We know spikes are bad, but……

[Harebrain]

@Hairbrain I know you've said you'd prefer not to discuss diet here, but if I had a spike like that I'd definitely be checking what I'd eaten to see if there was anything in it that might be the cause. The other thing I'd be doing was a another test straight away to see if it was possibly a case of rogue reading and/or mucky (AKA contaminated ) fingers. My personal preference is to avoid giving my poor elderly pancreas too much extra and avoidable work to do, so I work towards keeping my glucose levels as steady and stable as possible - high carb levels can knock me for six...

And I'd disagree with @SockFiddler in that I definitely believe that there are occasions when it's actually very useful to check at 1 hour (and sometimes other times too) to find out how we respond to certain foods. I've probably learned more doing these checks (and also using a Libre sensor occasionally to get a full picture of what's going on 24/7...) than if I'd simply relied on pre and 2 hours post meal tests all the time. It really depends on what we want to discover from testing (e.g.so we can adapt our diets accordingly if required) rather than just doing so at pre and post meal times because that's what/when we've been advised to do.

Robbity

Robbity

Thanks for that. I know the test is accurate because a) I've done it before and b) I know how many carbs were in my lunch.

I take your point about not wanting to pressurise the aging pancreas, however, how can I say this, I want to live my life and not be forever fretting about carbs as some do on here.

The rest of the time I keep my carbs lowish and my BG responds. The exercise takes care of the excess at lunchtime and I'm reasonably happy with the results.

I have however been very interested by all the comments made so far and would like to thank everyone for their input. It was all as helpful as I expected.

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[JohnEGreen]

"The current goal of diabetes therapy is to reduce time-averaged mean levels of glycemia, measured as HbA1c, to prevent diabetic complications. However, HbA1c only explains <25% of the variation in risk of developing complications. Because HbA1c does not correlate with glycemic variability when adjusted for mean blood glucose, we hypothesized that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications. We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression. Both the epigenetic changes and the gene expression changes persist for at least 6 d of subsequent normal glycemia, as do NF-κB–induced increases in monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression. Hyperglycemia-induced epigenetic changes and increased p65 expression are prevented by reducing mitochondrial superoxide production or superoxide-induced α-oxoaldehydes. These results highlight the dramatic and long-lasting effects that short-term hyperglycemic spikes can have on vascular cells and suggest that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications."

http://jem.rupress.org/content/205/10/2409.short

 

[Harebrain]

"The current goal of diabetes therapy is to reduce time-averaged mean levels of glycemia, measured as HbA1c, to prevent diabetic complications. However, HbA1c only explains <25% of the variation in risk of developing complications. Because HbA1c does not correlate with glycemic variability when adjusted for mean blood glucose, we hypothesized that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications. We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression. Both the epigenetic changes and the gene expression changes persist for at least 6 d of subsequent normal glycemia, as do NF-κB–induced increases in monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression. Hyperglycemia-induced epigenetic changes and increased p65 expression are prevented by reducing mitochondrial superoxide production or superoxide-induced α-oxoaldehydes. These results highlight the dramatic and long-lasting effects that short-term hyperglycemic spikes can have on vascular cells and suggest that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications."

http://jem.rupress.org/content/205/10/2409.short

This was what I was trying to avoid if you had read the beginning of the post. However looking at the actual article rather than the abstract which you reprinted here for transient read 16 hours I'm talking about less than 60 minutes, hardly the same thing, and the experiments were done at cellular level which hardly relates to the whole body experience

Thanks anyway.


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[Mike d]

Gee, ease up a bit .... the poster was simply trying to help, as were others. You're looking for absolutes. There are none.

 

[slinkimalinki]

Don't test 1 hour after food. Discard those readings and test only at 2 hours after eating. According to what you've written there, pre-meal is 5.6, 2 hours after is 5.4 - you're absolutely fine.

Wait for 2 hours after you've eaten before testing <3

Sock

You do need to test at one hour after, to catch the spike, and at 2 hours you should be back to your starting number. So test at the beginning of the meal, one hour after, then 2 hours after the first bite.

 

[Harebrain]

Gee, ease up a bit .... the poster was simply trying to help, as were others. You're looking for absolutes. There are none.

Ok, I apologise if I was too harsh and no I'm not looking for absolutes, I know that's not sensible. However that particular info is both a distraction and far too complex for most of us to understand (speaking for myself only of course). It is, I feel also not really on point.



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[Mike d]

Ok, I apologise if I was too harsh and no I'm not looking for absolutes, I know that's not sensible. However that particular info is both a distraction and far too complex for most of us to understand (speaking for myself only of course). It is, I feel also not really on point.Sent from my Lenovo P2a42 using Diabetes.co.uk Forum mobile app

This is a reachout forum ... and you won't find too many better. Impossible to put fences (be it you, me or anyone else) around queries or responses as our conditions vary substantially based on an infinite range of factors. None of us are medically qualified to offer anything other than our personal experiences and suggestions.

I've seen plenty of (former) members "crack it" as they didn't like what they read and disappeared soon after they came. Most stay around

 

[Harebrain]

This is a reachout forum ... and you won't find too many better. Impossible to put fences (be it you, me or anyone else) around queries or responses as our conditions vary substantially based on an infinite range of factors. None of us are medically qualified to offer anything other than our personal experiences and suggestions.

I've seen plenty of (former) members "crack it" as they didn't like what they read and disappeared soon after they came. Most stay around

Well, I dip in and out as and when and I shall continue to do so.

I think that my point in respect of this particular post was that before posting something like that you should at least read the actual research as this gives a very different favour to the information and this can be misleading.



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[Mike d]

Dip in and dip out all you wish ... I'm pretty much done. Luck to you

 

[Mr_Pot]

I thought the OP's question and his request for a simple answer with evidence was a reasonable one. It would seem from the responses so far that the answer is "we don't know". Which is a pity as I still don't know if having the occasional choc-ice is doing me any harm when my HbA1c is 37.

 

[Brunneria]

The problem is that saying 'I want hard scientific evidence, but I don't want it to be complicated, and anecdotes and personal experience are not scientific' makes it very unlikely that you will get an answer you accept. Or want.

I'm happy to trawl through scientific studies and read anecdotes. Heck I have plenty of personal ones I can come out with. But in the context of this thread, they will be rejected by the OP. So I will just go back to my personal policy of trying to minimise my standard deviation, watching my carbs, and appreciating all the wealth of evidence that is available - with the intention of avoiding long term complications.

 

[Pinkorchid]

I can never understand the... not over 2mmol rise after meals you surely have to be happy with the before meal level for that to work Some people could be quite high for whatever reason.. for example if someones level was 12mmol before their meal would they be happy with a rise of 2mmol to 14mmol then

 

[Mr_Pot]

I can never understand the... not over 2mmol rise after meals you surely have to be happy with the before meal level for that to work Some people could be quite high for whatever reason.. for example if someones level was 12mmol before their meal would they be happy with a rise of 2mmol to 14mmol then

As I understand it the 2mmol test is to find the effect of that particular meal not overall control.

 

[ringi]

I'm sure Jenny Ruhl, the author of blood sugar 101 would have some evidence. The majority of us use the ' not over 2 mmol after meals' rule.

The 2hr check is very good way to learn what the worse foods we eat are, so we can stop eating them. But we have to do better than that, otherwise, we will go on forever increasing dose of drugs like glic. Most people find that by keeping the 2hr under control their body improves enough that the h1 becomes reasonable without having to measure it.

I don't care what my 1hr is like with some (say 2 times a week) meals , provided that it is OK with most meals I eat. I care about what my 2hr is like with all meals. Hence I would not be happy with a 1hr peak that high on a meal I head every day.

For example, yesterday we had a meal out, I had glazed ribs and sweet potato chips (lower carb than normal chips), I could not test until we got home about 2hr after the end of the meal, at that point my BG was 5.5. I am happy with this so I will have the meal again, but would not consider having a meal like that often unless I proved with tests at 1hr,2h,3hr etc that it was OK. (Remember the peak can be after h1 for some meals.)

 

[Pinkorchid]

"The current goal of diabetes therapy is to reduce time-averaged mean levels of glycemia, measured as HbA1c, to prevent diabetic complications. However, HbA1c only explains <25% of the variation in risk of developing complications. Because HbA1c does not correlate with glycemic variability when adjusted for mean blood glucose, we hypothesized that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications. We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression. Both the epigenetic changes and the gene expression changes persist for at least 6 d of subsequent normal glycemia, as do NF-κB–induced increases in monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression. Hyperglycemia-induced epigenetic changes and increased p65 expression are prevented by reducing mitochondrial superoxide production or superoxide-induced α-oxoaldehydes. These results highlight the dramatic and long-lasting effects that short-term hyperglycemic spikes can have on vascular cells and suggest that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications."

http://jem.rupress.org/content/205/10/2409.short

Wow I think we would all have to be scientists to understand all that

 

[Pinkorchid]

As I understand it the 2mmol test is to find the effect of that particular meal not overall control.

Yes I realise that but if the level is high to start with then any food low carb or not will make it rise further and possibly more than 2mmol

 

[ringi]

I can never understand the... not over 2mmol rise after meals you surely have to be happy with the before meal level for that to work Some people could be quite high for whatever reason.. for example if someones level was 12mmol before their meal would they be happy with a rise of 2mmol to 14mmol then

You missing the point, the after meal testing it to learn what we can eat, we can't change the before meal BG by changing a single meal, but we can change the after meal increase. Hence the continuous improvement method is driven from what we can change in the short term, hence leading to long term improvement. Seeing the result of actions in 2hr is a very good method of self-motivation.

 

[ringi]

Yes I realise that but if the level is high to start with then any food low carb or not will make it rise further and possibly more than 2mmol

Not true, pure fat will not result in any increase, but it is true that worse someone's BG is the lower the carbs needs to be. This is however what is needed to get the BG under control.......

 

[kokhongw]

"The current goal of diabetes therapy is to reduce time-averaged mean levels of glycemia, measured as HbA1c, to prevent diabetic complications. However, HbA1c only explains <25% of the variation in risk of developing complications. Because HbA1c does not correlate with glycemic variability when adjusted for mean blood glucose, we hypothesized that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications. We show that transient hyperglycemia induces long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells both in vitro and in nondiabetic mice, which cause increased p65 gene expression. Both the epigenetic changes and the gene expression changes persist for at least 6 d of subsequent normal glycemia, as do NF-κB–induced increases in monocyte chemoattractant protein 1 and vascular cell adhesion molecule 1 expression. Hyperglycemia-induced epigenetic changes and increased p65 expression are prevented by reducing mitochondrial superoxide production or superoxide-induced α-oxoaldehydes. These results highlight the dramatic and long-lasting effects that short-term hyperglycemic spikes can have on vascular cells and suggest that transient spikes of hyperglycemia may be an HbA1c–independent risk factor for diabetic complications."

http://jem.rupress.org/content/205/10/2409.short

Besides the damages of the glucose spike...it seems that we often ignore the damages that can result from insulin spikes. Most seems to consider elevated insulin to be benign or inconsequential in the greater scheme of things...

 

[JohnEGreen]

Again you may not find this relavent but here it is any way.

Beta Cell Dysfunction Begins at 2-hr OGTT Test Readings Over 100 mg/dl (5.6 mmol/L)

When a team of Italian researchers led by A Gastardelli started examining beta cell response to glucose in people with normal blood sugars, they discovered that a small amount of beta cell dysfunction began to be detectable in people whose blood sugar rose only slightly over 100 mg/dl on a 2-hour glucose tolerance test. The beta cells are the cells in the pancreas that produce the insulin your body uses to control your blood sugar.
Analyzing their data further, they found that with every small increase in the 2-hour glucose tolerance test result, there was a corresponding increase in how much beta cell failure was detectable.

Conclusion/

When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.

https://link.springer.com/article/10.1007/s00125-003-1263-9?LI=true