Strategy for getting R insulin (UK NHS)

ert

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Well, it was quoted on DAFNE, and by my specialists, so I did do a quick check at the time.

If I try to argue a point with my specialist, he really needs NICE or Lancet articles.
I subscribe to the Lancet but am not sure if you have access to:
** The main article is for JDRF but if you access the references below, there are studies on adults to look up separately.
https://www.thelancet.com/journals/lanchi/article/PIIS2352-4642(19)30055-0/fulltext
Current NICE: hypoglycaemia (generally defined as blood glucose levels less than 3.5 mmol/L).
https://cks.nice.org.uk/diabetes-type-1#!scenario
They've had the cut off at 3.5 mmol/L for a while, here in 2013.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784865/
 
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MarkMunday

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... Can you point me to the source claiming brain damage starts below 3.5 mmol/L? ....
This is the conventional wisdom, which is not based on fact. Brain cell death is thought to occur when blood glucose drops below 1 mmol/l. Most hypos are treated well above this level. People with hypoglycemia awareness can function normally at 2 mmol/l with full cognitive function and no brain damage. That 3.5 mmol/l is an arbitrary number below which there may be stress response induced symptoms, like functional brain failure. Brain failure is fully recoverable and goes away when normal blood glucose returns.

The point at which brain failure and brain damage happens depends on various factors, including diet, activity levels and the amount of injected insulin. The most elegant solution is to wean the brain off glucose and get it to use ketones of energy. Blood glucose becomes much less of an issue for the brain. It is done by eating ketogenically and becoming fat adapted.

According to this NCBI article, brain cell death occurs at under 1.9 mmol/l but they don't say how they figured this out. If blood glucose drops very and low and very fast, it can cause coma. Then brain damage definitely occurs, but a 2007 study found that brain cells were killed by oxidative stress caused by glucose used to treat the hypoglycemia, not the coma itself. This study was done on rats so the analysis is more thorough, but the findings may not apply to humans.

The takeaway for me is that there are no convincing answers to the question of at what point hypos cause brain damage (brain cell death). It seems to be much lower than what we are told. Much of the narrative is speculative and used encourage responsible blood glucose control by T1s. I guess that is fair enough, but I really don't like scare tactics. As someone dealing with the harsh realities of T1 and everything that goes with it, I want to know the truth. :bored:
 
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deszcznocity

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This is the conventional wisdom, which is not based on fact. Brain cell death is thought to occur when blood glucose drops below 1 mmol/l. Most hypos are treated well above this level. People with hypoglycemia awareness can function normally at 2 mmol/l with full cognitive function and no brain damage. That 3.5 mmol/l is an arbitrary number below which there may be stress response induced symptoms, like functional brain failure. Brain failure is fully recoverable and goes away when normal blood glucose returns.

The point at which brain failure and brain damage happens depends on various factors, including diet, activity levels and the amount of injected insulin. The most elegant solution is to wean the brain off glucose and get it to use ketones of energy. Blood glucose becomes much less of an issue for the brain. It is done by eating ketogenically and becoming fat adapted.

According to this NCBI article, brain cell death occurs at under 1.9 mmol/l but they don't say how they figured this out. If blood glucose drops very and low and very fast, it can cause coma. Then brain damage definitely occurs, but a 2007 study found that brain cells were killed by oxidative stress caused by glucose used to treat the hypoglycemia, not the coma itself. This study was done on rats so the analysis is more thorough, but the findings may not apply to humans.

The takeaway for me is that there are no convincing answers to the question of at what point hypos cause brain damage (brain cell death). It seems to be much lower than what we are told. Much of the narrative is speculative and used encourage responsible blood glucose control by T1s. I guess that is fair enough, but I really don't like scare tactics. As someone dealing with the harsh realities of T1 and everything that goes with it, I want to know the truth. :bored:
This is exactly what my thought process was as well. I do not get any hypo symptoms above 3 mmol/L (based on Libre Optium readings). Only at a level of 2.4 mmol/L I get the cold sweat and shaking. Obvious to say I am keto adapted. When first diagnosed I got hypos at below 5.5 mmol/L. Also, I was reading quite a lot of literature from the 80s and 90s where everywhere they quoted that hypo level is below 3.0 mmol/L.
 
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shaunsilk

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I see this is an old thread but thought I would add something important to the last two posts, and that is: The brain and the body have two different bg values which is why you can read values of 2.5 on the meter and still feel fine, because the brain is not necessarily at that level! Usually it is good to treat the hypo as the brain can/will eventually catch up! This is a very important concept and bares repeating The brain is separated by the aptly named BLOD-BRAIN-BARRIER (the barrier bit). This means levels in the blood and or drugs etc just don't cross over, in fact many things CANT cross over and back from the blood to the brain and there are processes that keep the levels in the brain and the blood separate. Again this is why your meter can read (say) 1.2 mmol but you feel OK because the brain keeps its own glucose value and it almost certainly won't be 1.2 mmol when you do a finger capillary reading. So while your body hba1c maybe at 3.8 most of the time that won't be what the brain is! Usually you must be very low for a long time to cause brain damage because of this principle otherwise you would see masses of brain damage in type ones just from day to day and this is not what we see for this reason . So on one day you might be fine at 2.4 mmol (capillary reading) but end up hospitalised unconscious at a higher level, there is no direct correlation between blood-glucose and brain-glucose, and the best you can say is that the longer you spend very low the more-likely your brain will end up that low but it is of no certainty.

(mod edit to comply with rules)
 
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EllieM

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Hi @shaunsilk and welcome to the forums.

Speaking from personal experience of hypos (including ones that have induced unconsciousness) I have to say that the fingerprick bg correlates pretty well (for me) with the level at which I am in danger of passing out, possibly having a seizure. And impairment in my mental function definitely starts in the 3s so it would be incredibly unsafe for me to drive at a bg of less than 4.

So while your body hba1c maybe at 3.8 most of the time that won't be what the brain is!
Are you talking blood sugar (mmol/L) or hba1C (%)? I can assure you that as a (non keto) T1 my levels run higher. And though I appreciate your point (that the brain may not be running as low as the body?) I think you need to back up such a controversial statement with link(s).

As a T1 I have to assume that my meter is accurate as regards my mental acuity (no way to measure my brain bg), and to safely drive I need a bg greater than 4.
 

Dexta

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So on one day you might be fine at 2.4 mmol (capillary reading) but end up hospitalised unconscious at a higher level,[/QUOTE]

I can say that in my near 50 years of T1 I don’t believe I’ve ever gone severely hypo at a level higher than my meter has indicated when borderline. If anything the opposite applies.

When using a CGM we then have another variable where I usually find the meter readings will predict those of the CGM’s interstitial results by 10 to 15 minutes.

All very interesting.