The relationship between glycemic variability and diabetic peripheral neuropathy in type 2 diabetes with well-controlled HbA1c.

Abstract

BACKGROUND:

Diabetic peripheral neuropathy (DPN) is one of the most common microvascular complications of diabetes. Glycemic variability could be an independent risk factor for diabetes complications in addition to average glucose. Type 2 diabetes with well-controlled glycosylated hemoglobin A1c (HbA1c) may have different terms of glycemic variability and vascular complication consequences. The aim of the study is to investigate the relationship between glycemic variability and DPN in type 2 diabetes with well-controlled HbA1c (HbA1c < 7.0%).

METHODS:

45 type 2 diabetes with well-controlled HbA1c(HbA1c < 7.0%) and with DPN (DM/DPN group) were recruited in the study, and 45 type 2 diabetes with well-controlled HbA1c and without DPN (DM/-DPN group) were set as controls. The two groups were also matched for age and diabetic duration. Blood pressure, body mass index(BMI), insulin sensitivity index (Matsuda index, ISI), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDLC), and low density lipoprotein cholesterol (LDLC) were tested in the two groups. And all patients were monitored using the continuous glucose monitoring (CGM) system for consecutive 72 hours. The multiple parameters of glycemic variability included the standard deviation of blood glucose (SDBG), mean of daily differences (MODD) and mean amplitude of glycemic excursions (MAGE).

RESULTS:

The DM/DPN group had a greater SDBG, MODD and MAGE, when compared to the DM/-DPN group (p < 0.05). BMI, TC, and LDLC of DM/DPN group were lower than those of DM/-DPN group (p < 0.05). The patients with hypoglycemia were comparable between the two groups (p > 0.05). Univariate analysis showed DPN was closely associated with BMI (OR 0.82, CI 0.72-0.94, p = 0.005), TC (OR 0.63, CI 0.42-0.93, p = 0.02), LDLC (OR 0.4, CI 0.20-0.80, p = 0.009), SDBG (OR 2.95, CI 1.55-5.61, p = 0.001), MODD (OR 4.38, CI 1.48-12.93, p = 0.008), MAGE (OR 2.18, CI 1.47-3.24, p < 0.001). Multivariate logistic regression analysis showed that MAGE (OR 2.05, CI 1.36-3.09, p = 0.001) and BMI (OR 0.85, CI 0.73-0.99, p = 0.033) were significantly correlating with DPN. Glycemic variability, evaluated by MAGE, was the most significantly independent risk factor for DPN.

CONCLUSIONS:

There was a close relationship between glycemic variability evaluated by MAGE and DPN in type 2 diabetes with well-controlled HbA1c.

https://www.ncbi.nlm.nih.gov/pubmed/25530811

Full text:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4272789/

Hi Graham,
For those of us with badly controlled Reactive Hypoglycaemia these conclusions would appear to have more serious consequences than the Hba1c would imply.
regards
Derek

Derek wrote:Hi Graham,
For those of us with badly controlled Reactive Hypoglycaemia these conclusions would appear to have more serious consequences than the Hba1c would imply.
regards
Derek

It would seem that way Derek though the same would apply to poorly controlled T1's and also T2's on hypoglycemic drugs or insulin.

Yeah I had significant Peripheral Neuropathy, mainly feet "going to sleep" and tingling fingers, and a feeling of wearing Marigold gloves and velcro socks after eating for ages, while my A1c was I think 5.3%, since my BG was jumping up mainly to 8 - 10 but seldom more after eating this gives some indication as to how long it was low in between meals.

I ended up with a long term dead spot on one foot which gradually shrank away to nothing, the rest of it reversed rapidly.

So much for our clueless GP's "the only thing that is important is A1c" (he may be an excellent diagnostician and probably good with acute illnesses but they really shouldn't let him anywhere near chronic diseases, well OK maybe not his fault, he's just parroting what he was taught). Would have been good if my actual GP (the "diabetes specialist") knew what she was doing, then her immensely fat colleague might never have become immensely fat, or diabetic, eh?

chris c wrote:Yeah I had significant Peripheral Neuropathy, mainly feet "going to sleep" and tingling fingers, and a feeling of wearing Marigold gloves and velcro socks after eating for ages, while my A1c was I think 5.3%, since my BG was jumping up mainly to 8 - 10 but seldom more after eating this gives some indication as to how long it was low in between meals.

I ended up with a long term dead spot on one foot which gradually shrank away to nothing, the rest of it reversed rapidly.

So much for our clueless GP's "the only thing that is important is A1c" (he may be an excellent diagnostician and probably good with acute illnesses but they really shouldn't let him anywhere near chronic diseases, well OK maybe not his fault, he's just parroting what he was taught). Would have been good if my actual GP (the "diabetes specialist") knew what she was doing, then her immensely fat colleague might never have become immensely fat, or diabetic, eh?

Have you thought about consulting a die-titian 

OK I'll get me coat 

Who do you think got me into that condition in the first place? She made me gain weight which I'd never done before, left me semipermanently exhausted and constantly hungry with rapidly increasing blood pressure and WORSE lipids that I had previously, then turned around and accused me of "failing to comply with the diet".

Now I eat pretty much the EXACT OPPOSITE of what I was told, all my symptoms and most of the others I didn't bother to list improved, my BP came back down and is still normal 12 years later on a mere 5mg amlodipine, my HDL DOUBLED and my trigs fell to 1/10 of what they were and are generally around 1/5 of what they were.

A dietician with a clue could have achieved that but they didn't. N=thousands.

The main problem is that I'm now 12 years older. The only other thing that has happened is the thyroid which I am assured is non-dietary in origin.

HINT: if I'd continued eating what I was told to eat I'd be in a pine box long ago, probably with a below average number of feet.

chris c wrote:Who do you think got me into that condition in the first place? She made me gain weight which I'd never done before, left me semipermanently exhausted and constantly hungry with rapidly increasing blood pressure and WORSE lipids that I had previously, then turned around and accused me of "failing to comply with the diet".

Now I eat pretty much the EXACT OPPOSITE of what I was told, all my symptoms and most of the others I didn't bother to list improved, my BP came back down and is still normal 12 years later on a mere 5mg amlodipine, my HDL DOUBLED and my trigs fell to 1/10 of what they were and are generally around 1/5 of what they were.

A dietician with a clue could have achieved that but they didn't. N=thousands.

The main problem is that I'm now 12 years older. The only other thing that has happened is the thyroid which I am assured is non-dietary in origin.

HINT: if I'd continued eating what I was told to eat I'd be in a pine box long ago, probably with a below average number of feet.

We are the fortunate ones Chris, I bet the majority of diabetics never question the dietary guidelines and put their trust in HCP's, there is light at the end of the tunnel though with the increasing amount of Dr's and RD's sceptical of current guidelines for diabetes and not forgetting the media attention that low carb is getting. How long before the NHS realises the savings on the astronomical cost of diabetic drugs, Dr Unwin has shown the way but outfits like the BDA and DUK still promote a diet that will keep Big Pharma happy $$$$$

Quite, for every pound the NHS "saves" that's a pound the drug companies can't ass to their bottom line. Ooh, nice typo, I tried to type "add" to their bottom line.

One thing I've noticed is, when a "health scare" story hits the Grauniad, most of the comments are in favour of Conventional Wisdom or veg(etari)anism. When a similar story hits the Daily Fail most of the commentators know significantly more than the original journalist.

I think word is getting out there, slowly, one pancreas at a time.