T1DConquerer
Newbie
- Messages
- 3
- Type of diabetes
- Type 1
- Treatment type
- Insulin
Thanks for citing this great studyHi @T1DConquerer
Researchers from my Diabetes Clinic recently published this short study on different diets for Type 1s and the effect on ketone production. This is a preliminary study, but the authors conclude that the levels of ketones in the low carb groups stayed lower than they had anticipated and below the clinical threshold for DKA.
I have been given a ketone meter to track my ketones and was recommended to test in the morning (after overnight fast). My levels do rise as I decrease carbs, but I've noticed that being dehydrated can also cause ketones to rise.
I am not aware of eDKA being associated with keto diets. The range of blood ketones due to ketosis rarely exceed 4 mmol/l (72 mg/dl) and even intense sport activity will not raise it much higher. eDKA is usually levels of 10 mmol/l and above. There is no real evidence of DKA of any flavour occurring with blood sugar levels lower than 10 mmol.l (180 mg/dl) which is not as high as normal DKA caused by insulin deficiency.
, So it is usual for T1D and sometimes T2D to experience DKA when the pancreas output is too low, but is nearly always caused by very high bllood sugar levels of 20 mmol/l or higher, combined with insufficient insulin. eDKA is different as it occurs with an apparently working pancreas that has been interferred with such as when taking certain medications. The Gliflozins are one med that can give this, but there seems to be some evidence that the new meds that force GLP-1 to override the normal beta cell operation may overdrive the beta cells leading to a loss of insulin output temporarily. So maybe if you are in the honeymoon period, then I suppose it might affect you like that, but unless the GLP-1 is being forced by some other mechnism, you would probably experience high blood sugars at the same tinme. so not euglycemic.
The use of keto diet by someone using insulin is not generally linked to eDKA, but will increase ketone levels naturally and this is a known and expected event. Obviously, there is risk of hypo and matching insulin dose to diet can be tricky, especially when carb counting, and I believe that keto insulin users find they may have to add in a bit extra to cover protein intake as well (I have seen 50% meantioned as a rough guide, but I am no expert in this)
Now, weight loss injections like Ozempic and wegovy are contraindicated for T1D, probably because of this increased risk of eDKA. But there are T1D using these meds, and so far any incidence seems to be rare. But apparently possible, as described in the StatPearls document linked by @EllieM previous.
To quote from it
"Therefore, conditions like anorexia, gastroparesis, fasting, use of a ketogenic diet, and alcohol use disorder can lead to states of carbohydrate starvation" So the operative word here is starvation. a proper keto diet will trigger fat burning mode, which causes gluconeogenesis to create glucose for the brain and vital functions, I suppose there is a risk that there may be other conditions that interfere with the glucose generation operations, but then glucose would be below the 10 mmol/l threshold for eDKA. And this is not being reported.
I did find this case study report for DKA in a Type 2 patient
But he had bgl levels of 424 mg/dl on admission, so hardly eDKA. He was also re=classified as T1D on discharge-
Personally, I cannot get my head around why a T1D would want to use a keto diet anyway. i can see that carb reduction could help lower the swings and roundabouts and perhaps enhance control, but keto seems to be pushing it too far especially as you say, insulin users on a variable treatment regime adjust basal and bolus to suit, But fixed dose users should not attempt to go keto or ultra low carb IMHO.Appreciate your insight!
Just as a disclaimer, I don't claim to know all about physiology and human physiological processes, in fact, I'm still a newb when it comes to these things. But I've learned quite a bit in a short-time and want to be sure of all of the factors involved before I transition to a low-carb diet. Especially euDKA, how it can happen, and how it actually happens physiologically, whether or not the risks of euDKA are higher on a low-carb diet (which is probably true), etc.
I understand that during nutritional ketosis ketone levels of 0.5 to 3 mmol/L occur and this isn't really cause for concern in a non-diabetic person. If a type 1 diabetic for example was to go low-carb, he/she would also go into ketosis and have blood ketone levels within this same range (provided the carbohydrate is restricted enough to even go into ketosis). So long as this type 1 diabetic takes the insulin to cover the carb-intake, plus basal requirements, there shouldn't really be cause for concern, but it is more complicated than this:
I cannot directly post a link to the study below as I don't have enough posts to do so just yet, but traditional DKA (the hyperglycemic variety), although often associated with blood ketone levels 3 mmol/L and higher, can also occur with blood ketone levels as low as 1 mmol/L. This is why various leading diabetic institutions and societies put blood ketone requirements for a DKA diagnosis at >1.0 mmol/L for the sake of conservatism in diagnosis.
Per study:
"Our results showed that diabetic ketosis patients have blood ketone levels of 1.05–5.13 mmol/L, with 21.7% of ketotic patients having a blood ketone level of 3 mmol/L or more. If all the DKA patients (typical, atypical, and lactic acidosis-combined, n=255) were analyzed together, blood ketone levels ranged from 1.02–15.9 mmol/L, with approximately 30% of patients having less than 3.0 mmol/L."
So some of the patients were actually in diabetic ketosis rather than DKA and their ketone levels were anywhere from 1-5 mmol/L of which 22% were above 3 mmol/L and not in any DKA. This might be encouraging for soon to be/existing low-carbers. However, the fact that 30% of patients with actual DKA had blood ketone levels below 3.0 mmol/L is quite alarming.
Since DKA can also occur with blood ketone levels below 3.0 mmol/L, as low as 1 mmol/L even (well within nutritional ketosis), it might be safe to assume the same is true for euDKA.
And this goes to my main concern with euDKA is that it seems the risk of it occurring rises with a low-carb diet due to individual sensitivity and variability.
Say for example a Type 1 diabetic is eating a low-carb diet of a maximum of 50g carbs a day (I get that traditionally this is known as keto but there seems to be some marginal interchangeability, suffice to say, keto is certainly low-carb, but very-low-carb) This individual is taking sufficient bolus insulin doses for every meal, along with basal insulin requirements. As this person is in nutritional ketosis, the metabolic processes of lipolysis, beta-oxidation, and ketogenesis are going to be more prevalent, but sufficient insulin dosage should be enough to prevent excessive states of the processes. Here's the kicker: What if it doesn't? What if for whatever reason this individual, despite nominally taking sufficient basal and bolus insulin cannot prevent excessive states of lipolysis, beta-oxidation, and ketogenesis in his/her body because personally for him/her the carbohydrate-intake is just too low, and so since these fat-burning metabolic processes continue to occur excessively, a dangerously high ketone concentration is formed in the blood negatively altering the acid-base balance of the blood to metabolic acidosis. What if even 70g carbs a day is too low? It's so individual specific.
Also while the above mentions insulin insufficiency (which it's important to note, was not readily known that it was insufficient likely due to the presence of normal glucose levels), as the primary reason for euDKA, does insulin insufficiency even have to occur for euDKA to happen as opposed to hyperglycemic DKA? That is for some people, do the blood ketone levels associated with nutritional ketosis alone result in negative changes to the person's acid-base balance, and therefore metabolic acidosis? What if some people for whatever reason have a reduced ability to clear ketones efficiently, leading to their toxic accumulation? I suppose the entire scenario described in this paragraph may or may not be labeled euDKA, but likely another form of acidosis, but labels aside, it's still a risk-factor with a low-carb diet, no?
There are a lot of factors here at interplay and it can be hard to discern the main culprit/s. I understand that euDKA is rare even on a low-carb diet and that it's primarily caused by prolonged fasting (whether deliberate or due to illness), among other reasons, but it's important to dissect everything that's connected, so not only me but others can understand what they are getting into with a low-carb diet as a diabetic.
What do you make of all of this?
Lots of non diabetics want to do a keto diet, so why not T1's? We're pretty much like normal people.Personally, I cannot get my head around why a T1D would want to use a keto diet anyway.
T1D are normally at higher risk of DKA than normal people. The possibility of missing a dose can trigger it as can fasting. It is not so simple for a T1D to keep in ketosis anyway and adjusting doses can be tricky at low carb levels due to fat and protein interference, Keto is not just about carbs. T1D have higher glycogenesis due to Glucagon anyway.Lots of non diabetics want to do a keto diet, so why not T1's? We're pretty much like normal people.
I think I would be very close to keto levels on most days if it weren't for the two high carb Belgian beers I have almost every day.
I have no idea if I ever have been in ketosis, and it's not something I care much about either way, but I do know that more than about 7 grams of carbs for my first meal will spike me, no matter how I dose. So I have a very good reason to keep my breakfast very low carb.
Other carbs I eat come mainly from lower carb veggies and condiments, and hummus for my midnight snack.
T1D are normally at higher risk of DKA than normal people. The possibility of missing a dose can trigger it as can fasting. It is not so simple for a T1D to keep in ketosis anyway and adjusting doses can be tricky at low carb levels due to fat and protein interference, Keto is not just about carbs. T1D have higher glycogenesis due to Glucagon anyway.
Hi OldvatrAccording to NHS advice, ketone levels of 3 mmol/l or higher requires an urgent request for a blue light taxi to A&E. Also a reading of 2+ or more on weestix is a similar emergency.
I am using SGLT2 med, and my pee regularly registers 8 on the stix, but I am not in DKA. it is also a regular feature of ketosis that readings up to 4 are normal, and can go higher through exercise. So is that why the NHS states that keto diets are dangerous?
As far as I know, this is only true when either running high or being ill.T1D are normally at higher risk of DKA than normal people.
Missing needed insulin doses will make you rise, which is a risk for DKA. Why would fasting trigger DKA in T1's? (Provided we keep our BG at normal levels (so still inject for the glucose we produce ourselves.)The possibility of missing a dose can trigger it as can fasting.
I find dosing for protein and fats much, much easier than dosing for carbs. Keeps me level well below the prediabetic range.adjusting doses can be tricky at low carb levels due to fat and protein interference
This implies that the extra glucagon increases BG, so it's still about high BG and DKA, not eDKA.T1D can suffer a marked increase in glucagon following a meal, and this triggers gluconeogenesis to generate extra than necessary glucose from fatty acids in the liver, and this process also creates ketones as a byproduct.
I am aware that it is perfectly possible for T1D to follow keto. I am talking Risk, not certainty. But should all T1D be encouraged to go for keto?This implies that the extra glucagon increases BG, so it's still about high BG and DKA, not eDKA.
If BG rises above normal from either food or gluconeogenesis it means the T1 isn't adequately injecting to keep their BG in the normal range.
There are many T1s doing very well on keto type diets with hba1c's in the thirties whithout ever going into DKA.
But we T1's don't only inject for food, we inject based on BG and predicted BG as well. So there is no significant rise.But if your keto diet is starting with a baseline of 5 or 6 mmol/l then adding to that may still be significant and yet be below the 20+ that normal DKA presents as. Remember that the glucagon runs while metabolic glucose sleeps, i,e, it is happening during fasting periods.
Insulin users inject the insulin needed for this, it really isn't much different than endogenous insulin, if not exactly the same.For normal and T2D we actually resynthesise the ketones into COa and ATP for use in the mitochondria but that needs insulin to open the door for it to happen. This too is a risk factor at play for T1D and other insulin users.
No, why?But should all T1D be encouraged to go for keto?
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