Interesting. So would it be better to be 180 at one hour, 140 two hours postprandial, feed part of the remaining insulin so you never rise above 140 at the two hour mark, maybe even feed again a bit at the three hour mark and be normal at the four hour mark? If left to its natural DIA, with Apidra, I get close to 200 at the one hour mark, 160 at two hour, 130ish at 3 hour and 100 or less at four hour (those are not exact readings, just a generalization). If overbolusing you might be 160 one hour, 120 two hours, have to feed at least half, maybe more of the IOB at hour two or since insulin is peaking strongly, she will crash, which will raise her up to 150 ish again then she will come back to target third or forth hour. Only doable if I am home and watching; she cannot be expected to keep track of the clock watching necessary. There is no easy way…
You can’t keep a 13 year old blood sugars in a tight range. We just do the best we can. There are times I run in the high 200s just because. Not from eating too many carbs or not matching insulin to carbs but just because. And I’m not going to run around screaming “oh my god I just sustained permanent damage”. I try my best, my endo thinks I’m under control, and that’s all there is to it.
Jan, the evidence in the original post refers to type 2 and much to results on a 2 hour OGGT. (I dread to think what results most type 1s would have on a glucose tolerance test)
The majority of the studies may not have much relevance to type 1 at all.
Unfortunately there is very little long term research on the effect of post prandial readings on the development of complications in type 1.
The researcher E Kilpatrick has analysed the original DCCT data, to try to assess the effects of glucose variability. He included both the original 10 years of the study and its followup (I think there is now 16 years worth of data so it is long enough to show the development of complications). This data includes records of regular HbA1cs and also records of 7point blood glucose tests taken at quarterly intervals. Obviously not the best data but it does give some indication of the daily control of the participants.
Kilpatrick asked the question does increasing gluocose variability lead to an increased risk of microvascular complications and according to his findings.
It is the HbA1c which determines microvascular risk in type 1, no matter how the mean is arrived at. In other words in 2 people with the same HbA1c, one with lots of highs and lows, one with a more even spread have an equal risk of complications.
However, he did find that variations between HbA1cs, ie a period of good control followed by one of poor and back again caused a much higher risk.
He also found that for macrovascular complications the mean glucose, not the HbA1c was a better risk predictor.
He looked at the risk reduction for lower HbA1cs, the risk falls greatly for even quite small reductions at high levels but it is not the same at lower levels
according to him (for retinopathy) and I find this astonishing
’The absolute risk reduction in falling from HbA1c 10% to HbA1c 9.7% is the same as HbA1c 7% to HbA1c 5.4%’
A powerpoint summary showing some of his findings is available if you google kilpatrick HbA1c York. (unfortunately the pdf is not linking but the google quick view works)
Most of his analysis of the DCCT (and there are several papers on the different complications ) is published in Diabetes Care and available to read.
“It is the HbA1c which determines microvascular risk in type 1, no matter how the mean is arrived at. In other words in 2 people with the same HbA1c, one with lots of highs and lows, one with a more even spread have an equal risk of complications.”
“He also found that for macrovascular complications the mean glucose, not the HbA1c was a better risk predictor.”
What is the difference between mean glucose and HbA1c? Maybe my understanding of A1c is a bit off, which wouldn’t surprise me, but I thought A1c was measure of average BG.
I tried to google and find the info but couldn’t track down the specific reference.
This Kilpatrick study, is a lot closer to my experience as a T1 for 30 years, and the encouragement that my best docs have given me to stay in good control, than any of the studies that say “any number over 140 causes nerve damage”.
The Kilpatrick study also results in expectations for hour-by-hour control that are actually reachable for me and the other T1’s I know. Whereas the “any number over 140 causes nerve damage” attitude would make me want to just give up and die right now, the Kilpatrick study and the way it emphasizes good results for overall good control rather than predicting doom from a single number, makes the study actually useful to me.
Just my two cents. Obviously 90% of the board latches onto the “140 causes irreversible damage” school of thought but it has never appealed to me.
We were told that Clara could go to bed without correction if she were between 250 to 140. Geez!
Geez–indeed! 140-250 is quite a range. Once again, the phobia of overnight lows. Not that this isn’t something to be concerned with because it is, but I think medical people go a bit overboard here. Some people raise their BG to pretty high before bed & won’t go to sleep at normal BG. If I go to sleep high, I wake up high. Guess that means my overnight basal dose is right:)
Complicated. and it worried me, I took some time to find the answer, so I’ll quote from another more recent Kilpatrick paper
Actually the paper is quite a good summary of his work
http://jcp.bmj.com/content/61/9/977.full
"As the 1441 patients participated in the trial for an average of 6.5 years, it was possible to make 26 056 comparisons between HbA1c and a full 7-point profile.12 The linear relationship found (that mean plasma glucose (MPG, mmol/l) = 1.98 × HbA1c (DCCT)−4.29, r = 0.82) has since been used as the most accurate guide to clinicians and other healthcare workers when discussing glycaemic control with their patients.12 Nevertheless, the scatter of patients around this regression line meant that an individual with a MPG of, say, 10 mmol/l, could have an HbA1c anywhere between about 6% and 11%, and this has obvious implications when using solely HbA1c to set glycaemic targets. "
He postulatated elsewhere that one reason might be that some people were higher glycators and this would result in higher HbA1cs
Variability in the relationship between mean plasma glucose and HbA1c: implications for the assessment of glycemic control.
Kilpatrick ES, Rigby AS, Atkin SL.
However the plot thickens in that it now seems that the people in the intensively treated group also had lower HbA1cs fthan people in the normal care group at similar averages (???) Nowadays I would thinkalmost all type 1s use ‘intensive control’ methods…even if not always sucessfully.
In more recent studies the ‘relationship between MPG and HbA1c was found to be closer than in the DCCT,’ Kilpatrick remarks about this
‘However, it remains to be seen from any final publication how representative these mean blood glucose study patients are of the diabetes population as a whole, since there were many exclusion criteria to the study that could have removed the very people who might account for much of the scatter around the regression line.’
Here endeth the lesson, and I think I’ll give up research papers for this morning!
I think the assumption inherent in that instruction (which was the same thing we were told) was that there’d still be insulin from the dinnertime bolus in the bloodstream. Usually, little kids go to bed within 3 hours of having dinner, so there should still be active insulin doing its thing if she’s over 140. If Eric goes to bed with anything over 130, I use his pump settings to see how much insulin he has on board & still active and usually it’s around 0.5 U, which is generally more than enough to bring him back down (and it’s almost always within the 2-hour window, since we eat at around 6:30 and he goes to bed at 8 pm).
But, I do think the fear of overnight lows is what prompts them to set the upper limit at 250, and personally I’d be happier if it were 200 or 180 or something like that. On the other hand… people do occasionally die from sudden episodes of hypoglycemia during sleep, and kids are notoriously difficult to manage in that respect. So I can see why the medical community would rather risk long-term complications than short-term death of a child. I just keep my fingers crossed that the current trials of CGM in children under 7 means that Eric might be eligible for CGM soon - he’s much more likely to run high overnight than low, but either possibility is something I would like to eliminate.
Thank you very much Marie!
A r = 0.82 is not very good as you have pointed out. At present there is no accurate way to measure average blood sugar. The hand held meters with 5 second are way worst than the 60 second ones of ten years ago as far as accuracy goes.
If above 110 kills beta cells, then everyone should be diabetic… cause everyone i know of has post meal numbers above 110… for a good bit too (like until the 3 hour mark)
I am starting to believe anything but a normal bloodsugar causes damage to me, as anything but normal and I feel like crapola, but…how do I achieve this?
I have only recently (April 2010) been diagnosed with Type 2. I am on Lantus and Met. Two years ago I started getting numbness in my toes which has spread to all my toes, both feet with some burning pain. I just had an EMG done a week ago and the results showed Mild Sensorimotor Peripheral Neuropathy consistent with diabetes. Now tell me that you need to wait 20 or so years before you get complications? I always had normal bgl’s when tested at the clinic and I was tested a lot due to other medical conditions and not until diagnosis when my bgl within a three week period raised between 300-450, did I ever have an abnormal bgl at the doctor’s office.