IMPORTANT
If the info in this paper is true, then it may explain why these medications are associated with eDKA events
https://www.ncbi.nlm.nih.gov/books/NBK554570/
In particular I note the following text
"Additionally, SGLT2 inhibitors have been found to directly stimulate the release of glucagon from the pancreas, further worsening the glucagon/insulin imbalance, as well as suppressing the removal of beta-hydroxybutyrate and acetoacetate by the kidneys.[] Euglycemia is maintained due to the loss of urinary glucose [] and SGLT2 inhibitor-triggered hypoinsulinemia.[] SGLT2 inhibitors also increase ketone reabsorption, such that ketosis is common in patients taking SGLT2 inhibitors after a trigger such as pregnancy, alcohol, surgery, infection, or starvation."
(the [] are document references that I have removed )
I have seen marketing material for Empagliflozin being put forward as a treatment for obesity in the general public and also as a prophylactic for T2D in relation to heart protection. In that material it clearly stated that this drug used lipolysis (i,e, ketosis) as the mechanism, and that this was enabled regardless of insulin or glucose levels, thereby not requiring diet methodology. What this tells us is that the drug is a chemical override of the body's natural process, and is therefore overriding the normal feedback mechanisms that protect us during dietary ketosis. This drug takes about 3 or 4 days to clear from the body, so this means that the stranglehold on the glucagon remains in place long after the dose was administered. As a result, there is a mechanism here for overdosing. The glucagon it releases inhibits endogenous insulin production and emulates insulin deficiency while the empagliflozin is working. we can only halt it by extragenous insulin.
This is why Low Carb and or keto diets are contraindicated, and it is not a 'maybe', it is a real danger. I suspect that fasting and possibly even skipping a meal is a potentail hazard too. This makes this class of medications a potentially hazardous treatment but it is shortly to be offered to all T2D, all obese, and heart patients if the drug companies get their way. I personally was placed on one of these meds as a heart prophylactic. I have stopped it now because of other serious side effects that I was beginning to suffer and which could have turned into life threatening conditions.
I can only surmise that this medication should be stopped when the fasting blood sugar reaches normoglycemia (around 7 mmol/l) this is only my oponion and has no empirical evidence to back it up, but there will be a minimum level that it should not be used below. Note that it lasts a few days, so dropping the occasional day will not protect.
Note also that insulin users must ensure that they do not drop below this low limit. I would also include RH sufferers as also contraindicated.
The other thing that the original FDA trials data showed was that the drug was only effective for obese patients with BMI > 39 and who had a high baseline HbA1c. The drop in HbA1c after 6 months trial was around 0.65% at best. It was least effective in TOFI patients.
So diet control wins IMO.
