#Endocrinologists – The Practical Diabetic

Applying Motivation Theory to Diabetes Management

April 8, 2023leontribe1 Comment

Just after we got married, my wife and I embarked on an MBA (Masters of Business Administration). Along with teaching how the organs of business work, there were some interesting electives to choose from. One of the ones I chose was “Leadership and Motivation”. It provided guidance of how to lead people (as opposed to managing them), and how to motivate people. Obviously, in the context of an MBA, it was to help employees stay motivated to work on tasks deemed important to their employer, but I see parallels in the management of diabetes as well i.e. working on tasks deemed important for survival. For those not interested in the details, you can skip ahead to the tl;dr.

The 3C Model

The course was taught by Professor H.M. Kehr, formerly of UC Berkeley who created what is now called the “3C Model“; the Three Components Model.

I find it easier to remember it as the “Head, Hearts, and Hands” model. While relatively simple, the model brought together various motivational models of the time e.g. Csikszentmihalyi and Rheinberg. In this case the head, heart and hands are:

Head: Our logical thoughts regarding the task at hand
Heart: How we feel about the task at hand
Hands: Our ability to perform the task at hand

Other key concepts with the model are “volition” which, for the rest of us, is willpower and “flow”, a state of “effortless achievement”, which is sport is sometimes referred to as being “in the zone”. In short, when the head, heart, and hands are aligned, achievement is effortless.

Another key aspect of the model is the understanding that willpower is a finite resource which cannot be called upon indefinitely and, if pushed to its limit, leads to burnout. Burnout, of course, is a term familiar to many of us who manage diabetes meaning a complete abandonment of diabetes management.

Misalignment and Intervention

While alignment of the head, heart, and hands leads to a “flow state”, misalignment means willpower will be needed to achieve the task. For a task, such as diabetes management which is relentless, it is clear, without intervention, burnout is inevitable. Ideally, the intervention will either give the person a break from the task, allowing willpower to recharge, or make the amount of necessary willpower so small as to prolong burnout practically indefinitely.

Depending on which component is not aligned to the task, this dictates the kind of intervention to use.

When the head is the problem i.e. the person is emotionally aligned and has the skills, but there is a logical conflict, the person may need further convincing, have additional incentives put in place, or have the goals adjusted.

When the heart is the problem i.e. the task makes logical sense and they have the skills but it does not feel right, or they fear the task, emotional support, redesigning the approach, or focussing on the eventual outcome may help.

When the hands are the problem i.e. the person does not have the skills or knowledge to achieve the task, the answer may be education/training, coaching, or having others provide assistance.

Again, we start to see how this model could be overlay onto diabetes management and ensuring a specific approach is a good fit to the individual.

An Example of the Application of the Model

A classic example is the case of someone wanting to give up smoking. They know logically is makes sense (head), and may well have the skills to do it e.g. employing patches (hands), but their heart may not be in it or they fear failure. In this case we see suggested interventions which are often applied to help people give up smoking e.g. in New South Wales we have the ICanQuit web site and Quitline where people looking to give up smoking can call and get support and encouragement to help them on the path.

Application to Diabetes Management

The model provides insight into why intensive lifestyle interventions fail so often. While radical changes to diet or exercise in the management of diabetes frequently address the head and hands, the heart is almost always ignored and is the key point of failure. Very few of us deny the health benefits of exercise and most of us are capable of walking/running yet, like smoking, many of us fail to incorporate it into our lives. Simply put, our heart is not in it. Options to make exercise more palatable could be engaging a physical trainer to provide motivation (support), entering a charity fun run and then training towards the goal for the greater good (new motivators), or changing the type of exercise to something more enjoyable or aligned to the person’s lifestyle (redesigning the work).

In the case of Weight Watchers, the success rate is quoted at 11%. Even with intense coaching on top of lifestyle changes, one study showed remission for Type 2 was only achieved in 3.5% of participants. In the case of the Dr. Bernstein diet where the logic of the benefits of lowering dietary carbohydrates is sound (head), and there is no doubt, once the book is read, someone with Type 1 is equipped to undertake the program (hands), the majority of the strongest adherents, who literally commit to following the program to be part of the “international social group”, failed to meet the basic premise of sticking to 30g of carbohydrates per day. This is not the fault of any one program; the fact is changing habits and maintaining that change is hard and we need to consider the whole person to be successful. We must align the head, hearts, and hands for each person and provide the support that person needs. There is no “one size fits all”.

We also see this with diabetes technology. While the clinical studies speak at the benefits of, for instance, looping systems at improving outcomes (head), there may be a fear of using the technology due to a lack of skills/knowledge (hands) or the person simply does not like the idea of permanently wearing something on the body (heart). Professor Katharine Barnard-Kelly presents on this often at conferences and passionately believes “heart interventions” are effective at improving outcomes.

Professor Barnard-Kelly has also developed the Spotlight-AQ system which facilitates pre-clinic assessments to ascertain where interventions may be required e.g. the need for structured education (head/hands).

Putting the spotlight on my “Practical Diabetic Solution”, I think, if someone commits to replacing all meals, as I did, this would usually not be sustainable because the conflict with the heart e.g. no longer sharing food with family/friends would be simply too great. However, replacing non-social meals would not require the same level of willpower and the use of looping technology would greatly reduce the mental burden of daily management, assuming the person has the skills to use the loop (hands) and understand the benefits (head). To put it simply, the level of commitment and tool emphasis would be different for each individual, but a sustained improvement is better than one which fails to be maintained, however successful in the beginning.

How Can We Use This Model?

My vision is this could be used for self-assessment but also as a framework for the discussion between the health care team and the person with diabetes. For example, by considering why exercise may not work in the context of the three areas, a plan to address the disconnect can be intelligently devised. In the case of technology and medication, if one tool is not aligned, other tools can be considered instead with a closer fit, or other appropriate interventions considered.

tl;dr

The 3C Model of motivation, primarily used in the context of motivating employees, can also be applied to the management of diabetes and to frame conversations between health care professionals and their clients (people with diabetes).

The model focuses on three aspects of the individual, their:

Head: logical thoughts on a diabetes management approach
Heart: their emotional response to a diabetes management approach
Hands: their skills and knowledge regarding a diabetes management approach

When all three are aligned with the approach, its use as part of the diabetes management plan is effortless. When one or more are not aligned, interventions are required to reduce the excessive need of willpower to use the approach which could lead to burnout. Interventions may include:

Head: Education, adjustment to goals
Heart: Support, redesigning of the approach
Hands: Training, assistance

With a framework in place, it will be easier to identify appropriate interventions and optimise outcomes.

What Is Your (Diabetes) Type? A Guide For Those Suspecting Misdiagnosis

July 5, 2019October 26, 2019leontribe2 Comments

In my last blog I wrote about the different Types of diabetes. In this blog I will dig a bit deeper to create a scorecard so you can see how ‘typical’ you are and, if you are Type 2, give you a way to see if there is a possibility of misdiagnosis.

I am going to ‘borrow’ an idea from “Think Like a Pancreas” and have a tl;dr section at the end. If you want a quick summary to see if it the blog is worth the time to read, you know where to go.

The Prevalence of Misdiagnosis

Why am I so passionate about the possibility of misdiagnosis? Because it happens a lot. It is estimated that approximately 80% of MODY/NDM diabetics are misdiagnosed as Type 1 or 2. For LADA, misdiagnosis could be as many as 20% of Type 2s, and one study of 2 million diabetics showed that 97% of the Type 3c diabetics had been misdiagnosed as Type 2.

Why is it important? Because treatment, while not defined by Type, is informed by it. For MODY/NDM, the insulin production machinery is broken on a genetic level and for different gene mutations, the most effective treatment is well understood. Trying generic Type 2 treatments will, at best, be as effective but more likely be less effective. For Type 3c, the physical damage to the pancreas means alpha and beta cells are damaged and so it is not just insulin production that is affected. Treatment should account for this. For LADAs, drugs which work the pancreas harder, while appropriate for Type 2s will destroy the pancreas’ beta cells quicker and make the patient insulin-dependent so much quicker.

From a patient’s health perspective, a poorly targeted treatment means blood sugar control will not be managed as well as it could, leading to a higher risk of long term complications. Misdiagnosis is unfortunate for the doctors but can be devastating for the patient.

The Practical Diabetic’s Type Scorecard

Based on key parameters, it is possible to put together a simple scorecard to steer a clinician towards an appropriate diagnosis. I will focus on Type 1, Type 2, LADA, Type 3c, and MODY/NDM simply because Gestational diabetes is routinely tested for and Type 0 presents very differently to the other Types and is more easily diagnosed. I will also assume, like many of us, the patient has presented with a mild DKA for the first time e.g. thirsty, peeing a lot, lethargy, losing weight etc. so we are at the start of the diabetic journey.

For the purposes of the scorecard I am defining LADA as a Type 1 who still has sufficient insulin production to not be insulin dependent. A Type 1 who requires insulin to remain healthy is, for all practical purposes, a ‘normal’ Type 1, possibly in honeymoon.

The idea is to work out which columns result in a positive score and then get the appropriate definitive tests done.

	Type 1	Type 2	LADA	Type 3c	MODY/NDM
Young (<25)	+1	0	0	0	+1
Old (>25)	0	+1	+1	0	0
Low C-Peptide	+1	0	0*	+1	0
History of pancreatic damage	0	0	0	+1	0
First degree relative	0	+1	0	0	+1
Insulin resistance	0	+1	+1	0	0
TOTAL SCORE

(*) Some links characterize LADA as having a low c-peptide. From my perspective if you are a Type 1 with a low c-peptide to the point you need insulin, you have transitioned, from a treatment perspective, to a (possibly honeymooning) Type 1.

After my first article I got a lot of requests for the sources of my information (a good fraction of that piece came from “Think Like a Pancreas” and “Dr Bernstein” with NCBI and Google searches to fill in the gaps). Given this article could well end up in the face of someone actually qualified in medicine and you may need to fight for that definitive test, I’ll quote my links here:

LADA Characteristics
Some More LADA Characteristics
A paper on LADA and Insulin Resistance
MODY Characteristics
Type 3c Characteristics

These are all from NCBI. NCBI is a collection of peer-reviewed medical papers from around the world and cannot be easily dismissed by a health professional.

Hopefully the terms in the first column are relatively self-explanatory. C-peptide is a measure of your body’s insulin production and obtained from a blood test. “First Degree Relative” means a first degree relative who has some form of diabetes. Insulin Resistance can be determined by examining a patient’s HOMA-IR score (derived from their fasting blood glucose and endogenous insulin). Endogenous just means made by their pancreas as opposed to injected.

So let us run it for a sample patient. In this case I will choose me, two years ago when I first presented with DKA. You can read a bit about this in my About Me blog post.

	Type 1	Type 2	LADA	Type 3c	MODY/NDM
Young (<25)	+1	0	0	0	+1
Old (>25)	0	+1	+1	0	0
Low C-Peptide	+1	0	0*	+1	0
History of pancreatic damage	0	0	0	+1	0
First degree relative	0	+1	0	0	+1
Insulin resistance	0	+1	+1	0	0
TOTAL SCORE	0	2	2	0	0

The scores suggest either Type 2 or LADA. At the time, the hospital believed I was Type 2 and sent me on my way. It was my family doctor who had the smarts to get the right tests done.

Tests For a Definitive Diagnosis

For Type 1 and LADA, the definitive test is a blood test for the auto-antibodies associated with Type 1 diabetes. In 80-90% of cases these auto-antibodies will be present in the blood. If the progression of the disease is advanced, the immune response may no longer be present making a definitive diagnosis harder.

Assuming the test is positive, the next consideration would be the c-peptide level. If it is still normal/high and blood sugars normal, it may be a case that the patient can be treated similar to a Type 2 with regular monitoring to track the deterioration of the pancreas and the transition to insulin-dependence (a slow progression suggests LADA whereas fast progression suggests a ‘classic’ Type 1). If the c-peptide is low, the best option may be to simply consider the patient as a Type 1 and treat them accordingly.

For Type 3c diabetics, a scan of the pancreas will reveal the damage and provide a definitive diagnosis. With a better understanding of the underlying pathology, treatment can be appropriately designed.

For MODY/NDM, a genetic test will provide a definitive diagnosis. As mentioned before, the optimal treatment for the common variants of MODY are known so it is easier to treat and manage the disease once it is diagnosed. This paper reviews in finer detail some of the symptoms of the different forms of MODY as well as the first-line treatments.

tl;dr

There is a lot of misdiagnosis when it comes to diabetes with many Type 2s (and a few Type 1s) being put in the wrong bucket. The right diagnosis means the treatment can be tailored appropriately to ensure the best long-term outcome for the patient.

Using a simple scorecard we can inform the diagnosis and get the right tests done for a definitive answer.

The Types of Diabetes

July 1, 2019October 26, 2019leontribe4 Comments

Diabetics usually know of two Types of diabetes (imaginatively called Type 1 and Type 2). Not surprisingly, most diabetics in the world also fall under one of these two Types but there are others. In fact there are at least 6.5 Types (the half will be explained a bit further down) and not a complete consensus among the world’s diabetes associations. I will focus on the ones where debate in minimal.

The List

For those who do not like to read, here is the list of Types. The rest of this blog will go into detail about each of them, how they are derived, diagnosed and treated.

Type 1: About 10% of all diabetics
- LADA, aka Type 1.5: A subcategory of Type 1
Type 2: Almost all of the other 90% of diabetics
Type 3c: 0.5-1% of all diabetics (many others wrongly diagnosed as Type 1 or 2)
MODY/NDM: 0.24% of those with diabetes
Type 0: 1 in 2 million people
Gestational: Approximately 13% of pregnant women (1 in 7)

What Makes a Type?

Diabetes Types are NOT classified by how the disease presents itself. This is important because it means the Type does not solely dictate how to treat the disease. Diabetes Types are ‘etiological’. This is a fancy word which means they are classified by the cause.

Type 1

Type 1 diabetes is an auto-immune disease. This simply means the body’s immune system attacks the beta cells of the pancreas. How the immune system gets confused and attacks the body is not yet known. So, while the cause of Type 1 diabetes is known (the immune system) the cause of the cause (why the immune system is broken) is unknown.

Many websites out there characterize Type 1 as “not being able to produce insulin” but this is not the full story. As mentioned, diabetic Types are etiological so while most Type 1s produce little to no insulin (because the immune system is very good at its job), there are Type 1s, like me, who still produce enough insulin to live a relatively normal life.

In terms of diagnosis, when the patient first shows symptoms, a blood test for the auto-antibodies (the parts of the immune system which attach the pancreas) will confirm it is Type 1. If the person has been a diabetic for many years, as the beta cells of the pancreas are mostly destroyed, the immune response will be minimal, making a definitive diagnosis harder.

For treatment, while the patient is in ‘honeymoon’ (where their body can still produce some insulin) they may only need pills and a low carbohydrate/low GI diet to keep their blood sugars under control. However, eventually, the honeymoon will pass and they will need to inject insulin.

Type 2

Type 2 is the most common Type of diabetes and the cause is unknown. This is the bucket all diabetics fall into when the cause cannot be discerned and as this is literally 9 out of 10 diabetics speaks strongly to the fact that we are only beginning to understand this disease and what causes it. Sadly, largely due to unawareness of the various Types in the medical community, there is much misdiagnosis when it comes to a person’s ‘Type’ with far too many being incorrectly dumped into the Type 2 category.

A ‘typical’ Type 2 cannot make enough insulin to meet their body’s needs. The pancreas is limited in its production and the cells of the body do not use the insulin efficiently (insulin resistance). Like Type 1s, the beta cells will show damage in Type 2 patients but the cause of the damage is unknown. One theory is the immune system temporarily attacks the pancreas but then stops, causing partial damage, but this has not yet been proven.

A common myth is that Type 2 diabetes is caused by ‘lifestyle factors’ i.e. eating unhealthy food, being overweight and not exercising. This is completely untrue. Type 2 is associated to things like obesity but it is not the cause. Where the association likely comes from is that a common cause of insulin resistance is fat deposits around the organs (visceral fat). So, if you are overweight, you may be contributing to your insulin resistance. However the underlying production limitation is still there. While reducing your carbohydrate intake and losing weight may get you off the medications, you are not cured, but simply in remission. Your impaired insulin production is still there; you are simply not testing the limit any more.

An analogy would be to suggest that asthma is caused by running because when some people run, they get an asthma attack. While asthma attacks are associated with exertion, the cause is completely separated; the exertion simply tests the limits imposed by the disease.

Unlike Type 1, there is a strong genetic component to Type 2 (although there is no genetic test for the disease). Type 2 runs in families and is significantly more prevalent in some areas of the world more than others.

Given the cause if unknown, diagnosis comes from exhausting the possibility of the other Types (or it should!) and giving the patient a glucose tolerance test to establish they have an abnormal response when processing sugars.

While insulin is sometimes needed, Type 2 is usually managed through pills, diet, and exercise. Progression of the disease is extremely slow and many Type 2s never require insulin to stay healthy.

LADA (Type 1.5)

LADA is also an auto-immune disease and, therefore, is a sub-category of Type 1. LADA stands for ‘Latent Autoimmune Diabetes of Adulthood’ and what makes LADA different to ‘typical’ Type 1 is the rate at which the disease progresses. This is what the word ‘latent’ means and why LADA is different to typical Type 1. While a typical Type 1 will be on insulin somewhere between immediately to a few weeks after diagnosis, LADA patients can survive without insulin for years.

Generally, LADAs are diagnosed later in life (for me it was at the age of 43) whereas ‘normal’ Type 1s are diagnosed much younger. Because LADA affects older people and the patient may not require insulin straight away, it is often misdiagnosed as Type 2. A simple blood test is all it takes to separate the LADAs from the Type 2s.

This was the test that the hospital failed to do in my case. As a male in his early 40s with a bit of extra padding, the ‘experts’ simply assumed I was Type 2. As LADA eventually leads to ‘classic’ Type 1 where the body no longer produces insulin, it differs to Type 2 which often never progresses to such a state. Therefore, the treatment of LADA is different to Type 2 because the focus is on preserving beta cells and prolonging the honeymoon, whereas in Type 2s it is assumed the remaining beta cell population will stay mostly constant for the rest of the patient’s life.

This misdiagnosis leads to many cases where someone who has been told they are Type 2, gets sicker and sicker as the medications become less effective. Often the misdiagnosis is eventually found but only after the patient has been ravaged with diabetic complications which may last the rest of the life e.g. eye damage, organ damage, nerve damage etc. All it takes is a simple blood test when the disease first presents itself to get the diagnosis right and to save the patient’s quality of life and a fortune in medical consultations and treatments.

Type 3c

The first of the lesser-known Types, Type 3c is NOT auto-immune but is where the pancreas is damaged by something else e.g. cancer, pancreatitis, cystic fibrosis, surgery etc. The damage may have also happened years before symptoms begin showing.

Given the cause is different we begin to see that this is important in how we approach the disease. Whereas the immune system selectively targets the beta cells (the cells of the pancreas which produce insulin) but usually ignores the alpha cells (which produce other hormones used for blood sugar regulation), damage caused by cancer or a car accident is less selective. Therefore, treatment which assumes the patient is Type 1 or 2 may miss the mark and, like the misdiagnosis of LADAs, may lead to diabetic damage before the error is revealed.

Diagnosis is through examining the patient’s history to see if there is a likelihood of damage and scanning of the pancreas to see the physical damage.

MODY/NDM

MODY (Maturity Onset Diabetes of the Young) and NDM (Neonatal Diabetes Mellitus) are monogenic forms of diabetes. Monogenic simply means caused by one broken gene. The name ‘Maturity Onset Diabetes of the Young’ is similar to terms like ‘Juvenile Diabetes’ and ‘Adult Onset Diabetes’ in that they come from a time when our technology was unable to definitively define the cause. Today, these terms are limited in their meaning but continue to hang around. I, for example, was diagnosed with ‘Juvenile Diabetes’ in my early 40s.

Most cases of MODY/NDM involve one of three specific genes but 11 gene mutations have been discovered so far. As MODY/NDM are genetic they strongly carry down family lines. While as a Type 1, your children have something like an additional 10% risk of having the disease, with MODY/NDM they have a 50% risk, 1 in 2.

The mutated gene means that a patient with MODY/NDM cannot produce insulin effectively and medication which seeks to stimulate the beta cells in some fashion may be useless in MODY/NDM patients. There is also a form of MODY (Glucokinase MODY) which affects blood glucose regulation but the principle that treatment due to misdiagnosis may be ineffective or counterproductive remains the same.

As MODY/NDM are strongly genetic, the patient’s broken beta cell machinery goes into operation at birth (arguably before birth but the mother can help compensate). For NDM, symptoms appear in the first 6-12 months of life (it is very rare for Type 1 to make an appearance this early), while for MODY symptoms usually appear in adolescence.

Definitive diagnosis comes from genetic testing, which is readily available. While misdiagnosis is, again, common, the correct diagnosis is vital as different forms of MODY/NDM respond to different drugs or, in the case of Glucokinase MODY, no treatment may be needed at all (Glucokinase MODY has the patient run a slightly high blood glucose but often not dangerously so). The other reason correct diagnosis is important is because of the risk to a patient’s children of having the same disease. Knowing this means it can be tested for and treated before complications arise.

Type 0 Diabetes

This disease is also called Glycogen Storage Disease Type 0. While also caused by genetic mutations, rather than affecting the machinery that produces insulin, it affects the machinery which uses the insulin to move blood sugar into cells for storage.

One of the things insulin does is move glucose out of the blood and into cells. Excess glucose is usually converted to ‘glycogen’ and stored in the cells (mainly in the liver but also in muscles) as an emergency energy source in times of exertion. In patients with Type 0, they cannot produce glycogen and therefore they have no energy backup.

The upshot of this is a patient with Type 0 can faint doing something as simple as climbing a set of stairs. Because there is no backup energy source and because it is hard to shift excess glucose out of the blood, a Type 0 patient will have wildly fluctuating blood glucose levels and the usual diabetic treatments (insulin and glucagon injections) are completely ineffective. If you think you have it tough as a Type 1, consider the plight of the Type 0.

As the disease presents in a very different way to the other Types e.g. fainting when climbing stairs, misdiagnosis is less common. Treatment is difficult and the best protocols are still being determined.

Gestational Diabetes

As the name suggests, gestational diabetes occurs during pregnancy so this one is exclusively female. The mechanism is broadly understood; to grow a baby, glucose needs to reach the fetus. To make this happen, the woman’s body releases hormones which increase insulin resistance in her own body, limiting access to glucose and allowing it to get to the baby.

With increased insulin resistance, the pancreas needs to release more insulin to keep up with the woman’s energy demands (up to three times as much in fact) which can test the pancreas’ limits and lead to diabetes. Excess glucose in the blood can make the baby grow excessively, leading to birthing complications but can also damage the baby leading to miscarriage or stillbirth so it is important that Gestational Diabetes is managed during pregnancy and, thankfully, screening for it is common.

Once the baby is born and the pregnancy hormones disappear, the diabetes usually goes as well. However, in some cases, the damage is done and the diabetes remains, generally classified as Type 2 and treated as such. Arguably, the cause is known so it is not really Type 2 and is a continuation of Gestational Diabetes.

What is Your Type?

If you are a Type 2 and your treatment plan is not working well, it is worth considering that you may have been misdiagnosed. If, after reading the above, you feel you may be a candidate for a different Type, reach out to a medical professional to discuss your concerns. While medical professionals hate Dr Google and well meaning blogs, it is your life and you who will have to live with the complications if their guess was wrong. They can organize the tests to make a definitive diagnosis.