First, my limited understanding of ketosis - please correct any misconceptions I have.

If a person, diabetic or not, is metabolizing fat, they will produce ketone bodies that if above a certain level will (most likely) be detected by ketostix or other similar urinalysis reagent.

In Low Carbing, a person intentionally restricts their carbohydrate intake so as to force the body to switch to fat metabolization as a primary source of fuel placing them in a state of prolonged ketosis. If they consume carbohydrates in any quantity, their body will cease fat metabolism and switch to glucose metabolism - so it is one or the other at any given time. This poses little, if any, health risks (possibly a bit higher stress on the kidneys?).

In a diabetic following a non-LC diet, their goal (intentional or not) is to remain using glucose as their primary fuel source. If their body is unable to metabolize that glucose, either because they lack sufficient insulin or because they are so insulin-resistant that the glucose can't enter the cells properly, then even though they have sufficient glucose their body will still resort to metabolizing fat (and protein). This also places them in a state of ketosis, but for a very different reason. First and foremost, their body is metabolizing fat even though there is sufficient glucose still in the blood. The combination of both fuels being present while only one of them is being used (indirectly) results in a lowering of the blood pH levels to a dangerous level. This is the condition known as diabetic ketoacidosis.

So now we have the situation of a diabetic following an LC diet. Under normal conditions, if they are following plan, their blood sugar levels should remain reasonably low as long as they are ketosis. If, for whatever reason (too many carbs, missed medication, etc), their blood glucose level rises they will get knocked out of ketosis just like a non-diabetic. The problem is if they either experience increased blood glucose levels without getting knocked out or if they re-enter ketosis despite still having high blood glucose levels. Both conditions are indicative of diabetic ketoacidosis.

Any major misconceptions of fallacies so far?

So here is my question - does being firmly established in dietary ketosis increase the risk of incurring diabetic ketoacidosis if blood sugars get spiked? Perhaps what I am really asking is better understood by considering a hypothetical case.

Before I started low carbing it was not uncommon for my blood sugars to spike to 300 or higher. Now, let's assume that when that happened I was on the verge of developing diabetic ketoacidosis but didn't quite do it. Now shift to after I have been low carbing and maintaining myself in a firm state of dietary ketosis and I consume a bunch of bad carbs that cause my blood sugars to spike to the same level they did before. The question is whether I would now be more likely, less likely, or just as likely to develop diabetic ketoacidosis as a result?

A related question is how quickly can diabetic ketoacidosis develop? Minutes? Or does it require at least a somewhat prolonged period of time during which both high glucose and on-going fat metabolism are present?

Another related question. Before I was diagnosed with Type II, I had the classic symptoms of highly increased thirst, foggy mental processes, and also steady weight loss. My HbA1c levels were very high (12.8). Is it reasonably safe to assume that I was probably in a state of at least mild diabetic ketoacidosis during much of that time (several months)?

Thanks to anyone that can provide some insight.

IMHO, DKA is more related to T1 that do not produce any insulin and have so
called "brittle" diabetes, which is very hard to control. T2 it is not likely to develop this condition even after a carby meal while on LC diet. But I am no expert, so here is some info on DKA:






IMHO, what you describe is rather ketosis than ketoacidocis, converting fat and protein in glucose via gluconeogenesis and lipolysis, is not automatically equates to ketoacidocis. But this was already discussed on the forum, so may be this post will clarify it:
http://forum.lowcarber.org/showthread.php?t=79795


Thanks to anyone that can provide some insight.[/QUOTE]

Thanks. I looked at that post, as well as posts referred to by it, and I didn't see anything that really clarified what I was asking, at least not that I recognized as such.

I don't follow the reasoning in your quote above. Not saying it's wrong by any means, just that I don't follow it.

If someone has tons of glucose already in their blood from their food (so that their BG is 300 or 400 or more) and they lack the insulin to get it into the cells to get burned, why would their liver produce more glucose from protein - especially to the tune of losing a pretty steady couple pounds a week over a period of half a year or so? And if ketoacidosis is ketosis in the presence of very elevated blood sugar levels, then how can it be ketosis and not ketoacidosis?

I think the list of common causes in the first quote you refer to says a lot - one of the common causes is new onset of diabetes. This makes sense to me. A person with new onset and as yet undiagnoses diabetes is going to have insufficient insulin levels for the glucose they have. It makes sense that their body would have to start burning fat and producing ketones. If their diet was heavy on the carbs, which they can't use for fuel, then they would start losing weight even without dieting. That would seem to almost require them to be in a state of DKA - or at least moving in that direction.

Since I didn't test prior to being diagnosed, I don't know whether I had ketones in my urine or not.

Bill, Ketoacidosis can develop in a matter of hours but that's highly unlikely in a T2 who still produces some insulin and much more likely in an insulin dependent T1.
Type 2's are more in danger of a condition called a hyperosmolar state
The main differences between benign ketosis and ketoacidosis is the acid part which results from having high blood sugars (which contribute to a lowered blood pH) and ketonemia (ketones in the bloodstream) which also can tend towards a lowered pH. Under normal circumstances, the body's buffering systems are able to handle dietary ketosis and maintain blood pH within normal limits without breaking a sweat but when you throw in the additional burden of high blood sugars and the kidneys working overtime to try to get rid of the excess sugar and the excess ketones, the body's buffering system can become overwhelmed and you can start becoming acidotic. T2s produce insulin which tends to inhibit lipolysis and they are resistant to developing acidosis because of that.
As I understand it, a type 1 can be in trouble at a lot lower blood sugar than a type 2; anything over 250 is a big problem for a type 1 and ketoacidosis can start developing for them at that point but a type 2 isn't in serious danger until blood sugars are over 600 and then are more likely to develop a hyperosmolor state rather than ketoacidosis, not that the condition isn't equally serious...it is. When a T2 spikes their blood sugar, fat burning usually stops fairly quickly because of the resulting insulin spike.
A blood sugar spike of a few hours isn't likely to cause a problem, especially in a type 2, other than the sometimes uncomfortable symptoms of high blood sugar such as thirst, hunger and frequent urination. Elevated blood sugars over a prolonged period of time could start getting a T2 into ketoacidosis territory or hyperosmolar territory. The fact that you were losing weight indicates that you were headed for trouble and it's probably a good thing things were caught when they were. My symptoms were similar when my blood sugars went out of control with a weight loss of about 10 pounds in a few weeks.
Does this help answer at least some of your questions?

Yes, that helped a lot. I had never heard of HNS before. Thanks, Lisa.

Assuming that ketosis was being inhibited, what was the mechanism that was causing the weight loss?

I believe it is gluconeogenesis (muslce protein convertion into glucose) due to inability of cells to use dietary glucose (low insulin or IR), and glucose loss via urine. Technically, you must have really high BGs (over 300) on a regular basis to see massive weight loss.
here is some info on gluconeogenesis:
http://web.indstate.edu/thcme/mwkin...neogenesis.html
HTH

Again, I don't understand why, if the cells can't use dietary glucose, the body would start manufacturing more glucose. And, with an HbA1c of 12.8, my average BG was well in excess of 300 on average.

Inhibited doesn't mean totally or permanently. A body can only take so much. Type 2's can and do experience ketoacidosis, but it takes a lot more abuse and time (along with totally ignoring a lot of danger signs) for them to get to that state than for a type 1 and it tends to happen more gradually. The fact that you were losing weight while experiencing high blood sugars should tell you that you were burning your fat stores. Some of that weight loss may also have been water loss as your body attempted to get rid of the excess glucose via your kidneys; glucose takes water with it. For you, the threshold must have been reached where the insulin that you produce could no longer get the glucose from your bloodstream into your cells. Your cells, being starved for energy, began utilizing fat for energy.
The fact that your body's buffering systems were able to compensate and keep your pH relatively within normal range doesn't mean that your body has the ability to continue doing that forever.
Sudden weight loss should always be checked out by a doctor unless you are trying to lose weight.

Thanks again, Lisa. When I said "inhibited" I was only meaning "during the times it was inhibited".

One thing you said fills in another gap - I've always wondered what the cause was for the voracious thirst I had. I would wake up three or four times a night and just HAD to have a liter or more of water each time - which, of course, I would be sitting on the toilet getting rid of the last liter or so. Now it makes sense - the body is trying to cope with the huge excess of glucose by dumping it via the kidneys. Hence the need for a lot of water, hence the amazing thirst.

Am I correct in assuming that, during a period like this, your liver is unlikely to be converting much protein to glucose? Or is there something else that would cause this to happen at the same time?

One thing that is probably causing some confusion is that I am almost certainly using some terminology wrong. I've talked about possibly being in a mild state of DKA. What I have been thinking is that DKA is ANY time that fat is being (incorrectly) metabolized even though sufficient sugar is there and that DKA is a problem once it reaches a certain level. Now my thinking (correct me if I'm wrong) is that DKA is a name used specifically for this situation only once it has reached a certain level. Is there a term used to describe the general situation where blood pH levels are still acceptable but your body is burning fat when it shouldn't and when there is adequate glucose available?

I'm also still very unclear of the distinction between DKA and HNS. I read the discription in the link you provided, but readily admit that it was far to technical for me to grasp the meaning of much of what was being said. Do you know of a description of the two that a lay person can understand so as to grasp the basic distinction between the two?

Thanks again.

Correct. DKA only exists only once the acidosis part exists. Whether or not the acidosis develops depends on a lot of factors most of which are not usually present in a type 2.



Yes. It's called uncontrolled diabetes.




I'll try.

DKA occurs when you have an acid condition of the blood because of a combination of high serum glucose and ketonemia (ketones in the blood) that overwhelm the body's buffering system. The symptoms produced are distressing and uncomfortable leaving no doubt that something is seriously amiss.

HNS occurs mostly in type 2 diabetics and has a lot to do with how the body attempts to get rid of excess glucose. Basically, your body tries to dump the excess through the kidneys. This also involves a lot of water loss. The person experiencing this condition may or may not experience the symptom of increased thirst. If you drink enough fluid to replace what was lost, the osmolar balance shouldn't be affected. However, if you don't or don't drink enough, your osmolor state is affected and you have just as big of a problem as someone in DKA but for a different reason.

DKA: pH imbalance
HNS: Fluid Imbalance

Both have the same root cause: Hyperglycemia, but because the body is dealing with the situation in a different manner (largely depending on how much insulin is present in the bloodstream), the results, while equally serious, are different.

Does that help or have I just confused you more?

It helps.

Next set of questions.

I always assumed that "uncontrolled diabetes" merely meant that, primarily, blood glucose levels were well elevated regardless of whether fat was being metabolized.

I envision a continuum of conditions, starting from (1) normal metabolism where a person has normal BG levels and excess glucose is converted to fat and stored. The next stage would be (2) where glucose can still be metabolized and stored, but not all of it and the rest is left in the blood resulting in high blood sugars. The next step is (3) where the excess sugars are sufficient to result in them being dumped in the urine. Next would be (4) where fat is beginning to be metabolized. I don't know that (4) always occurs after (3). If they can happen the other way around, I don't know that they must occur that way. But I would have called (2) uncontrolled diabetes. It sounds like, now, this might not be the case. That uncontrolled diabetes describes the case not only where the BG levels are substantially elevated but where fat metabolism is also occuring, correct? If so, then is state (2) even possible? If so, what term describes it?

I'm slowly getting there and appreciate the help.

Bill, I think what you are looking for is something along the lines of precise demarcations of where one metabolic state ends and the next begins and I'm afraid that is well beyond my level of expertise.
To be honest, I'm not sure such a thing actually exists and I don't see it as a set of clearly delineated conditions but more of a continuum of overlapping metabolic states. I've honestly never felt a need for knowing the precise point at which I get into trouble because I don't make a habit of pushing my luck, so to speak, and do my level best to keep my blood sugars in check all the time. There are times when I'll get a spike despite my best efforts, like the occasional illness, and I know that for myself I start to notice a difference when I get much over a sustained level of 150 and start to feel 'yucky' for lack of a better term; unwell, fatigued, foggy.
If blood glucose is much elevated for a prolonged period of time, cells are likely not getting sufficient energy from glucose. Cells must have fuel or they die. If they cannot obtain fuel from glucose, they must obtain it from fat.
Where that point happens (at what level of blood glucose) is going to vary from person to person depending on several factors such as their level of insulin resistance and their ability to produce insulin. As I understand it, any time blood glucose is elevated, either the insulin production is insufficient or the insulin resistance is greater than current circulating insulin levels can overcome or both. Whatever the reason, an elevated serum glucose level means that glucose is hanging out in the blood stream where it cannot be used and is not being moved into the cells where it is needed. One of the symptoms of diabetes is fatigue (ie lack of energy ). If you think about the process of switching from glucose burning to fat burning even for a normal person starting a low carb plan, the 'switchover' isn't instantaneous but rather a gradual process that takes a few weeks to fully kick in.
Uncontrolled diabetes is a non-specific term which simply means that the current regimen is unable to maintain blood sugars within an acceptable range but other definitions give a blood glucose of 300 as the point at which 'uncontrolled' diabetes is defined. Based on what you are telling us, you were at that point.

No, I'm not looking for a sharp demarcation of states at all. As I said, I see it as a continuum of conditions. But even so, there are terms and descriptions that are used to describe various ranges along that continuum. The boundaries are not precise, I would be surpised if they were.

What I'm trying to gain an understanding of is what the basic order of things is. For instance, I know that, at some point, a diabetic starts metabolizing fat. I know that, at some point, their blood sugar starts rising. I know that, at some point, they start dumping sugar into their urine. I don't for a moment believe (could be wrong) that any of these are some kind of immediate on/off switch behavior. I would expect them to be gradual and progressive. But I would also expect for there to generally be an order that is followed.

For instance, would a T2 diabetic normally start metabolizing fat before their BG's have risen at all? My present thinking is that this would be unlikely - I would expect their BG's to start rising first and well before fat metabolism begins. But what about starting to dump sugar into the urine? Does this normally begin before any significant fat metabolism has started, or is fat metabolism usually well underway before sugar starts getting dumped into the urine, or are they completely unrelated. In other words, if you had two patients (neither of whom are low carbing) and all you knew was that Bob was dumping a little higher than normal sugar and Joe was dumping a little higher than normal ketones (and every other cause except diabetes related stuff is assumed to be ruled out), would you have any basis to suspect that Bob is probably dumping ketones or that Joe is probably dumping sugar? Similarly, if all you knew was that Bob was NOT dumping sugar and that Joe was NOT dumping ketones, would that give reason to suspect that Bob is also probably not dumping ketones or that Joe is probably not dumping sugar? Or does know the result of one test, be it positive or negative, give no indication as to the probably positive or negative state of the other test?

I'm not asking so that I can "push it". That's not my motivation at all. Nor am I particularly concerned about knowing what precisely was going on with me before I was diagnosed - I was simply using that as a specific example. I'm just trying to gain a better understanding of some of the finer points of this disease.

One point that I am still very unclear on - the other poster, Dina, has twice said that she thought that a T2 with very high BG levels would be undergowing gluconeogenesis and burning protein. That, based on my present very incomplete understanding, seems unlikely. Am I wrong? Does the liver of a T2 patient commonly convert protein to glucose even more as their BG's rise to very high levels? If so, is there a reason why the body would be doing this? I could see something along the following lines - there is insufficient insulin for the glucose to get into the cells and the cells only know that they aren't getting glucose to burn, so they sucrete hormones, enzymes, or what have you that trigger the liver to start converting protein to glucose. That seems unlikely, given that the cells (or something) are able to start switching over to a fat metabolism instead. But I don't know and am curious.

And, just want to add, that I really do appreciate you trying to explain things as much as you can. Thanks.

Initially, this can and does happen as the first response of the body to signals from the cells that they are not getting enough glucose is to produce more glucose through release of glycogen stores and gluconeogenesis. When that strategy fails, the body turns to fat burning. Many of us experience a process known as The Dawn Phenomenon (or DP) where blood sugars rise overnight due to a series of hormones that rise and fall during sleep that signal the liver to begin producing glucose even while low carbing and, in theory, burning fat stores for energy. This link may help explain that process a little better.



That depends, those of us who are T2 and desiring to lose weight (ie burn our fat stores) can do so through calorie restriction or carbohydrate restriction. Neither requires a rise in blood sugar.
For argument sake, a diabetic not practicing calorie or carbohydrate restriction would not start burning fat stores until the cells signal that they are not getting enough glucose (IR exceeds insulin production) and the initial strategy of producing more glucose doesn't work. So...yes, blood sugars would have to rise significantly before fat metabolism ensues.
In most people, glucose starts appearing in the urine when blood glucose concentrations reach 180 or higher.



Let's take Bob first. If Bob has sugar in his urine, he may or may not also have ketones. It depends on how high his sugar is and how long it has been that way but we cannot assume that the presence of glucose in the urine automatically means ketones are also going to be present.
Joe, on the other hand, would be assumed to also be dumping glucose in his urine if ketones were detected in the urine because in a non-low carbing diabetic, elevated blood glucose concentrations preceed ketone production.