Occasionally I experience dawn phenomenon, up to 2-3 times per week. This morning my BG jumped from level at 102 (when I woke up and took my thyroid pill) to 150 in an hour! I snoozed for 20 minutes and bolused at 131 for a correction and meal and got in some steps while puttering around. I also raised my basal 10 percent for an hour. I did okay with it by getting a little more activity but really feel like I ought to have given myself more insulin. Thoughts?
Why is it irregular? For now, let’s not consider differences in hormones or stress. That could be a factor too, but that is a harder thing to assess because there are so many reasons why hormones can fluctuate from day to day.
Think of your liver like a sailor on shore-leave. On some nights, it has just been paid and it goes out to the bars and spends it’s money buying drinks. It has a lot of money, so it buys a lot of drinks.
On some nights, it has no money. So the sailor sits quietly on the dock and carves his scrimshaw or plays his harmonica.
The more you eat, the more glucose (money) your liver (drunken sailor) will have available to spend.
On some days, if you have been eating full meals and have been less active, your liver is the drunken sailor spending money at the bar.
On other days, if your liver is not as fully replenished, it will be more stingy with it’s glucose and not give as much.
Everyone’s liver has about 100 grams of glucose it can store. And the amount is has at any given point is related to how much we eat and our activity levels and stress levels and all kinds of things that are happening with our body.
If your liver is at 80% it will share less than it will if it’s at 100%. If it is at 50%, it will share even less.
Your body has a built-in survival mechanism. It will never want to be fully depleted. The less it has, the more stingy it becomes.
We can see these things as diabetics. We can analyze our BG and know that our body is stocked up or depleted. We can look at our total daily dose and know how much we have been eating, if we are sick, tired, all kinds of things.
Others can never see these things.
It is hard to track stress or hormones. But it is easy to track food and activity and sleep.
Maybe a food/activity/sleep log can at least help you identify a pattern?
My answer’s not going to be as complex.
Pre-pump, If I woke up between 2 and 4 am I’d take a small dose of humalog, earlier the smaller, between 2 and 3.5 units. After waking up, 30 minutes prior to breakfast I’d take a few units and once the number was dropping I’d know it was a good time to start getting some carbs/coffee.
Post-pump, I schedule the basals to increase gradually between 2 and 4 am and then to go back down. Upon waking up, I multiply the basal by around 5 for 30 minutes and take a small bolus. If I wake up later or less rested I usually have to increase these numbers correspondingly. It seems as though once I have some carbs the number will want to go up so I’ll generally want the insulin to be working at that point.
This is actually pretty typical for me. ANYTIME I wake up during the night my BG starts to rise. If I wake up at 2AM it immediately starts to rise and 50 points would not be unusual. If I don’t wake up 'til 6AM then it will start to rise. If I wake up multiple times a night, then I’ll have multiple spikes! So usually I’m in range on waking and will need to take .5U+ depending on the BG.
@CatLady, are you seeing spikes upon waking for the day? Or spikes around 3AM (or whenever early, early morning) while you sleep? I was just curious since you mentioned that you woke up and took meds and bolused for a meal.
I used to have bad DP, when I take my thyroid supplements it usually behaves itself. But I would set my basal for higher amounts for a couple of hours in the dawn hours.
What drives you nuts is when it can’t make up it’s mind, I started getting DP for 2 nights, not for 2 nights, then a night etc for about 3 weeks. I didn’t want to change my settings because it wasn’t every night. I finally adjusted my pump up and the next day it went away permanently again. I have no idea why I got it, why it was random and why it went away lol…but it drives you nuts more when it’s random! When it was happening I looked at my CGM first thing in the am and would give a correction dose. If it got over 160 while I was sleeping my Dexcom would wake me up and I would give a correction dose.
That’s the best analogy ever!! I feel like I sorta knew this but the way you explained it now all the pieces have dropped into place!
Sometimes there’s a definite correlation between activity and the tendency to run low…but not always. I will have to pay more attention to what I am eating and how much activity I am getting in each day. The Health app on my phone will help with this
Spikes seem to start (when they do) around 5 a.m. but occasionally I’ll have a “feet on the floor” bump after being mostly steady at night.
Exactly! But know I have a better idea why this happens.
Thanks, everyone, for replying.
I may be wrong, but I think both DP and FOTF are a symptom of insulin resistance. The rise that begins before sleeping and after getting up vary from day to day because we can be more or less insulin sensitive. Exercise affects IR along with other factors.
While insulin resistance is a driver of type 2 diabetes, I don’t think that type 1s are immune.
I had long known about DP, but became aware of FOTF after starting MDI and getting a CGM. I, too, take thyroid meds fasting and wait 30 or more minutes before breaking fast. I was alarmed at the rise of BG during the wait.
I tried doing a correction dose, but was not particularly successful at getting it right. Long before I started MDI I was using Lantus in a split dose. The morning dose would be quite a bit after breakfast. I moved both doses up so that I injected Lantus at rising.
I don’t know if pumps can be programmed to increase the basal rate just a bit for the morning time. That’s assuming you’re on a pump.
I find that when I exercise after breakfast, I don’t experience DP and FOTF as much the next day. If BG is holding well I don’t do the Lantus dose until 30 minutes before breakfast and then bolus my usual 10 minutes before breakfast.
Who knows, if what works for me will work for you. Since you are CatLady, I spend my time after taking Synthyroid with one or two cats on me, drops my blood pressure right down.
Welcome and thanks for your reply. It is always good to find out how other people handle this kind of stuff.
Check out our cat thread: lots of cat pix and stories. My old cat Zane Grey was definitely my therapy cat but Leo just likes to knead on my abdomen usually right where I’ve placed a device.
The sailor analogy is really helpful. I think explains why a second or third meal depending on activity might appear to randomly deliver a major spike. Like on a day of inactivity.
Does the analogy follow at all to the random times there is a major crash? Like maybe the sailor’s friends show up and start buying rounds. I can’t figure out why a sputtering pancreas might suddenly have a second wind and overshoot the mark. I’m talking about a fast drop, like from 160 to 65 in half an hour, and then it’ll slowly creep up on its own to about 90. Where might that surge in insulin suddenly come from? These are the experiences that confuse me. The crash feels terrible and I’m almost relieved when it stays higher.
Are you taking insulin yet? Any other meds, like metformin or other types of meds like that?
I think it’s tricky when your pancreas is slowly becoming less functional. It will vary between providing sufficient insulin and NOT providing sufficient insulin. And then if you add other things, like metformin or some of the other drugs that get prescribed at this stage, and if you add some insulin to the mix, it can become difficult to know what’s going to happen.
It is hard for me to give advice based on personal experience. I was diagnosed when I was 5 (just a few years ago, ), and my pancreas gave out in a few days. So I did not have any of that experience.
Maybe some of the other adult onset people can share a little bit about their pancreas progression. @T1Allison went through a little bit of that at first.
I don’t know the Why of it, but empirically I crashed for years before I was diagnosed.
I passed out twice in high school.
I’d always keep pop tarts and jolly ranchers in my flight bag when I’d go fly in college (diabetes ended my career later which is why I mention it).
But yeah, I’d get weird lows regularly for about a decade before diagnosis. They happened more frequently the closer I got to diagnosis…at which point my A1C was 9.6%.
I hope you have a less messy path than I did. The fact you’re here and paying attention puts you lightyears ahead of where I was.
I’d crash often or go really high but not because I was still producing insulin but because of being discharged on metformin, basal insulin, and sliding scale boluses without ANY guidance on how to adjust these medications or the effects of activity!!! I got off the metformin pretty fast and on to basal/bolus…but still pretty much on my own to adjust things (like I knew what I was doing, NOT) so I went low a lot. Yep, sometimes I am still grumpy about this!
@CatLady I feel for you, still grumpy here too. Here’s insulin, 1 unit for every 3 carbs…a lot of crashing occurred until I started digging into the internet. Not even a hypo treatment warning.
Unfortunately my honeymoon period was mixed in with the misdiagnosis, no information and drugs that were tried that made me sick etc. So my sugars were all over the place. And add to that like @Catlady said, no guidance on dosing. So it’s hard to know what my pancreas was adding into the mix.
@Caterpillar But I wanted to second to ALWAYS keep a hypo treatment handy, always carry it with you, have it next to the bed and if others are in the house they need to be told to leave it because it’s so important to have it always available!
Thank you. Today would have been a good day to have more food with me as I was helping a friend move. I’m learning it’s better to over prepare/over pack.
I appreciate hearing about your experience. I can see the variability with diabetes can be a roller coaster, especially for LADA! It must have been pretty scary to fly knowing that your BG could drop unpredictably.
I’m the poster boy for insulin resistance, and I have some hopefully minor liver issues to throw in the mix (I’m a 2+ on a scale of 1 to 4, with 4 being full blown cirrhosis, even though I am not, and have never been, a heavy drinker), and I experience DP several times per week. It’s never a dip for me, always a spike, and it wakes me up - anywhere between 3 am and 6 am (I’m old enough that I have to get up to go relieve myself once or twice in the middle of the night anyway, but if I’ve spiked, I usually can’t get back to sleep). @Eric ’s drunken sailor analogy makes a great deal of sense to me (in addition to being hysterically funny) - thanks! I’ve always thought the DP was random, and my endo says it’s common and nothing to be overly concerned about so we never really addressed it, but anything that disturbs my already poor sleep is of concern to me. Now, based upon the ‘drunken sailor’, I will have to keep track of whether the DP correlates to the evenings my wife has later hours and we don’t eat dinner until close to 8pm - I’d hate to have to start eating dinner alone, but if that’s the answer, I’ll just add it to my list of grievances.
Mammals cannot convert fat to glucose, they lack the enzyme that converts acetyl-CoA (results from fat breakdown) to oxaloacetate (becomes glucose). Acetyl-CoA can enter the TCA cycle and provide energy (in the form of ATP), but fat breakdown can’t form any net glucose.
If fat breakdown produced glucose there wouldn’t be such a thing ketosis or a “keto” diet.
@Eric Make sure my biochemistry is correct on this!
I read a slightly different result in biochemistry - Can the human body create glucose out of fat? - Biology Stack Exchange
They assert that a small proportion of the fat can be converted to glucose, but most cannot:
Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.
This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).
The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose (http://www.ncbi.nlm.nih.gov/books/NBK22387/#A3079) in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)
I am not entirely sure that is right.
We can create glucose from non-carb sources. That’s the definition given for gluconeogenesis:
Gluconeogenesis is a process that transforms non-carbohydrate substrates (such as lactate, amino acids, and glycerol) into glucose
But I do agree that we need oxaloacetate for fat metabolism to occur. And we get oxaloacetate from pyruvate (mainly). And we get pyruvate from glycolysis (mainly). And glycolysis is primarily glucose-based.
So we need some small background of carb metabolism to be able to use fat as a fuel.
But I don’t think we need it to convert fat to glucose. That pathway takes much longer though.
But I might totally be missing the context of this discussion. Maybe you are saying we can’t convert fat directly?