Addressing Therapeutic Inertia, Basal Insulin Use in Type 2 Diabetes

Better glycemic control reduces complications associated with type 2 diabetes (T2D) by at least 50 percent; unfortunately, a large percentage of patients with this disease continue to exhibit poor glycemic control and subsequent increases in diabetes-related health consequences. This podcast will examine the significance of therapeutic inertia, which is the failure to initiate or intensify treatment in a timely manner using evidence-based clinical guidelines. It will also discuss different types of basal insulin, and how each can be implemented into T2D regimens.

This podcast is supported by an independent educational grant from Novo Nordisk, Inc. 

Additional Resource:

  • To view program information/faculty disclosures and claim your CE credit after the session, please click here.

Angela Thompson DNP

Angela Thompson, DNP, is a certified diabetes educator at Hendricks Regional Health (Danville, IN).

Richard Rosenthal, MD

Richard Rosenthal, MD, is an endocrinologist, an associate professor of medicine in the Division of Endocrinology, Diabetes, and Metabolism, and Associate Chief Medical Officer of Ambulatory Service at the University of Alabama at Birmingham (Birmingham, AL).




Hello everyone, and welcome to the podcast “Addressing Therapeutic Inertia and Basal Insulin Use in Type 2 Diabetes,” sponsored by an educational grant from Novo Nordisk Inc. This session was originally presented and recorded at the Practical Updates in Primary Care Virtual Meeting. I'd like to introduce your presenters, Dr Angela Thompson and Dr Richard Rosenthal. Dr Thompson is a family nurse practitioner and certified diabetes educator. Her current clinical practice is within a hospital-based endocrine clinic at Hendricks Regional Health in Danville, Indiana. Dr Rosenthal is an endocrinologist at the University of Alabama, Birmingham. He's an associate professor of medicine in the Division of Endocrinology, Diabetes and Metabolism. Additionally, he serves as the Associate Chief Medical Officer of Ambulatory Services. Please enjoy, and thank you for listening.

Dr Richard Rosenthal:

Good morning and welcome to our presentation this morning entitled, Addressing Therapeutic Inertia and Basal Insulin Use in Type 2 Diabetes. My name is Dr Richard Rosenthal and I'm a professor of medicine in the Division of Endocrinology, Diabetes and Metabolism at the University of Alabama at Birmingham. I will be joined today by Dr Angela Thompson, a nurse practitioner who practices at Hendricks Endocrinology in Danville, Indiana, and she'll join us for the second half of our presentation.

I have nothing to disclose in relation to this presentation, and Dr Thompson has nothing to disclose in relation to this presentation as well. Our learning objectives for today are to describe the impact of therapeutic inertia, barriers to treatment intensification and strategies for early treatment intensification. The second learning objective is to outline the pharmacondonamic and pharmacodynamic and clinical differences among basal insulin analogs. And lastly, to incorporate type 2 diabetes regimens using appropriate initiation and dosing of basal insulin analogs based on clinical guidelines, individual glycemic goals and patient preferences through interactive case studies that we'll do toward the end.

In regards to diabetes, you see across the country that the prevalence of diabetes has grown enormously. If you look on the far left of the screen in 2004, the prevalence of diabetes was more in the three to five or 6% range. And as we've progressed through the last two decades, there's been an explosion not only in the diagnosis of diabetes, but also the determination of patients who have impaired glucose tolerance who may go on to develop a diabetes.

Diabetes in the United States is very prevalent. As you see, 37 million people have diabetes. That's about one in every 10 people in the United States. One in five of those people don't even know they have diabetes, and that's where it's our job as clinicians to make the determination do they have diabetes and follow the standard set by various societies to make the diagnosis of diabetes with fasting glucoses or even hemoglobin A1C. Prediabetes is also very common. In fact, one in three Americans have pre-diabetes. Now that means that they do not have diabetes at that time, but they may go on to progress to developing diabetes mellitus and that encompasses about 96 million people.

The other issue is about four and five or eight and 10, however, you want to look at it, don't even know they have diabetes. So as providers, we need to make clinical decisions and testing our patients and getting them all proper therapy.

The problems with diabetes not only involve determining if they have an elevated blood glucose, but we also want to work very aggressively to get these blood glucoses down so they do not go on to develop some of the complications of diabetes that we'll discuss a little bit later. The amazing thing about diabetes is that the cost is enormous. Medical cost for diabetes patients are about twice as high as that for patients that do not have diabetes. And you see the figure on your screen approaches $327 billion. This is a very interesting trend graph here looking at patients who have total diabetes, which is basically those who have diagnosed diabetes and undiagnosed diabetes. The way this was determined was they asked patients if they were ever told they had diabetes, those would naturally be your diagnosed diabetes. The undiagnosed diabetes were patients who were never told they had diabetes mellitus, however, they had a fasting glucose of over 126 milligrams per deciliter, or they had an A1C of 6.5.

And from 1999 to 2000 up into 2000, 2015, the prevalence of total diabetes has increased from about nine to 12%. And the prevalence of diagnosed diabetes, as you see in the middle curve here, has increased from 6.2 to 10%, where basically your undiagnosed diabetes was relatively flat. So diagnosing diabetes has been a very common practice, and I think as providers, we've done a lot better job in the last one to two decades. As said in another way on the National Diabetes Statistic report from 2017 to 2020, 37.3 million people in the United States have diabetes. That's about 11.3% of the population. About 28.7 million are diagnosed and about 8.5 undiagnosed. These are type 2 diabetes that we're thinking about here. Type one diabetes has remained relatively flat, 1.9 million people with diabetes, and as I mentioned on the previous slide, 96 million people have pre-diabetes. That's about 38% of the adult population.

So we have a lot of work to do to improve these patients, not only with diet and exercise, which can be very helpful as shown in the diabetes prevention program. But also getting patients on proper medications and trying to get their A1C's to goal.

What is the clinical impact of diabetes? It's the major cause of premature death and disability in the United States. It's the leading cause of new cases of blindness in working age adults. That's why we encourage our patients who have pre-diabetes to see their eye doctor every one or two years. 50% of the non-traumatic lower extremity amputations related to diabetes and 35% of new cases of end-stage renal disease are related to diabetes mellitus. And lastly, there's a two to fourfold increase in cardiovascular risk. In fact, patients who have diabetes who have not had a diagnosed coronary event are at the same risk of having another or having their first coronary event as a patient who has established coronary disease who has already had a problem with an event.

So we really look at patients with diabetes as having a coronary equivalent. Said in another way, 82,000 amputations are performed each year because of diabetes mellitus. About 12 to 24,000 people are felt to lose their eyesight for diabetes. You see the large number of patients with instate renal disease and 280,000 people die from diabetes and it's complications each year, and that's increasing. Why do we try to get our patients in good control? This is an older study from the United Kingdom Prospective diabetes study that was put out in the BMJ in 2000, and it looked at how we do in lowering patients A1C's and what we see in our patients and what I encourage my patients to do is to get that A1C down. If you have a patient in your clinic and their A1C is nine and you can get them from nine to eight, they're going to have a 37% reduction in their risk for microvascular complications, whether it be retinopathy, nephropathy and neuropathy.

The risk for stroke down 12% decreased risk of MI was statistically significant with a reduction in 14% and a statistically significant reduction in any diabetes related endpoint by 21%. So clearly improving blood glucose is adding in medications has been very important. When you think about diabetic retinopathy, it's frequently present at the diagnosis of diabetes type 2, and that's why we send our patients to see an ophthalmologist right away. On the other side, a patient with type one diabetes, we're not as concerned about them at the time of their diagnosis. They really haven't started to develop the outcomes or the complications related to diabetes.

Diabetic retinopathy can progress and lead to several problems including microaneurysm, retinal hemorrhages, severe diabetic proliferative retinopathy. And it also may lead to macular edema. And when we're managing these patients, not only do we need to get their blood sugar in good control, we need to get their blood pressure as well as their cholesterol levels to where they need to be.

Some of these patients may require laser treatment, they may require photocoagulation, and as you're aware, the cost of diabetic retinopathy is enormous. Diabetic neuropathy is another condition that we don't want to hold lightly. In fact, when I see patients in my clinic, I have a sign on the back of the door to make sure they always take their shoes and socks off so we can examine their feet, make sure that their nail care is good, make sure that their pulses are intact, that there's no infections that they may need to be a candidate for diabetic shoes and diabetic peripheral neuropathy is one of the most prevalent of the distal poly neuropathies and it affects up to about 50% of patients with diabetes. Not all the patients have symptoms, but some of them will have numbness and tingling, and we can use our tuning for, we can use our light touch to see where they stand in regards to neuropathy and it really can have an effect on their quality of life. And that's why it's important to address diabetic peripheral neuropathy.

One of the things that Dr Thompson will talk on as we progress through the program in the second half of this is the importance of trying to get better glycemic control. This study out of the American Diabetes Association showed that about 50.2% of providers failed to get patients to their A1C goal. And the American Association of Clinical Endocrinologists showed in a study and that basically, two-thirds of patients were not getting to goal. And as providers, we're not adding in medications. I think in the last five to 10 years, with the advent of easier-to-use insulins and more oral agents, we're starting to use double and triple therapy. But as providers, we need to think about trying to get our patients in better control and help prevent some of these microvascular complications.

When we delay a patient in treating them appropriately, there is a significant increase in problems in regards to the cardiovascular system. As you see here, MI by 67%, stroke by 51%, heart failure by 64%, and they're composite by up to 62%. This is a very nice slide or supplement that was in the recent diabetes care. And at the end of each year, these guidelines of how we treat our patient are something that you should refer to. In this presentation I'm not going to go into all the details of when you should add in an oral agent or when you should add in an insulin. The key point to remember is if you're not at goal, you need to think about what is the reason you need to add in another agent. Do they have underlying heart disease? Do they have underlying diabetic nephropathy? Is it time for them to go on to a basal insulin and not be afraid of any of those treatment options to treat our patients?

The second figure also gives additional information about consideration of adding in a GLP one receptor agonist or possibly a basal insulin to help improve the patient's blood glucose. And as I mentioned earlier, help improve their glycemic control. I'm going to now turn over the presentation to my colleague, Dr Angela Thompson.

Dr Angela Thompson:

So now we're at the part of the presentation that we're going to be discussing the therapeutic inertia as it relates to both the patient and the provider factors and the suggested interventions including the newer insulin formulations. So therapeutic inertia by definition is that underuse of effective therapies in preventing serious clinical endpoints despite the abundance of evidence showing benefit including deficits with the lack of screening risk assessment, preventative measures attention to adherence barriers and referrals. The provider related factors that lead to therapeutic inertia include the overestimation in the quality of the care, the use of soft excuses to avoid intensification, the lack of materials, time, training to appropriately escalate care to meet the recommended targets. This includes complexities of navigating ever-evolving guidelines and the insurance coverage for the treatments prescribed. There are several approaches that have been identified in the literature to address provider inertia, and they include adopting monitoring systems to assess the quality of care as a whole.

Through this type of analysis of process and outcome indicators, clinicians can evaluate their own performances, identify critical areas and adopt suitable strategies in a virtuous quality cycle. Additionally, implementation of software or algorithms that are embedded in the informatics clinical folders to help with this therapeutic decision-making can better stratify patients according to their cardiovascular events, whether they are previous or whether they have risk factors for cardiovascular events. The presence of chronic kidney disease, age, fragility, etc, therefore, identifying the most appropriate decision aligned with those current recommendations by the American Diabetes Association and whether these individuals are candidates for new therapies.

Ongoing opportunities for education and training to increase the knowledge and also help facilitate behavior modification, including having educational tools and guidelines embedded in an electronic EMR alongside other opportunities for learning such as podcasts, journals and workshops are helpful. And then there's additional consideration for more frequent visits and enlisting other team members that can assist with the patient education, assist with barrier identification and even treatment implementation have all been proven solutions to mitigating provider therapeutic inertia.

The patient-related factors that contribute to therapeutic inertia are plenty, and they include denial of having the disease, low medication taking adherence, diabetes distress, and or depression. There's cost and coverage issues along with fear of hypoglycemia. Oftentimes low literacy and low healthcare literacy are problematic. Competing priorities if you have patients who have multiple medical conditions that they are trying to manage, including family and work. There's dexterity and visual impairments, especially in our elderly patients. And then certainly social determinants of health have been shown to be significant barriers to not only adherence but to gaining control of diabetes. And there's a lot of evidence that's shown that these patient-related factors are a very strong predictor of therapeutic inertia, far more than provider factors. Therefore, understanding these barriers to a patient's willingness or even to their ability to engage in the treatment plan is essential to combating patient therapeutic inertia and improving outcomes.

Strategies to ally patient-related therapeutic inertia include identifying those barriers that are impacting care so that individualized solutions can be implemented. Also using shared decision-making that involves that patient in the decision. Utilization of smart goals that can help foster behavior change or clinical goals through a structured action plan have been shown to be effective, followed by early implementation of combination antihyperglycemic therapy can help patients achieve these glycemic goals much sooner, and also with a reduced burden of multiple medications and co-payments for your patients. And finally, close and consistent follow-up to evaluate not only the efficacy of the current plan, but determine any alterations that are needed is appropriate and strongly encouraged.

So we're going to talk about utilization of insulin in the context of therapeutic inertia, just what is that connection. Well, with the introduction of these ultra rapid-acting insulins, they include insulin aspart, which is also called Fiasp and Lyumjev, which is also called Lispro-aabc. These new generation insulins, they're different from their short-acting counterparts because they have additives to enhance the absorption, which accelerates the onset to about two to five minutes. And this allows for a lot more flexibility in dosing up to 20 minutes after starting a meal. And clinical studies have demonstrated that these ultra fast acting insulins provide significant reductions in one in two hour postprandial glucose levels, thereby improving the time and range A1C reductions, matching the physiological secretion of insulin with similar safety in terms of hypoglycemia to fast-acting insulin. And so these characteristics have the potential to improve adherence and to reduce patient related therapeutic inertia.

So we're going to talk about the first-generation basal insulins in comparison to the ultra-long-acting basal insulin to see how this could impact therapeutic inertia with these first generation basal insulins, in particular in pH. It is a very inexpensive insulin, so it can certainly be used in those individuals who have cost or coverage issues. However, it has an increased risk for hypoglycemia as well as a requirement that twice a day dosing be utilized in order to cover 24 hours duration of action. Additionally, it has far higher pharmacodynamic variability and intra individual variability, which can cause a lot of differences from one day to the next in the glucose control and also in the risk for hypoglycemia. This is in comparison to insulin glargine and the biosimilars as well as Insulin Detemir, who have a longer duration of action up to 24 hours, minimal variability and a lower risk for hypoglycemia when looking at comparison studies.

And so having a lower risk for hypoglycemia, having a requirement for daily dosing over twice a day dosing has the potential to improve therapeutic inertia in your patients. So with this second-generation basal insulins also called ultra long-acting insulins, they have the potential to improve adherence and to reduce therapeutic inertia in patients more so than even the basal insulin counterparts. There are two ultra-long-acting insulins and they include U300 glargine, which is also marketed as Toujeo, as well as insulin degludec, which is also marketed as Tresiba. With U300 glargine, it's actually the same molecule as U100, but at the higher concentration. It provides a relatively flat or peakliss insulin. And so absorption delayed, there's a longer duration of action of 36 hours as a result.

With degludec, it's actually a novel accolade basal insulin. It has a unique mechanism of action. It's a protracted absorption involving the formation of a depo of multi-hexamer chains. And so this causes a reversibly bound to or reversibly binds to serum albumin that leads to a slower release, a longer half-life of 42 hours, and a flatter more stable glucose lowering effect. And these ultra long-acting insulins have shown clinically to have even less pharmacodynamic variability and intra-individual variability because of these longer duration of actions and just because of the way they're made. Clinical studies comparing long-acting insulins with ultra-long-acting insulins have also shown a significant reduction in hypoglycemia and overnight hypoglycemia up towards 40%. Each of these insulins allow for higher dialing capacity for especially those individuals who require more than 80 units per injection, they're ideal. They have a more flexible dosing because of the longer duration of action, and they don't have that rebound hyperglycemia often seen with longer-acting insulins in their delayed doses. So all of these factors make ultra-long-acting insulin a very viable option in preventing patient-related therapeutic inertia.

These are some of the characteristics or specifics about dosing and storage and prescribing that I have listed on the slide. And what I wanted to point out is that the ultra-long-acting insulin preparations are really unique in the fact that they do have, as I mentioned before, these larger dialing capacities. They can actually dial up to 160 units in a single dose. They also hold larger amounts of insulin, thereby reducing the number of prescriptions that a patient has to obtain in order to be able to maintain control of their diabetes. They have a longer storage life, so that improves adherence if the individual does not have to throw away a pen after 30 days because of the potential loss in potency. These particular ultra-long-acting insulins have a shelf life of eight weeks after opening. So there are some pretty exciting developments in the field of basal insulins. And those are with the emerging treatments of weekly basal insulins.

The very first one that is underway in phase three clinical trials and already completed phase two clinical trials is B I F. It is a weekly basal insulin that has already completed studies looking at the feasibility and the safety of a loading dose as well as efficacy and the titration and conversion from the ultra long-acting and the long-acting basal insulins to a weekly basal insulin. And the studies have demonstrated that it's just as effective as the ultra long-acting and the weekly insulins, but there might be actually a lower risk for nocturnal hyperglycemia, hypoglycemia with these particular agents as well as a reduced weight gain or less weight gain in comparison to the current long-acting insulins available.

The other weekly basal insulin that is currently under study is Icodec. Icodec is, also completed their phase two clinical trials, which looked at the same loading dose and titration schedule and conversion from long-acting insulins to a weekly acting insulin. And I've got some information about that particular basal insulin as far as its pharmacodynamic and pharmacokinetic characteristics as well as the steady state and glucose-lowering effect. So on this particular slide, I just have a summary of some of the phase two clinical trials looking at loading dose and optimal titration. What I wanted to really summarize with talking about these two weekly basal insulins is the potential for them to improve adherence with our patients because you're not having a daily injection, you're reducing it to a weekly injection.

In studies in the past, looking at patient factors related to therapeutic inertia, having increased complexity and more frequent dosing has always been seen as a disadvantage and a barrier. Additionally, if these insulins have the potential to improve or maintain the same clinical goals and reach A1C targets with less weight gain and hypoglycemia, that's also going to improve adherence and address one of the key patient-related factors to therapeutic inertia, which is hypoglycemia.

And so now I'm going to transition to my colleague, Dr Rosenthal, for him to discuss case studies.

Dr Richard Rosenthal:

Thank you Dr Thompson for that excellent description of the current basal insulins that we have, some of the future studies looking at newer weekly insulins that are coming out as well as discussing the points of clinical inertia, a problem that we face as providers and trying to get our patients to goal. And hopefully with these newer insulins and these long-acting insulins, that'll be a little easier for our patients to reach their glycemic targets. I'd like to go over a few case presentations.

Case presentation. One revolves around a 59 year old female who has a history of hypothyroidism, obesity and reflux disease, and she's referred for poorly controlled type 2 diabetes. About three years ago after failing metformin when her A1C was 9.4%, her intern has tried an SGLT two inhibitor, so she had persistent UTIs, a side effect that's seen in about 10% of patients on this class of Drugs. And she stopped it and her A1C was up to 9.8%. She did not want to take a GLP one agonist because she had had some chronic GI disturbances and her son who actually happens to also have diabetes reports that she's had some recent polyuria polydipsia and has lost some weight.

So when you're thinking about the next step to improve this patient's glycemic control, which of the following would be best suited for the patient? A, would you check the thyroid levels to ensure adequate replacement? B, would you add in a sulfonylurea. C, would you start basal insulin therapy and encourage frequent sugar checks and adjustments in dosing to reach a fasting sugar in the low 100s and continue the sitagliptin. Or D, would you refer to a bariatric surgeon to treat her obesity. This patient clearly has a hemoglobin A1C above goal. Checking thyroid levels would not be beneficial, although it would be helpful to make sure that she was adequately replaced. It would not help her improvement in her sugars. Adding in the sulfonylurea would not get this patient to go, and I don't think this patient necessarily needs to go see a bariatric surgeon without really working on diet and exercise and trying to get the A1C to where it needs to be. Adding in a basal insulin would be the correct thing to do.

There's really no reason to stop acidic lifting product because it has very favorable effects in helping control post real sugars. If this doesn't work and you're not getting your patient to where they need to be, you may want to consider prandial or rapid-acting insulin at meals to try to get the patient to the correct goal.

The next case I'd like to go over is about a 72-year-old gentleman who has a history of type 2 diabetes, hyperlipidemia and gout for the last 18 years. He presents with an A1C of 9.1% and he admits to avoiding finger stick blood glucoses due to discomfort. He says what some patients always say, "I know when my sugar's high or low." He's had recent eye surgery for proliferative or retinopathy and reports that when his uncle started insulin, he ended up having a lower extremity amputation the same year. Currently he's on glimepiride metformin and saxagliptin.

In addition to educating this patient, which recommendation is the most appropriate? Would you stop the glimepiride to ensure that the patient at least avoids getting low blood sugars? Would you have him go see an educator to get on an insulin pump in a continuous glucose monitoring system? Would you go up on his metformin by 50%? Or would you review in the importance of better glycemic control, discuss a basal insulin pin technology and start eight units at bedtime?

This gentleman clearly has some fears about insulin. A lot of patients feel that if they start on insulin, they may have a bad outcome as related to this gentleman's uncle, when in fact his uncle probably ended up having a problem with peripheral vascular disease and neuropathy because he didn't get on insulin soon enough. So we need to educate on these type myths and explain that the better glycemic control is important to help preventing some of the complications. Sure, stopping the glimepiride may help avoid some low sugars, but it's not going to get him to goal and doubling up or increasing the metformin a little bit is not going to be enough to lower an A1C by two to 2.5%. So starting on a basal insulin, titrating that insulin, consider adding in mealtime insulin if you're not getting the goal, would be the appropriate answer.

The third case I'd like to go over is a patient who is 56 years old. This gentleman has a history of type 2 diabetes, hypertension, and hyperlipidemia. He had a positive stress test recently. So you basically feel that this gentleman has underlying coronary disease and you see the list of his medications. He has a strong family history of diabetes. In fact, his father died at MI at an early age. This gentleman is overweight, his pulse is 92. He does have an S4 gallop and the rest of his exam is normal. His A1C is clearly not at goal, neither is his LDL cholesterol. You'd like to see that below 100. To optimize this patient's regimen and reduce his risk, what would be the next most appropriate thing to do?

Would you increase his metformin, he's not at goal, he's not at the max dose. Would you also increase his Glyburide? Those may help a little bit. However, they're not to the point where you're going to get an A1C to six and a half to 7%. Adding in a TCD like Pioglitazone is going to cause some more weight gain. It may help with some other features with the patient, maybe if he has underlying liver disease or fatty liver. But again, a low dose of Pioglitazone is not going to lower an A1C by three or 4% when he is al already on several oral agents. Stopping the sitagliptin and adding in an oral GLP-1 agonist may help some, but again, not getting the patient to goal. So the correct answer here would be D, which would be to start a basal insulin, try to get this patient to goal into the load one to mid 100 range. And if you're not getting at goal with the basal insulin, think about adding in a mealtime insulin. As. A lot of times patients need combination basal bolus insulin to get them to appropriate goal.

So in summary, today we've spent a lot of time talking about the epidemiology of diabetes. We've talked about ways to prevent long-term microvascular complications. We've talked about some of the faults we may have as physicians and providers in managing patients due to clinical inertia that was well elucidated by Dr Thompson. Dr Thompson also went over several options of treating patients with basal insulins. Talked a little bit about the pharmacokinetics and pharmacodynamics and making your choice for a basal insulin. And hopefully these case presentations showed you a method of thinking about your patients, thinking about their hemoglobin A1C and also trying to come up with an option to treat them to get them at goal. So I thank you for your attention today and I want to also thank Dr Angela Thompson, our expert on clinical inertia as well as insulin products that she discussed today. And I hope you enjoy the rest of your day.

Moderator: Well, thank you so much to both of you, Angie, and to Rich for the presentation because this is a challenge for all of us in primary care. So let's get straight to the Q&A and we've got a number of questions that I don't know we'll get to all of them, but when you add in a basal insulin, how do you decide to decrease or discontinue even a concomitant oral agent in their regimen? And let's start with Rich.

Dr Richard Rosenthal:

I think that's a good question. When we add in basal insulins trying to get their A1C's to goal, you got to remember an insulin may cause hypoglycemia. So I always think about if I am going to withdraw a drug, I think about a drug that may potentiate low blood sugars like a sulfonylurea. So if they're on a glyburide or a glipizide, I at least cut it in half or may even discontinue it. And then as we advance forward, we determine we need to add in other agents. Because at the end of the day, you want to make sure your patients aren't getting lows. An occasional high we can treat, but a low is hard to treat.


Oh, absolutely. I agree with that. So I've always had some resistance with patients to starting or initiating basal insulin therapy. So how do you address that resistance to initiating that therapy?

Dr Richard Rosenthal:

I'll make one comment then I think Angie probably would like to add a little bit because she does a lot of this in her practice. I think a lot of it, there is some aversion to that, but a lot of these patients are already checking their fingers and I reassure them that actually the needles on the basal insulins are a lot easier than the Accu-Check or the blood glucose on their checking on their fingers. So that's how I address them. Angie, how do you look at those issues?

Dr Angela Thompson:

Well, I think one of the number one fears that patients have is that they're going to have pain and just the fear of a needle. And so they envision that needle being the same size as what you would give for an immunization. So demonstrating the insulin administrative in the office and then showing the actual what the needle looks like almost always alleviates that fear and they're ready to move forward. And then I never use it as a punishment. I always talk to patients about how diabetes is progressive and that there may come a point in time in their disease process that they're going to need to start utilizing insulin. So they realize early on that that's just a part of what's going to happen.

Dr Richard Rosenthal:

The other thing too is to avoid the myths. I saw one yesterday who I wanted to add in basal insulin. She said, look, when my aunt added in basal insulin, she went on dialysis. And it was like, no, she went on dialysis cause she didn't add it in early enough. So reassuring that insulin doesn't mean you're going to have a complication is also an appropriate way to manage it.


Agreed. I had the same thing with, oh, I don't want to take blood pressure medicine because when my mother did that, she had a heart attack. It's because we didn't start things early enough. And I think diabetes is the same, progressing nature of the beast. So, well, let's see, when you're titrating a basal insulin, when would you make the decision to add in a mealtime insulin to control their diabetes? Angie, why don't you do that one?

Dr Angela Thompson:

Yeah, I have two items that I look at. First, I look at their total daily dose and compare that to what would be a equivalent weight-based dose for a basal insulin. And if you're looking at the ADA guidelines or standards of medical care, the recommendation is once an individual's basal insulin is 0.5 units per kilogram per day, and they're still not meeting their A1C goals and having hyperglycemia around meal times to consider initiating a bolus insulin or rapid-acting insulin. I think now with sensor technology, that's another means of being able to determine whether or not they are still having hyperglycemia postprandially and basal insulin's really only going to regulate their overnight and in between meals. So if you still see those large peaks and the long duration of peaks occurring around mealtime, then that's an indication that they would need a fast-acting or rapid-acting insulin.


Sure. And another question that has come in is, would the use of ultra-long acting insulins reduce the need for frequency of finger stick controls or are you trying to get most of your people on CGMs and things like that? Rich, why don't you do that one?

Dr Richard Rosenthal:

Well, I think the CGM is a good thing. Along the lines of what Angie said, an ultra-long-acting is mainly controlling that fasting and in between meals. I look at the A1C values a lot because if you're trailing around with an A1C down in the high seven, low eight range, it's not that they need more and more basal insulin. A lot of times their problem may be they need a mealtime insulin. You may want to just start that, a fast acting insulin with their largest meal. And I use a rule of thumb that check your sugar two hours after a meal and the goal by the ADA is probably to keep that below 140. That's pretty hard. We accept up to 180, but if they can check their sugar two hours after a meal and you're seeing numbers in the low to mid 200, their problem is not the basal insulin. They need a mealtime insulin to bring that down. And again, I go with the very slow process of adding that in and not trying to potentiate a low blood sugar.


Those hypoglycemic events are such a challenge throughout the disease process, so I appreciate that greatly. So, Angie, I know that a lot of our patients struggle with the cost of all of this, so if you have someone, like one of the questions, no insurance or especially with someone newly diagnosed, what is your suggestions on those who don't have insurance or how to treat patients who have either no insurance or are underinsured to get those lower costs?

Dr Angela Thompson:

I think there are a couple different options that can be explored. Certainly utilization of a low-cost, intermediate-acting insulin is an option, which is your NPHs. They're 25 to $30 a vial. There is also a pen option for the Glargines that I believe now is capped at $99 at Walmart a month. For those who struggle with that cost, you also could employ the pharmaceutical companies. I know Lilly started during the pandemic offering. They have a Lilly Cares program and they oftentimes cap the insulin cost at about $35. For most individuals who are uninsured, as long as they don't have a really high income, but they do base it somewhat on the income. So if they're individuals who have a lower income bracket than they oftentimes get it lower or even a little higher if they have higher income, but still need help. So that's really been a great tool, although other companies that make insulin also have a patient savings option. And again, it's income-based and so that they can apply for that. And oftentimes they will get covered in a matter of just a few days with the paperwork being sent there.


Okay. So the response is fairly quick?

Dr Angela Thompson:

It is fairly quick. It's typically a turnaround time, once the application's completed, the patient would have to sign a few sections of it. The provider would have to document the type of insulin, the dosing and send a actual prescription. It's typically within a week, at most. Sometimes it's shorter than that.


Okay. Because that's important too.

Dr Angela Thompson:

And then delivery, delivery sometimes it depends on the pharmaceutical companies. Some deliver at the provider's office, some now deliver at home, and so it's typically good for a whole year and you would just reapply at the anniversary of the next.


So most of those are shipped directly to the patient or to the provider. It's not something-

Dr Angela Thompson:

Yeah, it's either one or the other. Lilly ships directly to the patient. I believe that Sanofi and Novo ship to the providers.


To the providers.

Dr Angela Thompson:

Hm-mmm (affirmative).


With shipping, that can be a challenge these days, which is a challenge for all of us for many things. But it's nice to know that those programs are there. And I think in the economics of healthcare, we just need to be aware of what patients can pay for instead of them just walking out of our office knowing that they can't do any of that and so they'll just have to forego those treatments, which is sad to me. So I think that it is really important for us to know that these options are out there for when we have a therapeutic inertia or we're just not getting anywhere. And what we do with adding basal insulin and mealtime insulins as well.

I really appreciate each one of you or the both of you for doing what you do on a daily basis. It really helps us in primary care do what we do in treating patients with diabetes. It is such a challenge each and every day. And I'm also thankful that we've come so far in healthcare with the treatment of diabetes.