@Ronnie5cakes, I undertook to read all that you were told during Monday and add if there was something that occurred to me.
There is so much to get one's mind around: so many insulin types with different consequences; 42 recognised factors that can affect BG; is PERT providing full digestion? The consequence is that the "numbers" are our best attempt to make D management a science and in practice it is much more of an art. Throw into that mix that we all are different and one person's metabolic response to any one scenario could be very different to the next person - thus shared knowledge can help but might further confuse.
An observation about insulin, if I may. To our body insulin is just .... well ... insulin. Your body doesn't know if the insulin is natural or extraneous. It doesn't know that some clever engineering has made extraneous insulin to be rapid or slow release. Insulin as a hormone "facilitates" the movement of glucose out of your blood. If insulin is there in your blood your body will make use of it to draw glucose from your blood into your cells for repairing damaged cells, making new cells and generally doing all that good stuff that our muscles and organs need. If your BG is already low, excess insulin will topple you into that hypoglycaemic state. One of the essential regulating mechanisms for turning up or down our natural insulin production comes from our pancreas in the form of a rarely mentioned hormone called somostatin; we're told no pancreas = no insulin, no digestive enzymes and possibly told no glucagon; we take measures to mitigate against those missing hormones. Intellectually I realised that I had to mentally and thus manually totally replicate all those missing hormones, but I didn't know the brain needed one's pancreas to do the practical regulatory work using somostatin from my non-existent pancreas.
T1s go through a transition of declining natural insulin production as their autoimmune condition progressively destroys that insulin making process and this transition can be irregular from possible surges of natural insulin. T1 BG management can be very confusing, particularly in their early years, with no way of knowing until after a day has passed whether their natural insulin has been even or irregular through any 24 hrs .
Whereas we both now produce zero natural insulin; there is an advantage in that certainty - one confusion factor is eliminated. A 2nd advantage is that, as far as I know, we have no particular susceptibility to other autoimmune effects or considerations.
Our T3c may be perceived as if it is T1 in its later stages, but it is also very different in origins. T1s unquestionably have their unique considerations. As we do with our different and abrupt start point.
Firstly (and in my opinion most important for me) is your basal right? The Fundamental Principle is that if our basal (=background) insulin is not right then bolus is trying to compensate for that, which has a significant bearing on getting one's bolus ratios correct. Getting your basal right first is a key opening thing yo do and it may be the main reason why you're on the current roller-coaster
The profile of a basal such as Levermir is short enough to be administered 2 x daily; change of Levermir doses is practical from one day to the next and different doses for am and pm is appropriate to get one's basal closer to matching what your body is doing day and night. A disadvantage is that daily BG management is reviewing both bolus and basal. The mental juggling has unquestionably increased.
Lantus = slower/longer profile. But it's profile is not quite covering 24 hrs and that profile is not totally even across those 20+ hrs. So timing of Lantus is relevant; where should the missing last 4 or so hours of Lantus be timed to end up? Eg Lantus at 8am and it is winding down c. 4am - just when either or both the Dawn Phenomena (DP) or Foot On The Floor (FOTF) are potentially kicking in.
I am a big fan of Tresiba; it has a very long lasting profile, c. 40 hrs with an extremely even release during 37-38 of those 40 hrs. So today's dose is topping up yesterday's dose. This can be perceived as inflexible, changes of dose can take 3 days to have an effect. BUT my perspective is with the correct Tresiba basal dose there is a very stable platform for safe, level BG at nights; with only infrequent adjustments to Tresiba through any 12 month period. ALL other extraneous insulin comes from your easy changeable bolus, along with food and exercise/ activity. Whatever Tresiba is bringing to the daytime party is whatever it is; and it should not, must not, be added to the "thinking" (sometimes over-thinking).
@rebrascora and
@Wendal covered:
enough Creon?
Libre limitations;
treating hypos (including we're all different);
effects of exercise/activity;
general good BG management (with ref to trial and learning, a range of actions could be needed);
some reassurance that there was a light at the end of the tunnel;
try to pace yourself,
tackle this marathon one bit at a time;
make full use of the Libre Logbook (it is far superior to the Dexcom G7 for recording data)
use the Libre alarms as alerts;
and several other gems or gold nuggets in the responses generally.
So lots to dig into there.
I had one extra thought - have the courage to lean on the trend projections from Libre. If you go hypo have you got the Alarm set at the top of its Low range and did you heed the 1st Alert? At the end of a day a hypo means you had too much insulin ion board. And you couldn't respond quickly enough. Can you retrospectively analyse how that occurred.
If you then go hyper did you overreact to that hypo and thus end up with too many carbs on board? Was there a lesson you could learn from that? Generally its very hard to break the hypo / hyper roller coaster and that instability breeds extra hypo/ hyper cycles.
Your reply to me today was overly flattering: I still sometimes feel like a Newbie; but my 1st year without any CGM made me determined to do better, once I saw a graphical display showing how erratic my BG Management actually was.
pthb.nhs.wales
