Apologies to anyone following this for the sudden burst of activity meaning that you have to read a load of posts that you weren’t expecting. I’ve had a bit of a brainstorm and generated a bunch of titles that all need addressing for Diabetes Awareness Month, and as T1, awareness of us, the 10% is a broad necessity. I’ve been sitting on the train and writing my tomes, and as such, releasing them after I’ve had a chance to read them!
But coming back to the title. I, and many others with the Libre and CGM systems, have all found that there is a significant difference between what many healthcare professionals (HCPs) in the Diabetes world believe and tell patients versus what we have seen with full traces of our glucose levels. Coming back to a point I made in my post about clinic appointments in July time, the registrar with whom I spoke was unaware of the action time of fast acting insulins.
The advice regularly given is that you can bolus anywhere from 15 mins before to just before eating and it will do the job fine, with some HCPs recommending that you can bolus anywhere from 10 mins before to just after eating. Many people take these kind of approaches, however, it’s not really sensible.
When you treat in this fashion, you get significant post-prandial spikes. But why are these recommendations made? They come from the marketing of the pharma companies that have told and possibly believe that the action times of these insulins is very fast. Well I’m here to tell you that they aren’t.
I’ve had a number of conversations with people on a large Diabetes related forum who insist that as the dietitian told them it was okay to inject post-prandially, then that’s what they would do, so they could adjust dose based on what they ate. How about doing it the other way. Bolus on what you know then top-up later if necessary… And try to always do it as a pre-bolus, except in the circumstances where this is really not possible e.g. when you are eating out.
Why is this an issue? Well there is plenty of evidence to suggest that the old adage that as long as your two hour post-prandial spike is ony 2mmol/l above your pre-meal bg value, then you are unlikely to suffer any issues, is not quite true. In fact any spike between eating and that time can and is doing some form of damage. As long ago as 1998, this report highlighted that post-prandial spikes could enhance diabetic complications and in 2005, this one, by the same author, reported that post-prandial spikes elevated the Atherosclerosis risks. This particular google search provides access to a number of papers that also discuss these risks. I’m not suggesting that the HCPs we are talking about here are unaware of these issues, but some might be less aware than others.
With regard, then, to the bolusing guidelines for current fast actings such as Novorapid, Apidra and Humalog. Why is the 10 mins pre- to just-post an issue? Well, if you look at the time to action on the Libre or any CGM, you start to see that there is an interesting correlation between following these guidelines and the way blood glucose levels get elevated. Primarily, I and many others have found that with these guidelines we see what can be huge post-prandial spikes. And this is the issue. These are damaging.
In fact, by observation, we’ve found that the reality is that subcutaneous bolusing typically needs to occur between 30 and 45 mins before eating as otherwise the insulin hasn’t yet started its action. Now this doesn’t work for everyone, unfortunately, and therefore for any individual, trial and error is required. With pre-bolusing, the post-prandial rise can be controlled reasonably. I can maintain a flat or minimal rise by hitting so far in advance.
But this timing is also out of kilter with what many HCPs know, as we’ve discussed, and is more akin to the older “fast” insulins such as Actrapid (which never did). They are often surprised when this is disclosed.
Now this doesn’t take into account those with Gastroparesis or Delayed Gastric Transit. Those are much harder to deal with and the pre-bolus is a recipe for hypo disaster in that context. I’ll write about these complications another time, but suffice to say that it may be the single most unreported and heavily experienced complication of T1. It requires a whole different management regime.
I’d like to see more use of CGM and FGM technology and patient led research such that HCPs are provided with better information based on what is observed. I’m sure there is a distribution of action times that could statistically be provided to HCPs such that these could be shared with their patients. It would allow better advice at the time of insulin prescription for all HCPs. It should also, perhaps, be part of the clinical trial process that takes place in the UK before a product is allowed on to the market.
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