Robbity@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
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"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
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.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
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.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.Sent from my Lenovo P2a42 using Diabetes.co.uk Forum mobile app
Well, I dip in and out as and when and I shall continue to do so.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
As I understand it the 2mmol test is to find the effect of that particular meal not overall control.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
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.
Wow I think we would all have to be scientists to understand all that"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
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 2mmolAs I understand it the 2mmol test is to find the effect of that particular meal not overall control.
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
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
"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
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