Requesting Opinions from Type 2s

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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Editing my post cause I thought I was replying to someone else, sorry, same basic principle holds true though.

Hi David,

I know that there are really no set in stone rules when it comes to diabetes and that everyone is different, however, part of my reason for posting what I did is maybe some who think they are type 2 are really type 1

With you not having insulin resistance, which is a hallmark of type 2, could you be type 1, not type 2? A lot of adults are mistakenly diagnosed as type 2 when if fact they are type 1

@Gina @Stang777 Sorry to be so heady but this community is so very smart. I am pretty good at keeping it very simple… 8))

In a nutshell some people believe that type 2 diabetes is caused by loss of a certain cell called the beta cell in the pancreas. The beta cells produce insulin While that is true, other organs contribute to the the development of type 2 diabetes.

It’s important for people with type 2 diabetes to know that. Organs such as the liver, skeletal muscle (skeletal muscle is regular old body muscle) and body fat also known as adipose tissue contribute to the development of type 2 diabetes.

(Side point. Did you know that muscle is a storage site for glucose? That is why it is such an important organ).

The liver produces sugar/glucose when body is in a fasting state (while we sleep) and sometimes it produces so much glucose, metformin is not enough. BTW, chemicals from metformin target the liver to help control the amount of glucose it delivers to the blood. When metformin isn’t sufficiently effective, some physicians recommend a long-acting insulin also called basal insulin to help remove some of glucose from the blood so when the individual wakes up, their fasting blood glucose is within a normal range.

Diabetes is a complicated disease. It’s one of the reason why there are so many drugs manufactured to help manage it.

Now, let’s not forget that the cells that make insulin in the pancreas are still progressively being destroyed, so two organs (pancreas and the liver ,for this sake of this explanation) contribute to the development of type 2 diabetes.

I hope this simplifies things.

Be well. 8))

I think we have a lot of uncertainty about the “causes” of type 2 diabetes. In truth we mostly never talk about the “etiology” (causes) of T2 because we just don’t understand the causes. We know risk factors, but those are not causes. From what I have read, Genome Wide Association Studies (GWAS) can explain up to 80% of the risk of T2. Williams Textbook of Endocrinology is a good source of what is currently taught in endocrinology about this topic. There is certainly lots of research going on about physiological role of things like the role of Free Fatty Acids (FFAs) in the development of T2, but there is no good understanding of the process. Unfortunately there is a great deal of misunderstanding both in society and in the medical profession about the concepts behind “association,” “risk,” and “cause.” Obesity is associated with diabetes, we have not proven that it “causes” diabetes.

When people do talk about how to classify (i.e. “typing”) type 2 diabetes they don’t revert to “causes” like in autoimmune T1, instead the often revert to talking about classes of defects that are present. That is why I consider the work of DeFronzo and Schwarz important.

In practice today diabetes diagnosis is just “messed up.” Type 2 is a huge heterogeneous bin that really just means “diabetes of unknown cause.” If you have abnormal blood sugars your doctor can diagnose you as having T2 with 90% accuracy, a far higher accuracy then their diagnostic performance in general. If you have a specific form of diabetes (like autoimmune T1 or MODY) and you are lucky your doctor will give you additional tests and you may get a specific diagnosis. If you don’t test positive for any specific type of diabetes then you have Type 2 diabetes which is a “diagnosis of exclusion.” There isn’t any test for Type 2.

Yes many people have insulin resistance, but as DeFronzo has noted that by the time you are diagnosed with full blown T2 you have already lost 80% of your beta cell function. And I have come to believe that pre-diabetes is just diabetes. And we really have to face up to pre-diabetes being truly abnormal glucose regulation and it warrants being considered to be an actual disease state.

ps. Since my c-peptide is now 0.4 mg/dl my doctor has at times started classifying me as ideopathic T1 but I test negative for autoimmune T1 as do some non trivial number of people who carry the T1 diagnosis.

pps. The reason that basal insulin helps fasting blood sugars is not because of increased glucose uptake it is because insulin suppresses gluconeogenesis (much more powerfully than metformin).

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@Brian_BSC just trying to keep it simple for the masses. 8)) Perhaps when I am at the AADE Convention this year we can discuss this face to face? Feeling really bummed that I put the etiology word out there because it seems like it destroyed the context. Oh well 8((.

I’m sorry for the length diatribe, I hope you didn’t take it as a criticism. I have some sensitivities about things. I don’t like the way that everyone leaps to the conclusion that lifestyle causes diabetes. And I have a suffered a bit of incompetence and mistreatment at the hands of the medical establishment (as have others here). So I am at times aggressive about getting things right. And while there are many people here with a wide range of understanding and background in diabetes it is important to understand that there is a wisdom of crowds here. There are literally millions of years of experience of people living with diabetes. And for many of us having diabetes has driven us to learn about the condition.

I would love to meet you at AADE but I have not decided whether I can really afford either the time or the cost to attend.

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@Brian, we met last year. Don’t you remember. I had the miniskirt on and the trampoline shoes! 8))

I’m so sorry. I’m sure if I saw you I would remember. I attended ADA, AADE, FFL, Innovation Summit, Unconference as well as all my work conferences. My mind turns to jello with the thousands I met. I’m sorry. I do hope to meet you “again.”