Requesting Opinions from Type 2s

The following statements are not mine.

“Type IIs don’t have enough effect from their insulin due to resistance or eventual beta cell destruction to get their fasting blood sugar down to a good level. They DO have the ability to manage the fasting margin, so if they can get help from basal to bring the baseline down they can regulate up or down within that margin. In other words, a type II with appropriate basal who is at 170 will eventually come down to their set point, wherever it was titrated to.”

I’m not sure if I simply do not understand what is being said or if I disagree with these comments.

I would appreciate it if those of you more knowledgeable about Type 2 (which could very well be just about everyone) could comment on the above. Thank you in advance!

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Well, I’m clueless. Is it an injecting insulin type question? Or does basal have a broader meaning somehow? I’ll check in, myself, my friend, to read answers from those more knowledgeable!..

I have no clue how true those statements are. From my experience, even though my basal is set right (with insulin assistance), eating will drive my BG up and it will stay there for extended periods unless “something” is done to change that. Sometimes, exercise will help, sometimes drinking a lot of fluids will help the kidneys eliminate the sugar – slowly, but most often my BG will settle into a new high point and stay there. Basal insulin will just keep my liver from “assisting” my BG up, up and more up.

Note, I have not experimented with skipping insulin in quite a while, so I don’t know what would happen now for sure, but the last time I did, the only interesting observation that I made was that there seemed to be a ceiling, above which my pancreas seemed to help prevent me from crossing. I have since had highs above that point; however, so I do not want to repeat that experiment now.


That’s EXACTLY the point of the original quote. As a result of insulin resistance (often exacerbated by beta cell destruction) T2’s cannot produce enough insulin to mobilize glucose derived from digestion of carbohydrates so BG levels rise after eating carbs. Unless they are at a relatively late stage of beta cell loss, they probably retain enough insulin producing capacity to cover basal requirements. So if they don’t eat anything and you can get BG down to the “normal” set point levels (say 5-6 mmol/L = 90-110 mg/dL) BG levels will hold at that point because much less insulin is needed to keep BG at the set point.

You can see this by considering the insulin requirements of typical T1s (who are not producing any insulin but are insulin sensitive). Using myself as an example, my basal pump rates average about 0.75 units/hour. 90 g of carbs would require a bolus of 10 units (equivalent to a peak demand of perhaps 3 units/hour). We can estimate that a non-D might have similar sorts of insulin demands. An insulin resistant T2 might require a basal rate of 3 units per hour and a peak of 12 units/ hour to deal with the meal. If his/her beta cells were still functioning they could probably manage the basal but not the bolus requirements.

Of course once a lot of the beta cells are gone, all bets are off.


I’m still confused, I suppose, but I’ll take your word for it. My beta cells do not appear to be all-that helpful, though not “gone” (as exhibited by my last fasting c-peptide test, which was well below the lab’s reference range, but not zero). My average basal rate is around twice yours, though my requirements for meals is more like 3 times yours, or so. On the other hand, I have never seen a number over 350, even in the worst of circumstances. On several recent occasions, I had a pump failure that resulted in rapidly increasing BGs over just 2-3 hours. To me, it seems like basal needs are definitely not handled well by my beta cells, but, perhaps - since I have not tested lately - on the extremely high end, the beta cells kick in. It seems more like glucose insensitivity (sort of what @Lloyd described once, though his threshold was more like 220). My beta cells aren’t (apparently?) dead - just on “early retirement.”


I basal is 18 units in the day and 12 units at night. This ensures that my levels stay low. However when I eat something I have to make corrections if there are any cards or sugars. Average for a normal meal 3 units of Apidra. If I take a higher dose of basal I can go without the correction however I do not know what the meal is going to be or what is in it. So have to act retroactively.

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The difficulty in talking about T2 is a microcosm of the difficulty in talking about diabetes in general: cases vary and each one is singular and individual. In the case of T2, that effect is exacerbated by the fact that the behavior of a T2 frequently changes over time, particularly as beta cells dwindle. So, a statement that is true and accurate in the beginning may well not be after a few years have gone by.

That being said, the original quote contains a joker—the word “eventually”. In the general scenario described, someone’s post prandial BG might come down, all right, but if it takes 5 or 6 hours to do it, that’s not acceptable. It means you’re living a major chunk of your life with unacceptably high BG levels, and we don’t need to discuss what that entails.

Furthermore, as hinted earlier, once enough beta cells are gone, T2 looks an awful lot like T1 for practical purposes. I’m certainly in that category. After 20 years of fending off this beast, I need both basal and bolus insulin to stay in a good range. Either one alone doesn’t cut it. I began with bolus insulin by itself. It didn’t take me long to figure out, from rampant DP and other clues, that basal insulin was needed, not optional.

Digressing slightly, the thing that offends me the most about this is that as my A1c began to climb inexorably and it was obvious (to me at least) what was happening, nobody (nobody!) even suggested insulin. I had to march in and demand it. That speaks volumes about how the medical establishment views T2 . . . but that’s another rant for another time.


David. Never been to an Endo and my GP I see when I am home every couple of months basically lets me do what I want as long as the levels remain constant and low. In my line of work there is no ways that I could survive without insulin. I eat in a devac do not know what is in the food and have no means to buy my own food.
Yes I use lantus in the morning and night. I use only 15 units. In the day I correct with Apidra after meals as then am I only able to find out how it effected me. I test after the meal make a correction and account for exercise because if it is high I will go for a walk to take the edge off. It has been a lot of trail and error but could not survive without the insulin. I had lost 26kg and have slowly been able to add some weight again.

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@David_dns…Thank you…Still one general language question. Is Basal a term that is ever generic to insulin production in the body? or is it always about injecting insulin?..

The body only makes one kind of insulin. The rate at which it’s secreted is based on what is happening at the time—when food is consumed and blood sugar spikes, a lot of insulin is released to deal with it. In between times, the release is slow and gradual in order to keep BG on an even keel. Very similar to what a properly programmed pump does.

By contrast, injections happen at a single moment in time and aren’t spread spread over minutes or hours, nor are they self adjusting the way your body’s builtin governor is able to do. Thus the need for different types of insulin: fast acting (bolus) and slow acting (basal).

This is a super idiotic concept of natural insulin production, but it’s actually how I came to conceptualize it early on. I know that this is not physiologically correct, but I think of it conceptually this way, and it helps me----

Healthy Beta cells continuously ooze bubbles of insulin… Some of them pop spontaneously and release into the bloodstream continuously throughout the day. This is natural basal production or “phase 2” S some call it. When glucose rises in response to eating or some other event, stress, dawn phenomenon, etc— those bubbles start popping and releasing insulin instantly into bloodstream much more rapidly— or a phase 1 insulin response… I suppose it could be considered the natural bolus mechanism.

Again I’m aware this is an idiotic oversimplification— I do think it’s valuable to put things into outrageously simple terms in order to manage them from a practical perspective though.

Hello everyone,

I thought I might send these quotations from my dissertation.

Etiology and Pathogenesis of Type 2 Diabetes Mellitus

Describing the etiology of type two diabetes mellitus, (T2DM), Surampudi, John-Kalarickal and Fonseca (2009) described the multifactorial nature of T2DM. Surampudi et al. (2009a) reported that individuals with T2DM present with “elevated fasting and postprandial glucose levels” (p. 216). The development of T2DM is gradual in nature and progresses from “normal glucose tolerance (NGT) to IGT [impaired glucose tolerance] and finally to T2DM” (p. 216). The progression from normal glucose tolerance to impaired glucose tolerance is attributed to “the interplay between IR [insulin resistance] and defects in insulin secretion” (p. 216).

Further highlighting the etiology of T2DM, and the role insulin resistance (IR) contributes to the development of T2DM Surampudi et al. (2009b) stated the following:

Insulin resistance can exist in many organs and tissues as the liver and the muscle. Some of the results of Insulin resistance include the overproduction of glucose by the liver (despite fasting hyperinsulinemia and hyperglycemia) and decreased glucose clearance by peripheral tissues.” (p. 218)

Regarding the pathogenesis of type 2 diabetes mellitus and the contribution of other organ systems in the development of T2DM Kalra (2013) stated that the “traditional gluco-centric approach to diabetes, the beta cell is thought to be seat of diabetes pathophysiology” (p. 1). However, insulin resistance is “mediated at the level of three organs [the] liver, adipose tissue, and muscle” (p. 1).

I include this quotation because it appears what the individual is trying to express is that s/he has been prescribed basal insulin to control hepatic glucose output so s/he doesn’t wake up elevated as a consequence of glucose the liver produces while s/he is fasting (during rest). This person could have been prescribed basal insulin because the insulin “controls” the hepatic production of glucose more effectively than metformin (which works on the liver) The fasting margin is likely the upper and lower boundaries of what one’s fasting glucose should be according to clinical guidelines.

I don’t know what the “set point” is. Most people with T2DM or w/o T2DM are unaware what their fasting blood glucose on any day. That’s why we check it so that we can know whether it is low or high. Too, there are so many factors that determine whether one’s FBG are within those clinical “margins.”

I hope this is helpful.

Ok, first, this is a bit of a confusing read. You may want to edit it. If you have (four) leading spaces in a line the forum can interpret that for special formatting (called a code block). That leads to weirdness.

So let me ask you, are you really doing you dissertation on the “Etiology and Pathogenesis of Type 2 Diabetes Mellitus” or is this a section?

And as to the quote from Surampudi, I don’t have any quibble with it but it might not be the most authoritative source. A better source would be Ralph DeFronzo who has literally hundreds of pubmed citations. His 2008 Banting award lecture presented a model of eight fundamental defects associated with T2. One of those defects is the increased production of glucose by the liver but another is also a set point problem which is really a defect with the hypothalamus. DeFronzo’s paper would be considered far more authoritative. More recently Stanley Schwarz has argued for a reclassification of diabetes based on fundamental defects. He recognizes defects in a manner that is consistent with DeFronzo. His paper in Diabetes Care can be found here. There has been some discussion of Schwarz and background information here at TuD.

I appear to have some mix of the defects with my set-point and excess glucose production with my liver (I also have insulin deficiency). None of the available medications worked to correct my chronic high fasting blood sugars but once I started a basal insulin my fasting blood sugars became immediately controllable. Unfortunately I was repeatedly denied a basal insulin by the health care system and had to make my own decision to start managing my diabetes with insulin. I do hope that things change in the future.

@Brian_BSC, Thank you Brian. No my dissertation is not on the etiology of type 2 diabetes. I actually doing a study using avatar-based technology (cartoons) with the objective of increasing access to diabetes self-management education to those who don’t have access to it. Particularly those of low socioeconomic status. The education is basic at best, however, basic is better than nothing.

Respectfully, without discussing which research is more authoritative (I think all are doing their best to add to the evidence base) I was attempting (it seems unsucessfully) to draw attention to the context of the original poster’s comment pertaining to the mediators of type 2 diabetes. It’s not only at the pancreas, as your post and personal experience, rightfully highlight.

I was attempting to emphasize that diabetes is mediated by organs other than the pancreas as your post also highlights. I believe the individual, @rgcainmd was quoting would find (if s/he doesn’t already know) that type 2 diabetes is mediated at organs other than the pancreas.

Unfortunately, that is a common perspective.

My focus was on this part:

"Type IIs don’t have enough effect from their insulin due to resistance or eventual beta cell destruction to get their fasting blood sugar down to a good level.

True, but only partially.

This is why it is so important for PWDs who are prescribed the various classes of medication understand what organ system the prescribed medication is working on.

Thank you so very much or the reference to DeFronzo and on “set point.” I’ll be sure to read it (after my dissertation hearing).

And thanks for the suggestion on editing.

Be well.

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Wow, this whole thread has my mind boggled! I am a diabetic 2 and w as diagnosed 6 months ago and take two metformin a day and will start testing my bc once a day soon. I feel like reading all of this is way over my head! Just found this site today too…

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Hi, :slight_smile:

The insulin the body produces is called endogenous insulin. Basal insulin generally refers to injected long acting insulin. Basal insulin equals background insulin. It is meant to replace the insulin that pancreas is always secreting. It is not meant to cover food that is eaten. Someone who does not produce insulin needs to inject a long acting insulin so they have background (basal) insulin going at all times, because those who do produce insulin are producing insulin at all times.

When someone who produces insulin eats, the pancreas produces and secretes more insulin than it normally does to counter the food that is eaten. When someone who does not produce insulin eats, they need to take a different type of insulin to cover the food they are eating to avoid a spike in their blood sugar level. The insulin that is used for food is usually a fast, or rapid acting insulin and the shot that is done at that time is referred to as a bolus.

In addition to that, those whose body does not correctly utilize the amount of insulin they produce can also benefit from using both basal and bolus insulin.

I hope I explained that in a way that is easy to understand by all

@Gina5 it’s over my head too :slight_smile: but it;s important stuff they are talking about @jojeegirl is doing some research work

This gives a simple overview to how it works for you and me.
For me, the more carbs we eat the more carbs we want. They don’t give up easy and it’s biochemical

Hi Thas,

Did you know that most people with Type 1 diabetes do not test at zero c-peptide, even after having it for 50 years? They have found that most with Type 1 still produce a very small amount of insulin regardless of how long they have had it. The amount they produce, however, is just not enough to do any thing.

I am Type 1 and my c-peptide level at diagnosis was .2 and the low end of normal for my lab was .8. My doctor said that indicated no production of insulin.

Also, most people with Type 2 produce a level of c-peptide that is much higher than the normal range, but they are resistant to insulin so the body is not able to utilize what they produce effectively.

To put it in perspective, your c-peptide was 0.2 and your doctor considered that to be essentially zero. But from papers I’ve read about Type 1s, researchers seem to consider about 0.2 and above to be enough insulin production to have some positive impact on diabetes control, even though it’s not enough to keep someone alive.

The study that found that many Type 1s produce insulin even after 50 years found that 67% of those tested had a c-peptide level of 0.03 or above. So that is a very, very small amount, too small to really do anything, BUT it is useful in the sense that it means there are a very small number of beta cells that are functioning, which could be used from the perspective of a cure (having those cells proliferate, etc.). I believe that same study found that only 2.5% or so of Type 1s had a c-peptide of 0.1 or greater. Of course, these numbers might vary slightly because I don’t know the exact reference ranges of the labs, nor do I have the study on hand to refer to (but if someone wants references, I can dig them up).

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Most, but not all. My c-pep came in at 0.3 the last time we tested it.

What this really does is illustrate for the umpteenth time one of the basic fact of diabetes: blanket rules just aren’t dependable. Each case is individual. Another example: the vast majority of T2s have some significant insulin resistance. I have little or none. My TDD is around 20-25 units which is relatively low by any yardstick.

It’s like Judith says: if you want to treat diabetes “by the book”, you need a separate book for each diabetic. :smiley:

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