Basal Discussion Deep Dive for Everyone

Type 1 & LADA
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I think putting my deep dive questions in my “Basal Rates & Hormones” thread was confusing some people as to what I was asking yesterday, so I want to start a new thread to just discuss the ins and outs of basal insulin for anyone: man, woman or child.

What does basal insulin really accomplish? @Eric, @TiaG and @ClaudnDaye all had good things to say in the other thread.

We all are told it is what insulin is needed to keep our bg flat in the absence of food.

  1. Does it strictly address sugar released from our liver throughout the day?
  2. Does our basal rate also address non-gendered hormonal swings that cause resistance (i.e. Dawn Phenomenon)?
  3. Why does just a tiny amount of extra basal throughout the day lead to such deeper, more persistent lows that an equivalent amount of correction dose would NEVER get close to causing? (in my experience, anyway)
  4. Why are basal induced lows (with tenths of units of insulin for me) so much different to treat and watch on the Dexcom than bolus induced lows?
  5. How (and why) does dietary carb reduction lead to overall basal need reduction? (@Eric, @TiaG introduced this in the other thread, and I look forward to more insight on that when people have time)
  6. If we are experiencing (men or women or children) something wherein we need extra basal due to illness, or seasonal change, or hormonal shift, do was also need a corresponding percentage increase in our bolus insulin? If basal needs are increased due to resistance or sedentariness or whatever, would bolus also need a similar increase for accomplishing what it needs to accomplish? If basal needs a boost…maybe bolus doesn’t need a boost since basal has everything under control? Or is it that the insulin we’re using is going to be resisted no matter if it is used as basal or bolus so it all has to increase?
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@T1Allison
These are not simple yes-no answers. I have a few factors to mention for 1 and 2, but it is extremely mind-numbing.

The reply I was working on makes me think how humbling it is that what we are trying to do with a few different rates of insulin or food could ever do what the human body does. We can never really come up with simple numbers that take all of the factors in.

Anyway, just a warning on my reply, if you want mind-numbing, I can post it.

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I’m begging for mind-numbing. Begging, I tell ya.

And I’m adding a sixth question to the original post.

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The human body is so much more complex than we may realize. And every single thing we do interacts in so many different ways. So the question about if basal insulin only covers us when we are not eating is not a simple yes or no.

If you do not eat, the only glucose being released into your body is from your liver. So in that sense, basal insulin only addresses the liver’s release of glucose.

But where it gets tricky is that other factors affect us when we are not eating, and particularly when we sleep.

Just as one small example, we have the nighttime release of growth hormone, which then stimulates the release of a different hormone called insulin-like growth factor 1 (IGF-1).

IGF-1 is made by the liver, and it helps in the oxidation of fatty acids for fuel. IGF-1 release is reduced by the presence of insulin, hormones like cortisol, and estrogen, and it is increased by exercise, fasting, and sleep.

The simple takeaway is that IGF-1 is increasing your oxidation of fat.

But…increased uptake of fatty acids, also inhibits the uptake and phosphorylation of glucose.

So on the one hand, IGF-1 increases at night and helps increase your utilization of fat for fuel (makes sense, since we are not eating at night, right?). But then on the other hand, the same thing reduces our ability to metabolize our blood sugar.

Further compounding it, is the fact that diabetes is linked to changes in IGF-1.

So just as a simple example, nocturnal surges in growth hormone secretion are partly responsible for increases in blood glucose levels (not directly, but indirectly.

And all of that stuff I mentioned is without food. And also, all of the stuff I mentioned can go a hundred different ways depending on hormone levels like estrogen, cortisol, and also how much you are eating.

It’s like a choose-your-own-adventure story book. You can read it every night and go a hundred different ways and never end up at the same place in the book.

It’s egotistical for us to think that we can ever do manually with a few button pushes what the body does automatically. The body is so much more complex than we ever give it credit for.

Here is one reference for the example I am using. The purpose of this link is just to show how much other stuff is going on that we aren’t even considering when it comes to our basal needs.

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This is a great start. :grin: I look forward to much, much more of this.

These mechanisms don’t have to be perfectly understood to be useful. But I think the basal rate questions posed are valid questions worth discussion. I’m guessing you probably agree with that statement.

If my basal needs never fluctuated, I’d set it and forget it. But Crockpot Diabetes does not exist for certain segments of the diabetic population. So that’s why I think this is worthy of discussion.

I’m approaching this from the premise that more knowledge, more observation, more discussion, more questions, will help improve decision making for some of us when deciding what lever to pull (basal vs bolus) in dynamic situations that we did not cause, we did not choose, but we are along for the ride for anyway. Bolusing the hell out of an underlying basal need change will not fix it in any kind of predictable, safe, or useful way, IMHO. But basal changes of minute quantities have such a powerful impact on our blood sugar. I just wonder why minute basal changes do so much more than surfing boluses will ever do from a mathematical and biological perspective.

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Of course, I am not saying it is not worth analyzing and discussing. I am just saying that us trying to come up with simple answers to explain it all is a bit overly-optimistic. We can come up with answers, but they will be incredibly complex.

I agree with that :arrow_up:

Part of the reason is that you bolus for food. And you basal for no food.

Additionally, food has to be converted into glucose that your body uses. Liver glycogen is much closer to a usable state. So liver glycogen can go in and out much differently than food.

Kind of as an example to put it another way - a 100 point spike from food will not be the same as a 100 point spike from liver glycogen. They are not the same.

Somewhat related -
I have always felt like strong basal amount helped me negotiate meals much better.

Basal is the foundation of the house. A strong foundation means you can do much more with meals.

Having a slightly higher basal amount than I actually need means I can eat like a jackass.

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If FUD puts out a cookbook, I want it to be titled “How to Eat Like a Diabetic Jackass”.

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This is good stuff.

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In my experience with insulin resistance, it always required more basal to deal with it but not necessarily more bolus.

  1. Does this mean that the insulin resistance induces the liver to put out more glycogen, and the extra basal is managing it?
  2. Or does it mean that the factor causing the insulin resistance (i.e. one example, increasing levels of progesterone during pregnancy) acts as a Proverbial Bouncer at the Nightclub Door of Insulin Acceptance at the cellular level…and the extra basal just gets the extra factor (progesterone, in this case) out of the way for the rest of your basal and regular boluses to be accepted properly?

Basically, for insulin resistance, which requires an increase in basal, is it truly causing the liver to put out more glycogen or is it that more basal is needed to do the same job due to a different hindrance in the process.

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If my blood sugar is high from glycogen either way, and if it is more ready to go into cells than food breaking down, why wouldn’t a correction bolus bring down my bg much much faster than tiny amounts of extra hourly basal? It is the same insulin, after all. But they fix the problem sooooo differently if I pull the correct lever.

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My suspicion is that this pattern is really due to liver insulin resistance. I’m actually not sure how much peripheral insulin resistance plays a role compared to liver insulin resistance but I suspect it’s a more minor process. When people are able to “reverse” the symptoms of T2 it’s mainly through stark fasting and calorie restriction that strips the fat from the liver and other visceral organs. So I’m not sure how much insulin resistance at the cellular level plays a huge role or if it does it’s reversible with this liver-fat-stripping.

As for why it takes a higher basal rate than bolus – well consider a few things.

  1. If you have an hourly rate of 0.4 units per hour, that actually translates to a steady state insulin level in your blood of MORE than 0.4 units per hour. i can’t remember how much more but it’s closer to 0.5 I think?
  2. When you give an insulin correction dose of 1 unit, the peak insulin level in your blood is much less than that.

So the first step is to do the math and figure out if those correction doses are actually amounting to a cosntant, steady-state level of insulin equivalent to what you would get with at 20% + temp basal.

I also wonder if there’s a certain amount of time that the insulin needs to be pinging the liver to say “hey, start storing sugar” before the liver does so. I guess it depends on whether this increased insulin resistance is occurring as a result of gene expression differences (for instance, making more or fewer receptors on cell membrane), which take at least a few hours to days to change, or if it’s really just the presence of those hormones at certain concentrations, in which case it could ramp up or down in 10 or 15 minutes. But if it’s the former, or on a slower timescale, then you’d need that continuous, steady level of insulin to shut off the sugar-dump signalling – and correction doses just won’t get you there.

But I don’t know if this is right. Id’ need to do more googling to find out.

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another factor for this complicated menu you laid out: alcohol consumption. I found out (thru seat of the pants experience, firstly, and later confirmed thru reading) that drinking too much alcohol in an evening (let’s say 6-8 neat bourbons or so) takes the liver a while to work thru…and alcohol processing is a very high priority task for a liver, taking precedence over the liver’s release of IGF-1 and associated glycogen release, and also takes precedence over gluconeogenesis (important factor, especially in low carb diet I was following).

In short, I woke in early morning hours with a 56 BG, (and a headache) wondering …what happened here?? I should have cut my evening basal dose, but I didn’t know this specific effect of alcohol at the time.

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There are a lot of factors, but one simple possibility is that taking 2 units of insulin over 4 hours is utilized more effectively than taking it all at once.

The absorption stuff, and the surface area of a larger bolus versus tiny little “spits” of 0.05 units every few minutes that your pump does for basal.

But I don’t understand the premise if this :arrow_down: question:

Are you correcting high BG’s with basal?

Are you seeing a 200 BG and taking 2 units of bolus, and then saying that took too long. So the next time you see a 200 BG, you just increase basal instead, and say “that was much faster!” ?

I am just not sure how you are comparing the two things - basal versus bolus for corrections.

On a different idea from that :arrow_up: stuff, are you clear on the idea that your body does not release liver glycogen during times when you have large amounts of insulin? That your body only releases liver glycogen when you have smaller amounts of insulin in your body?

Have we already established that idea, or is it worth going over?

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That is worth going over.

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Empirically, when I’m experiencing what seems to be insulin resistance due to progesterone or [insert other hormone here], that after I try two or three correction boluses to bring down a “stuck” 160, or 190, or 220, whatever the “stuck” number is, I examine if it makes sense from a cyclical perspective that I might need extra basal. If timing makes sense, I’ll start with adding +10% temp basal and see where the numbers float down to for their next hovering point. If they come down from let’s say 220 to 160, I will probably add another +5% or +10% temp basal and see if I can get them down to the 120 area.

Those temp basals equate to not much more than 0.1 units per hour at my maximum settings…so why can 0.1 extra basal an hour do what three correction boluses of 1-2 units apiece Not Even Budge. Like literally, the correction boluses will not budge it. Not even a wiggle. But an increase in basal that is tiny? Then suddenly the whole orbit lowers by 40 points or more, easily.

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Well, this is hard to say exactly what is bringing it down, right? If you do bolus and then later do basal increases, isn’t it the total increase of insulin that brings it down, not just one or the other?

So two things come to mind.

  1. It doesn’t matter what you call it, bolus or basal, it is the amount of insulin you are giving to correct the high BG.
  2. Second, it may be the thing I mentioned, where a larger bolus doesn’t work as well from an absorption standpoint. Smaller bits over time may work better for you.

Have you tried an IM shot for that sort of stuff? If you were to do the same thing for a high, but do it with a pen and go IM, I bet that would be more effective than anything else.

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I know there are all kinds of exceptions. However, if we start looking at all the different possibilities and say “but, but, but”, we can end up swimming in circles. So I just want to give a very general rule for this this sort of stuff works. And not get too caught up in all the millions of scenarios and different things happening.

Just very basic…

As discussed previously, the body uses liver glycogen for fuel when you are not eating. It doesn’t need it when you have food in your stomach and then glucose in your blood right after a meal. But when you do not have a meal, your body needs fuel which it gets from the liver.

In the normal non-diabetic body, when you eat, your body releases insulin. And your liver reads that increase in insulin as a signal. It says, “Hey there is more insulin here than usual, so that means Allison is eating. Since she is eating now, I don’t need to release glucose. Now would be a good time to bank some of this food for later use!”

Your body is so smart. The body wants to preserve itself, so at times of being fed, it takes some of that food and stores it for later.

Another way of viewing this is simply that higher amounts of insulin (when in a fed state) equates to higher amounts of carb storage.

When your body has less insulin, it will not store as much. Your smart liver says, “There is not much insulin here. That means Allison has not eaten much recently! Now is not a good time to store food.”

So while this is a very simplistic explanation, it is however clearly demonstrated by microbiology.

When insulin is absent from cells, Glycogen Synthase Kinase 3 (GSK3) phosphorylates Glycogen Synthase. This phosphorylation inactivates Glycogen Synthase. Glycogen synthase is a key enzyme used in glycogenesis (the conversion of glucose into stored glycogen). And when Glycogen Synthase is inactivated, glycogenesis is not possible.

So if my simplistic explanation does not seem like it is correct, simply look at the more scientific explanation in the few sentences directly above, and see that it really does work that way.

When fed, your body stores more. When unfed, it stores less and releases instead.

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Anymore I typically am not using combination approaches due to my big picture tracking of things. If I’ve seen my breakfast bolus start to lose efficacy over a few days, I’ll just start with adding temp basal bc it’s what is historically needed, and it does the job. But if I wasn’t adding that temp basal, the amount of correction boluses would far exceed the amount of basal insulin I’m getting and it wouldn’t come close to producing the same results. Which is what makes me think the hourly basal has to increase to handle the general resistance from the hormone factor…but it’s amazing that such a small hourly change produces such large-scale results. Which doubly means that the margin of error is quite small…as evidenced by my tanks this week.

Here’s a recent post on this:

And another example:

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Let’s just try for a minute to look at is differently. Let’s think about if it was a delivery problem.

If you were to do the correction boluses as extended, instead of as a normal bolus, would they work better?

Let’s suppose instead of increasing your basal by 0.5 units per hour for 4 hours (2 more units), instead you did an 2.0 unit extended bolus, and you extended if for 4 hours.

Would that work worse, better or the same?

I bet that your body would not be able to tell the difference. Those two things are identical.

Because the terms bolus and basal can get fuzzy sometimes, let’s change the argument for just a moment, and say that it is an issue of how you are delivering the correction. Can you consider it in those terms for a minute and see if that analysis changes perception?

I don’t know if it will change perception, but just wanted to examine this as a possible delivery issue.

In my mind, your body doesn’t care if you call it bolus or basal, it only cares about the timing and the amount of your delivery. If delivering it slower over a longer time works better, why not do it that way?

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Totally open to considering different angles, but this is going to get farther from 12 years of cyclical observations of patterning. How many extended boluses would I have to run to cover insulin resistance over a 2.5 week timeframe? And how would the math of extended correction boluses compare to temp basals? If it’s all the same, it seems terribly clunky when temp basals accomplish the same thing without blocking my ability on the PDM to meal bolus.