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Bgs below traditional diabetes cut offs can cause damage

I assume that therefore the issue is artificially lowering BG below 4.

I wouldn't assume that at all. I suspect that there are a number of life threatening non diabetic conditions associated with low fbgs that have high mortality (eg eating disorders ?)

However, fascinating though this topic is (and I'd love to see the source for @Oldvatr's hospital study), I'm not sure how relevant it is to the original question, which is whether people are suffering diabetic damage at levels below the traditional diagnosis level.
 
And why were they inpatients?
More questions than answers in this one
That report should not be taken too seriously. It smells ;like a postgrad research project where a student has gained access to the local hospital database and tried to analyse a hunch into reality. As I said, 1,000 deaths in 3,000 patients dying within 6 months after afmission is suspect, to say the least and suggests a systemic error in the analysis.
 
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I wouldn't assume that at all. I suspect that there are a number of life threatening non diabetic conditions associated with low fbgs that have high mortality (eg eating disorders ?)

However, fascinating though this topic is (and I'd love to see the source for @Oldvatr's hospital study), I'm not sure how relevant it is to the original question, which is whether people are suffering diabetic damage at levels below the traditional diagnosis level.
I would love to see the source of the Italian Study on which the OP article is based. Jenny Ruhl is a writer I respect, but why can I not find that report in the ether. Dr Google has not produced it and I normally get answers on my firsy trawl. I have used many different pathways to find it, but to no avail. The Chinese study I found does have similar conclusions, but also differs in its ranges. It too is very coy about what the mortality event prevalences were, so what is it that the FBG is worsening? all cause death is a catch all and not very helpful.

My GP is not impressed when my bgl was runing below 7 mmol/l, and he has asked me to adjust my lifestyle changes to aim for a daily average of 7 or above.

I was of the impression it was due to the fear of insulin driven hypo events being embedded within that average and being masked when averaged out, Certainly my hypo events were much less severe than those of my T1D friends who often need hospital admission. I still meet the DVLA requirements for hypo reporting having never required assistance. But I an pretty sure this low FBG observation is deep seated and is why keto diets are such an anathema to the medical profession.

But without the source material we are not able to examine the evidence ourselves, I reapply the question asked in a recent post. What do we know about the study cohort participants in regards to diabetic status and medications?
 
Dr Bernstein's diabetes solution has target of 83mg/dl with less than +/-10mg/dl after meals. Divide by 18 to get mmol/l, so a target of 4.61mmol/l and above 4.04mmol/l and below 5.16mmol/l after meals. HbA1c should be in the 20's with the around 4.6mmol/l equating to an HbA1c of 26mmol/mol.

I am still nowhere near those values :(

I doubt I will ever get my HbA1c in the 20's but I do hope to get them into the 30's but still a work in progress ;)


My non-diabetic brother had an HbA1c last year with a 26mmol/mol as part of a 55 year+ check-up.
 
The following is a report on glucose care for inpatients who are diabetic.
https://www.ncbi.nlm.nih.gov/books/NBK279093/

The ADA has adopted the ranges suggested in this report (control within range 7.8-10 mmol/l) and my recent experience of care in a UK hospital echoes a similar care plan is in place here too (in my case the upper control limit was 12 mmol/l. A bgl level below 5,6 was considered a hypo requiring urgent carb treatment, which shocked me. but now i see where it is coming from).

The book referenced is a reference book for HCP's

If the Italian study is referencing recent hospital database records, then it is possible that they were using a similar control algorithm for inpatient care. The same can maybe explain that strange NHS study that used the NHS South coast UK database, but that is from GP records so is not so regimented. It does explain why my T1D buddy has been advised to run his pump control between 8 and 12 mmol/l.

It has for some time been a conundrum to me as to why the HCP;s were using control regimes higher than recommended in the general media sites such as here and DUK. There does seem to be a concerted pressure to move the control ranges higher, but I have not seen the science behind these movements. My supicious mind says it is a cost cutting measure to reduce the number of confirmed diabetics being registered. And of course to bolster Eatwell as the fount of all food.
 
I wouldn't assume that at all. I suspect that there are a number of life threatening non diabetic conditions associated with low fbgs that have high mortality (eg eating disorders ?)

However, fascinating though this topic is (and I'd love to see the source for @Oldvatr's hospital study), I'm not sure how relevant it is to the original question, which is whether people are suffering diabetic damage at levels below the traditional diagnosis level.

I may be misinterpreting but I thought what we were covering included concerns over low BG levels causing damage.
 
One thing to consider is that in the outside world, diabetes is largely controlled by exogenous insulin treatment and generally within an ageing and aged cohort. For FBG to be falling into the low reaches of the
'safe' range will probably involve excursions both above and below the target range, Since FBG is a spot check, it does not necessarily catch these excursions, and even an averaged set of results does not either. it is like the weatherman reading the temperature or sun strength at one point in the day. What is needed is a max/min type meter doing continuous sampling to capture potential harmful events.


There is also the problem that according to the iSO standard requirement a meter must report within ~/- 0,7 mmol/l of the true value of a reading which becomes significant when measuring the FBG level. For example reading of 4,0 could be actually 3.3 mmol/l. Conversely, the 3.3 value could be reported as 2.6 and recorded as such by the hospital. And the meter could not be accused of lying.
Even a true value of 5.6 mmol/l could be recorded as being between 4.76 and 6.44 mmol/l and still be considered as accurate,

The other problem we see is the actual method of measuring FBG. The FBG value from the lab report in hospital or annual checkup is generally expressed in whole blood calibration, but modern bgl test meters now report the value in plasma calibration. If you are using a meter from 2006 or older then these were all calibrated in whole blood units. I believe even recent lab results are still whole blood because they are from a venous drawn sample, whereas the hospital ward testers will be normal hand held bgl meters in plasma or could be results reported from blood tests in the lab. ,

Conversion is easy - plasma readings are 12% higher than whole blood values.
This means that a hospital record could be 12% lower than what we are measuring. So read those Italian reported values with care. We do not know what their units represent.

Also, when the bgl meters changed to read in plasma, the NICE levels did not change, and still reflect the whole blood as seen by the HCP's and the lab. So in home control should actully be using a raised set of values to control to if using a modern meter.
 
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I think I have finally found the relevant Italian Study
https://link.springer.com/article/10.1007/s00125-003-1263-9

They use an OGTT oral test and a euglycemic clamp to measure the insulin in the blood. This method does not actually measure beta cell failure or beta cell decline but is a measure somewhat crudely of the insulin resistance and weskness of the insulin response (speed of action to recover from glucose spike). The aithors admit this in the body of the study, so their conclusion does not seem to be proven by this study, It is I think conjecture that the drop in glucose being weaker in some subjects is beta cell failure, and not an increase or decrease in either adipose or muscular IR, or other varying parameter such as GLUT 4 or glucagon response changing.

Nope this is not the Italian Study. It is a Texas USA study where two of the authors are from an Italian University in Pisa.
 
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Then the title is misleading?
What I meant to do was warn people that I had read that you don't have to be in the traditional "diabetic" range of BG, or even have reached the "prediabetic" range, for damage to occur. That retinopathy and neuropathy can start at much lower BGs than many of us realise. I certainly hadn't realised before that neuropathy could start so early on in the disease progression process.
However I think that the discussions of the possibility of low BG causing harm, though not what I originally meant, are interesting and a reasonable development of the original post.
 
One thing I pick up from the Texas Study was that the sample cohort had a very high preponderance of at least one parent being a diabetic even among the 'normal' group. (51%) The bgl readings were plasma calibrated it seems. They used radioimmunology measurements to measure insulin and c-peptide.

The test was not an OGTT. It was a primed infusion with titrated glucose to maintain a normal bgl of 5,6 mmol/l The infused glucose had a tracer which was measured. Once the basal rate had stabilised, then the infusion was increased to provide a step function for two hours and the insulin clamp works by infusing exogenous insulin at a fixed rate, then adding in infused glucose adjusted to bring the levels back up to 5,6 mmo;l. I am not sure how this tests the beta cell output response at all. but they seem to think it does.
 
What I meant to do was warn people that I had read that you don't have to be in the traditional "diabetic" range of BG, or even have reached the "prediabetic" range, for damage to occur
Thank you for the clarification. That is what I understood your title and original post to mean.

However, I would like further links to why you believe this to be true. Specifically about type 2 diabetics.

Given the conclusions in the links quoted, it seems to accept that many will have to do the best they can, and that the lower levels may be impossible in a practical sense and cause unnecessary anxiety, which is also bad for blood sugar levels.

I feel your title is scaremongering.
 
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What I meant to do was warn people that I had read that you don't have to be in the traditional "diabetic" range of BG, or even have reached the "prediabetic" range, for damage to occur. That retinopathy and neuropathy can start at much lower BGs than many of us realise. I certainly hadn't realised before that neuropathy could start so early on in the disease progression process.
However I think that the discussions of the possibility of low BG causing harm, though not what I originally meant, are interesting and a reasonable development of the original post.
What I find worrying about the info we uncovered wrt low FBG is that reducing the bloods below the 'normal; value of 5.6 does not reduce the risk of CVE, and actually is seen to be associated with reduced lifespan as a result. Whether this applies to all diabetics, or mainly insulin users, or even medicated people has not been tested as far as I can tell, but the current dive to the bottom to get remission may actually be harmful it seems.

I knew that there had been some studies on T1D diabetics where a bathtub curve was seen when plotted out as bgl vs all cause mortality in groups where intensive intervention and aggressive control was in use.

I don't think we have seen any evidence yet that associates retinopathy or neuropathy with 'normal range control regimes. The OP article was only talking about beta cell damage, and provided I found the right study paper, then it seems that there is some misinterpretations being made. The conclusions in the study report are not supported by the evidence (as declared inside the paper itself by the authors).
 
But you’ve made a post and highlighted the risks of excessive readings at these times so why do you not take these? It seems illogical, at the very least, not to even do so as a monitoring sample taken occasionally or to establish levels for regular meals.

How about hba1c as these are also used as a measure of risk of complications?

Why only use fbg, which whilst it has its merits also has limitations for interpretation of the overall picture?
I don’t think it matters which BG test you use to determine where you are on the range of normal through prediabetic to diabetic. Though I have read – also in Jenny Ruhl's book, that the 1st/2nd phase insulin responses are the first to go when you get diabetes – these are shown broadly, though not perfectly accurately, by the OGTT, and further, that the FBGs are the last to go.

My FBGs have come down from diabetic to just normal since 2017, but my OGTT is only down from very rubbish (diabetic level) to pretty rubbish Just under diabetic level, but at the very top of the pre diabetic range, since this time last year. An improvement, but not a roaring success, as obviously, according to the article I quoted above, complications of T2 can easily happen in the prediabetes range and even possibly earlier. I shall have to try to lose a bit more weight once my bowel problem is resolve (or not), but now is not a good time. Ruhl doesn’t say, but I’m assuming that HbA1c is in between. My own HBa1cs show as rather lower than they should be because I have an abnormal red blood cell count, so I don’t rely on them.
 
Have you asked for a fructosamine test instead?
Thank you for your suggestion. But no, I've never heard of them. What are they? But I don't think it really matters enough for the GP to be giving me extra tests. I know I have prediabetes and they don't treat that except by telling you to lose weight Last year's OGTT came out diabetic but this year's is only prediabetic albeit just one decimal point from diabetic! At the moment I'm concentrating on the coming bowel biopsy, and T2 testing is not a priority.
 
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