Correlation or causation?

Greetings all,
I haven’t been here in a while, i hope all is well with everyone. Something i noticed recently that i wanted to share and gather members’ thoughts on is the following chart, that graphs 7d rolling daily average BG (in mmol/dl) and rolling 7d average bolus units. There is a striking apparent link, particularly since i started with a CGM in June ‘20. On days my BG is high, i tend to inject more insulin ; on days it’s low, i tend to inject less. On the face of it, you’d expect the opposite, assuming my carb intake is the same, i.e. more insulin should push my BG lower. So given we observe the opposite, i.e. more insulin seems to correspond with higher BGs, reading between the lines, this would suggest i am chasing my BGs rather than leading them, which obviously isn’t the best place to be.
Does anyone else monitor these numbers, and observe similarly? Perhaps it is simply a case of varying carb/conditions that require dosages to vary, and since one can’t always be on top of these (they are so complex), naturally one ends up ‘chasing’ by injecting more when they see an excursion. So perhaps there’s nothing interesting to observe here, except the sign of the correlation appears wrong to me, on first observation.
I would love to hear members’ thoughts.


Based on what I’ve seen when treating my own high BG excursions, I’ve concluded that when my BG is high, I become more insulin resistant than when my BG is normal, so I need extra insulin. Your observation is consistent with that.

I would agree that preventing a high takes less insulin than correcting a high, and I attribute this to better insulin sensitivity when in range.


Indeed; so no conclusions can be drawn without carb intake numbers.

IMO until we can determine those we will always be up **** creek without a *******.


As well as the sensitivity issue, once your BG is high your liver will make and release more glucose into your blood stream. So you will need more insulin to stop your liver doing that!

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I didn’t know that, and thought I knew the opposite. But when I search to see if hyperglycemia suppresses hepatic glycogenolysis I don’t quickly get a clear answer, especially in type 2. Is anyone here in a position to shed some authoritative light on this?

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If your BG is high, that indicates that you have insufficient insulin in your bloodstream.
Facilitates glucose entering cells via glucose receptors
Increases the uptake of glucose in the liver
Decreases gluconeogenesis ( the formation of “new glucose”)
Promotes glycogen synthesis
Facilitates glycogenesis (storage of glucose in the lever as glycogen)
So when you don’t have enough circulating insulin, as demonstrated by your high blood glucose level, those 4 things are impaired, and so:-
Glucose cant enter the cells efficiently
Less glucose enters the liver, so the blood glucose goes higher still
More “new glucose” is formed in the liver and released into the blood
Less glucose can enter the liver to be stored as glycogen.

Higher BG results in beta cells producing more insulin. A side effect of this is that the alpha cells produce less glucagon. The liver cells in question release glucose in response to glucagon by breaking down the glycogen they store and adsorp glucose in response to insulin by building glycogen. Muscle cells also store glycogen so do the same thing, but the liver is the thing that works fast.

For T1Ds there are no beta cells (or, LADA, there is significant reduction) so the alpha cell glucagon production isn’t regulated in that way. We do still have a glucagon response but that is an independent result of low BG.

We (T1s) have to inject insulin to deal with high BG. In effect we have to externally control the response to high BG that is otherwise provided by the beta cells.

T2 and T1D are, in some sense, quite opposite in effect, at least if “T2” is classified as “insulin resistance” and T1 as “an absence of insulin production”. There are also lots of different drugs for T2, including having more insulin simply by injecting it, but for T1 insulin is always required and the other drugs (e.g. metformin) merely spice it up.

We assume that glucose transport into cells is controlled by insulin and is proportional to the amount of insulin. In T2 the amount of insulin required is greater (the correction factor is lower - lower BG drop for same insulin), in T1 in the absence of insulin resistance it’s pretty constant. (Obviously we see different insulin sensitivity, but that’s maybe a factor of 2 change at most.)

So the amount of insulin we need to correct high BG is determined only by the BG, except that many but not all T1s observe “sticky highs” and apparently reduced insulin sensitivity at high BG.

It’s clearly possible in theory to max out the liver ability to adsorp glucose; adsorption means converting it to glycogen and there is a simple chemical limit on the rate at which this can be done. I’ve not seen any information about this, but I do see BG behavior where I can inject more insulin without effect but then, some hours later, the insulin seems to start to kick in. That seems to happen if I exceed maybe an IOB of maybe 10IU (using the Omnipod calculation of IOB, which is hardly perfect.) So far as actual limits are concerned I’ve seen non-Ds eat utterly incredible amounts of carbs at one sitting and I assume they don’t hit 500, so I think the limit of a fully functional liver is probably not of any concern to us.

So far as the liver’s ability to adsorp glucose is concerned apart from the above paragraph the only way I know to interfere with this - to stop it being proportional to the amount of insulin - is alcohol. The same liver cells that product glycogen are also the ones that metabolise alcohol and alcohol takes precedence over glucose. Consequently alcohol raises the blood glucose resulting in continuous excess insulin production in people who are not T1D which in turn results in catastrophic low blood sugar when the alcohol has been eliminated from the system. T1s have another option - we may see a rising BG but we don’t have to respond to it by injecting excessive amounts of insulin, at least here we have a choice :slight_smile:

So yes; in the absence of alcohol and saturation of the liver’s ability to adsorp glucose in T1Ds it depends only on the amount of insulin available and the amount of glucagon available; not the BG.

Then in T1s there is no insulin production, only injection, but then there is glucagon production in T1s with functioning alpha cells (remember that some T1s don’t have a pancreas at all). Glucgaon production goes up suddenly at low BG (the glucagon response) and, IRC, DKA can stimulate it (but I’m not sure I’ve got that right). Apart from that it should be pretty much constant; in people with both alpha and beta cells it actually goes down as BG goes up, in people with only alpha cells it is a baseline constant, in people without either it is 0.