet he was just assuming lows. He might not have believed her. Perhaps he had never seen such an a1c before. You are a diabetic married to a diabetic? Interesting.
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I’ve seen this article referenced many times on this site. I’ve read it in the past.
I think it adds value in explaining that an average is not the whole picture.
However, those are actually not graphs of actual people with a 7% A1c. They’re graphs showing 3 different bg patterns that all have the same average. One of the most important things that graph shows IMO is that individual 1 is at a higher risk of severe hypoglycemia. That’s a short-term threat that obviously needs to be addressed.
I don’t think anyone is saying glycemic variability is irrelevant. I think the point was that the A1c is the best indicator of your risk of long-term complications.
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From the same article, the point I was making earlier that the A1c is a validated measure that permits risk conclusions to be made across a population but is not able to validly draw that same assessment at the individual level.
A1c is a valuable measure for how a population is doing with diabetes, but for individuals themselves, knowing what goes into a person’s A1c is really important.
I guess what I’m trying to get at is that from everything I’ve read: glycation in and of itself is the most significant factor when determining the risk of complications.
Here’s an article discussing how the glycation of proteins in the body contributes the the development of complications:
http://www.jpma.org.pk/full_article_text.php?article_id=5295
We’re limiting hyperglycemia to reduce our risk of complications (and to be comfortable and think clearly on a day to day basis). There’s a reason why the A1c is important on a population level, and it’s not simply because it roughly equates to an average.
“It was not until 1968 that the significance of in vivo glycation was recognised, prompted by the discovery of glycated haemoglobin (Hb A1c) 4. Further work showed that glycated haemoglobin measured in diabetes reflected the average glycaemia over the preceding 120 days i.e., the life span of the protein5. Following the discovery of glycated collagen6, it was quickly realised that glycation may have a role in diabetic complications.”
The article goes on to explain how glycation plays a role in the development of complications. Hyperglycemia leads to glycation (at different levels for different people) and glycation leads to complications. The A1c helps us estimate how much glycation is occurring, guiding us in our management goals so we can limit our risk of complications.
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We know that the individual A1c test measures the percentage of hemoglobin (red blood cells) that are glycated or have attached glucose. Do we know that this hemoglobin glycation percentage is the same accross all body tissues? I’m sincerely asking this question and don’t know the answer to this.
I thought the intention of the A1c test was to simply use the hemoglobin glycation percentage to understand the average blood glucose exposure.
I’ve written before that my A1c number implies a higher glucose exposure than I actually experience. I am a high glycator. I’m thinking there are likely also low glycators in the population. Their A1c is under-representative for their actual glucose experience. They are actually exposed to more glucose than their A1c shows.
I am not trying to be argumentative for the sake of argument alone. I don’t understand everything about the science. But then again, the inherent nature of science is never fully conclusive.
Thank-you @katers87 for this exchange!
Let me dig up some research I did a few months ago on this topic. I came to the conclusion that the A1c was the best indicator we had (I’m pretty sure that glycation doesn’t occur at the same rate everywhere though).
I feel a whole lot more comfortable about my glucose control, now that I wear a CGM that is accurate both during the day, and at night (unlike the crappy Enlites I used to wear that always showed false lows when I’d lie down), than simply relying of spot-checking my bg’s during the day, or getting an A1c test periodically. My CGM proves to me that I didn’t screw up by eating a meal late in the day that might elevate my bg’s way above my target range. Because I’ve got that feedback every day, I’m able to both predict and control my bg’s better than before. That is a HUGE DEAL for me.
We can all agree that a1c doesn’t tell the entire story of an individual’s blood sugar management. That’s a no brainer, and it’s well explained in articles like the one linked to…
I think the reality is also impossible to escape that all things being equal (eg assuming no dangerous hypos etc) that its the best indicator of risk… that’s not to exaggerate it’s precision… but certainly Sam with an 8 a1c is at higher risk of adverse outcomes than Sam at 6 and so on… that’s pretty indisputable in my thinking
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I’d give you 5 “likes” , if I could, but I hit “like” the one time that is available. 
I read through your linked article. First of all, my ability to fully understand what is written there is compromised by my lack of formal biochemistry education.
Having said that, I can make a few observations. This report is primarily based on in-vitro studies, not studies on the glycation process in humans.
I also notice that the author published this in 1991. Has there been any subsequent work to either confirm or refute his findings?
It discusses some of the advanced glycation end-products (AGE) that were studied in the Joslin Medalist study.
"Complication associations with AGEs
Given the lack of correlation between current HbA1c and complications, we assessed markers of long-term glycemic control in the Medalists by evaluating the early glycation product fructose-lysine/fructosamine and AGE concentrations including CEL, an AGE derived from methylglyoxal ; pentosidine, a glycoxidation product; and CML, a glycoxidation and advanced lipoxidation product. CEL and fructose-lysine CML were significantly elevated in the Medalists as compared with nondiabetic, age-matched control subjects (n = 23, mean age 67.7 years) (Supplementary Table 3).
A combined biomarker of CEL and pentosidine was highly associated with complication status. Subjects with both CEL and pentosidine ≥median levels (“high CEL and pentosidine”: CEL ≥5.3 μmol/mol lysine and pentosidine ≥1.0 pmol/mg protein) were the most likely to have any complication (P = 0.001) or suffer from nephropathy (P = 0.007), neuropathy (P = 0.005), or cardiovascular disease (P = 0.002). Subjects with either CEL or pentosidine (but not both) at or above the median had an intermediate risk of severe complications, and subjects with both CEL and pentosidine below the median had the lowest complication risk. The odds of complications in Medalists with high CEL and pentosidine as compared with those with low CEL and pentosidine were 7.2-fold for any complication, 1.3-fold for retinopathy, 3.1-fold for nephropathy, 2.5-fold for neuropathy, and 2.3-fold for cardiovascular disease (Fig. 3A).
The relationship between current AGE concentrations and risk of progression to PDR was examined in Medalists with longitudinal follow-up. Increased risk of PDR was seen in subjects with high CEL and pentosidine as compared with the rest of the cohort (P = 0.05) (Fig. 3B). A combination biomarker that also included CML and fructose-lysine segmented by median (“low CML and fructose-lysine”: CML <59.8 and fructose-lysine <1,004 μmol/mol lysine) was even more strongly associated with PDR outcome (P = 0.02) (Fig. 3C). None of the four subjects with low CEL and pentosidine (CEL and pentosidine levels below the median) and high CML and fructose-lysine (CML and fructose-lysine levels above the median) progressed to PDR over the course of follow-up. Conversely, five of seven subjects with high CEL and pentosidine and low CML and fructose-lysine progressed to PDR."
http://care.diabetesjournals.org/content/34/4/968.long
I agree it’s old though. I’ll keep digging 
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