What Does Insulin Do? Basal Vs Bolus

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It surprises me how often questions come up online about what insulin does and the purposes of basal and bolus insulin. As usual, there is a tl;dr at the end, although this blog article is relatively short.

The Two Roles Of Insulin

The most well known role of insulin is its role in taking glucose from the blood and moving it into the cells of the body. In fact there are parts of the body which do not require insulin to access blood glucose, such as the brain (the thing that uses most of the fuel and is too important to go without it), and the liver (the thing that makes the fuel when fasting). For most of the rest of the body though, to use glucose as a fuel, requires insulin.

The second and less well know role of insulin is in helping regulate the liver. In “What Is Ketosis And Diabetic Ketoacidosis?” I talked about this in detail. In short, when there is less insulin in the blood, the liver becomes more active at producing fuels for the body and when there is more insulin the liver is substantially less active at doing it.

So What Does This Have To Do With Basal and Bolus Insulin?

For those that do multiple daily injections (MDI), the two roles of insulin are reflected in the two types of insulin used i.e. rapid- and long-acting insulins.

The role of a long-acting insulin is to mimic the slow and continual release of insulin from the pancreas to offset the slow and continual release of glucose from the liver, keeping the liver in check and blood sugars stable.

The rapid-acting insulin is designed to mimic the release of insulin by the pancreas to offset spikes in glucose from things like exercise, and carbohydrate intake.

In the case of a pump, the basal rate and bolusing reflect the same thing.

Consequences for Insulin Use

The big takeaway from all this is, if you are not doing things which cause glucose spikes, your blood sugars should be flat and in range. If, when you fast, your blood sugars and trending up or down, your long-acting insulin/basal rate needs adjusting.

Get your basal right and it will be a lot easier to manage your blood sugars.

tl;dr

Insulin serves two purposes in the body: moving glucose from the blood into cells and to assist in the regulation of the liver’s fuel production. Rapid- and long-acting insulins tries to reflect these two roles. A consequence of this dual-role is, at least in theory, if a person is not eating or undergoing anything else to spike their glucose levels, their glucose levels should be flat and controlled exclusively by their basal insulin. If glucose levels are not flat the person’s basal insulin routine/rate needs adjusting.

You Do Not Need To Eat Carbohydrates!

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There is some debate over the appropriate amount of carbohydrate in the diet of diabetics (and muggles for that matter). If you want the summary, here is link to tl;dr, otherwise keep reading.

On one side of the argument we have Dr Bernstein and the Type One Grit advocates. They promote very low levels of daily carbohydrate (around 30g) and see excellent control because of this. The risks of hyperglycemia are small because of the lack of carbohydrates and Dr. Bernstein argues the risk of hypoglycemia is small because of the correspondingly smaller amounts of insulin used and the strict control of the carbohydrate count at each meal (typically 6g/12g/12g for breakfast/lunch/dinner).

On the other side we have high carbohydrate advocates, such as Forks Over Knives and the unfortunately named ‘FOK Diet’. FOK promotes a plant-based diet high in carbohydrates and low in animal fats. The thinking here is to reduce insulin resistance in the body and, through this, provide better control. Clearly, the focus is on Type 2 diabetics but the FOK folk also promote this diet for Type 1s. The argument is that while control can be achieved through a low carbohydrate approach, the health cost of high levels of animal fats is too high; you are replacing one problem with another. Hypoglycemia is avoided by eating lots of carbohydrates. Hyperglycemia is avoided by making sure you eat low GI (glycemic index) foods, preferably plant-based. It should be noted that FOK do not say high levels of dietary carbohydrates are necessarily good or essential, they simply say high levels of animal fat are bad.

I am not intending to resolve this debate with this blog article but I do consider where the body gets its energy from and answer just how essential carbohydrates are. From there, it is up to you. In full disclosure, I do not eat a lot of carbohydrate. As a Type 1 LADA in honeymoon, I believe the best thing I can do for my pancreas is to give it as little work to do as possible and a low carbohydrate regimen achieves that.

What Foods Give Us Energy?

There are four main components of food which give us energy. These are:

  • Fat (yielding 37 kJ/g or 9 kcal/g)
  • Ethanol (aka alcohol) (yielding 29 kJ/g or 7kcal/g)
  • Protein (yielding 17 kJ/g or 4 kcal/g)
  • Carbohydrate (yielding 17kJ/g or 4 kcal/g)

There are a few other sources of energy, such as organic acids and alcoholized sugars, but we will keep things simple with the main ones.

What Food Gives Us Glucose?

Of these foods, the only ones which get converted to glucose are carbohydrates (whenever you eat them) and proteins (significantly when you are fasting via gluconeogenesis). For a recap of what gluconeogenesis is, refer to “What is Ketosis and Diabetic Ketoacidosis?” where I wrote in detail about how the body finds alternative sources of energy when fasting. In short, when there is insufficient dietary carbohydrate, the liver engages the following processes:

  • Glycogenolysis: The release of glucose into the blood from the glycogen energy stores of the liver and muscles
  • Gluconeogenesis: The conversion of amino acids from proteins into glucose
  • Ketosis: The conversion of fatty acids from fat into ketones (an alternative fuel for some parts of the body)

So even if we are not eating carbohydrate, the liver can release glucose into the blood to fuel the body and, when this runs out, it can convert the body’s protein supplies.

What Food Elements Are ‘Essential’?

So we know, from an energy perspective we can possibly make do but perhaps carbohydrates are needed for something else. In fact, while proteins and fats are necessary to build the structures of the body, this is not the case for carbohydrates. Here are some of the uses of fats, proteins, and carbohydrates:

  • Fats: Break down into fatty acids in the body and used for:
    • Regulation of vitamin intake
    • Hormone regulation
    • Insulation and protection of organs
  • Proteins: Break down into amino acids in the body and used for:
    • Build structures in the body like muscles
    • Facilitate communication between cells
    • Act as transporters for other molecules
  • Carbohydrates: Break down into glucose in the body and used for:
    • Energy

That is it. Carbohydrates are used for energy or stored for use as energy later on. There is nothing essential about carbohydrates.

So, assuming you could eliminate carbohydrates, fats, or proteins completely from your diet, could you survive?

For carbohydrates, as we can make glucose from protein via gluconeogenesis, we know they are not essential.

For fats, there are two essential fatty acids: omega-6 and omega-3. Essential meaning the body cannot synthesize enough of them on its own to maintain function. Without omega-6 and omega-3 the body simply cannot function.

For proteins, there are nine essential amino acids. Of these, you may have heard of Phenylalanine, which is one on the substances the sweetener aspartame breaks down into. Another is Tryptophan, made popular by the myth that it causes the drowsiness of excess turkey eating.

Do Our Bodies Need Glucose?

There is a common myth that the brain requires carbohydrate to function. This is not true; the brain runs primarily on glucose, from any source but, more importantly it can also utilize ketones to run as an alternative fuel source in times when glucose is in short supply. In fact there are four main fuel sources the organs of the body can use to fuel themselves.

  • Glucose (fuels the kidneys, brain, liver, fatty tissues, and muscles)
  • Fatty Acids (fuel the muscles)
  • Ketones (fuel the brain and muscles)
  • Amino Acids (fuel the liver)

Source: https://www.ncbi.nlm.nih.gov/books/NBK22436/

Clearly glucose is the most versatile fuel source, covering all the bases but the only parts of the body solely dependent on glucose are the kidneys and fatty tissues. Everything else can supplement with alternatives.

I tried to find the maximum rates of glucose production possible through glycogenolysis and gluconeogenesis but came up short. Of particular interest is the rate of glucose production for gluconeogenesis because the liver only keeps enough glycogen stored for a couple of days. After that the only way for the body to generate glucose is through gluconeogenesis.

The story all students are told before going on school camp is the rule of three: you can survive three days without water and three weeks without food. If this is true, as we know glycogen stores are only good for a couple of days, this means the body can get by on gluconeogenesis alone until, presumably, the available protein stores run out. Of course, with enough protein in the diet, we can keep the glucose production going indefinitely.

tl;dr

Unlike fats and proteins, carbohydrates are not essential because the body has ways of generating glucose outside of the digestion of carbohydrates. This is not true for essential amino acids and essential fatty acids which are needed to maintain the health of the body and which can only be obtained by the dietary intake of proteins and fats, respectively.

Moreover, while the kidneys and fatty tissues rely exclusively on glucose for energy, the rest of the body can access alternative fuel sources, such as amino acids, fatty acids, and ketones.

Finally, we know the body can generate enough glucose for its needs outside of carbohydrate ingestion because a person can survive with no food for up to three weeks. Given the liver and muscle’s glycogen stores are only good for a couple of days this means the process of gluconeogenesis (the body’s conversion of amino acids to glucose) is all that is required to maintain blood glucose levels, and as long as a regular supply of protein is provided, this means the process can continue indefinitely.

You do not need to eat carbohydrates!

What Is Ketosis And Diabetic Ketoacidosis?

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There is a lot of confusion around ketosis and diabetic ketoacidosis. Some people think they are the same thing; others think ketosis leads to ketoacidosis. Neither of these notions are true.

To better understand the differences, let us understand precisely what the terms mean. As a disclaimer, the metabolic processes of the body are extremely complicated. There is much more to it all than just the liver and insulin but using these gives us a practical working model. As usual, if time is short you can go to tl;dr.

I have used a lot of internet searches and Wikipedia pages on the human metabolism to put this blog together. A couple of key sources of information were:

https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0008/220679/nepean_guide_DKA_2007.pdf

https://www.ruled.me/what-is-gluconeogenesis/

The Role of Insulin

To understand ketosis and ketoacidosis, we need to understand the role of insulin in the body. It is generally understood by many diabetics that insulin is needed to move glucose from the blood into cells. What is less well know is that insulin is also a control switch for the liver.

While the pancreas releases insulin based on the levels of glucose in the blood, the liver releases glucose into the blood based on the amount of insulin. Other hormones also influence this process but ignoring these external factors for simplicity, the liver and pancreas work together to keep the glucose in the blood stable, both producing small amounts of glucose and insulin respectively to keep the other in check. The doctors call such an equilibrium ‘homeostasis’.

If we consider the role of food, when carbohydrates are consumed, blood glucose goes up and insulin production is increased to move the glucose out of the blood. Similarly, the liver’s production of glucose goes down. When blood sugars return to a base level, the liver and pancreas also return to their homeostatic rate of production.

When someone chooses not to eat, the opposite occurs. With glucose in the blood not being replenished by food, glucose levels drop and the pancreas produces less insulin. This, in turn, encourages the liver to produce glucose to give the cells of the body the energy it needs.

Prolonged Fasting

In a world before widespread food transportation and refrigeration, winter meant a time of limited carbohydrates. Fortunately, the human body has some backup measures when times get tough.

The glucose stores of the liver are good for a day or two. As these run low, and insulin levels continue to drop, a new process ramps up. The protein sources of the body are broken down into amino acids and converted by the liver into glucose in a process called gluconeogenesis (other substances in the body are also used, such as lactate and glycerol but let us keep things simple).

This can keep the body going for a few days to a few weeks, depending on things like diet (protein sources can be found in the winter, after all). After this, and the insulin levels drop a little further, the fat stores of the body are broken down into fatty acids. Different parts of the body can use fatty acids and amino acids as alternative fuel sources to glucose so, even with a low carbohydrate diet, the body can maintain the necessary energy levels.

If carbohydrate fasting continues, insulin levels keep dropping and there are sufficient fatty acid levels in the blood, another process kicks in to convert fatty acids into ketones, yet another fuel source which can be used by the brain and muscles (a commonly held misconception is that the brain can only use glucose as a fuel source; it is simply not true). This final process of converting fatty acids into ketones is called ketosis.

Ketoacidosis

In a body with a low but sufficient level of insulin, ketosis is regulated and poses no threat. In the muggle (non-diabetic person) body, it is very difficult to go below the threshold where ketosis becomes a problem. To do so requires literal starvation or large amounts of alcohol over an extended period of time. Starvation can be understood as an extension of the explanation above. Alcohol causes a problem by blocking the liver’s ability to generate glucose from the energy stores and amino acids, forcing the overproduction of ketones.

For the diabetic, where insulin production is impaired, it is much easier to go below the threshold. This is why insulin-dependent diabetics, whose pancreas cannot maintain a basal level of insulin, do so through a pump or via the injection of long-acting insulin. For non-insulin-dependent diabetics, one path to ketoacidosis is feeding the body fast-acting carbohydrates which flood the blood with glucose and overwhelm the pancreas. The insulin in the blood becomes depleted and the liver goes unchecked.

With no insulin to regulate it, the liver goes into energy production overdrive, running all of the energy production processes as quickly as possible. The body is flooded with glucose and ketones and, while the excess can be removed from the body through urination, even this has its limits. The ketones begin to accumulate, changing the pH (acidity) of the blood. This has knock-on effects throughout the body leading to sickness and often vomiting. If not dealt with, ketoacidosis can lead to coma and death.

The Key Differences

While ketosis is a state of low dietary carbohydrate, ketoacidosis is a state of low insulin in the blood, which is almost impossible to generate through a lack of eating, except in extreme cases of starvation. A diabetic who maintains a basal level of insulin in their blood will not go into diabetic ketoacidosis (DKA) from a low carbohydrate diet. It is simply not possible.

The manifestation of the two in the body is also different. While someone in ketosis will have a low/normal blood glucose and generally feel fine, someone in ketoacidosis will have elevated blood sugar levels, be urinating frequently e.g. a full bladder every 30 minutes, may feel thirsty and be dehydrated, and feel ill. Unfortunately, there is no over-the-counter test for serum insulin levels (the amount of insulin in the blood) or blood acidity levels, which would provide a definitive answer to a concerned diabetic.

EDKA

A rare form of DKA is Euglycemic DKA (EDKA). In this case, the body is flooded with ketones but blood glucose levels are normal. This usually occurs when there is extremely low insulin levels in the blood and the liver also has low glucose stores. This is something to watch out for if, for example, you are fasting. It is also the reason why it is vital to ensure you always have a sufficient basal level of insulin.

As EDKA does not present with high blood sugars, it is often missed by doctors. If you suspect you could have EDKA tell your health care team of your suspicion and insist they measure your blood pH which is the definitive test for DKA and EDKA (reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5592704/).

In terms of treatment, DKA and EDKA are treated the same way: hydration and insulin to bring ketosis back under control.

tl;dr

Ketosis and diabetic ketoacidosis (DKA) are not the same thing. While ketosis is triggered through an extended lack of dietary carbohydrate, DKA is triggered by the exhaustion of insulin in the blood; the consequence of which is the liver over-producing fuel for the body, including ketones which, when they accumulate, can turn the blood acidic and lead to death.

Treatment for DKA is re-hydration and the re-introduction of insulin back into the blood.

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

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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 1Type 2LADAType 3cMODY/NDM
Young (<25)+1000+1
Old (>25)0+1+100
Low C-Peptide+100*+10
History of pancreatic
damage		000+10
First degree relative0+100+1
Insulin resistance0+1+100
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 1Type 2LADAType 3cMODY/NDM
Young (<25)+1000+1
Old (>25)0+1+100
Low C-Peptide+100*+10
History of pancreatic
damage		000+10
First degree relative0+100+1
Insulin resistance0+1+100
TOTAL SCORE02200

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

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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.

Who Is The Practical Diabetic?

leontribe1 Comment
Me

My name is Leon Tribe. I was educated as a physicist but now work as the National Director for a large multinational organization and occasionally speak at conferences on technology and diabetes.

I live in Sydney, Australia and I am a Type 1 Diabetic. As I write this it has been two years since my diagnosis and I am still insulin free with normal blood sugars. More of that in another post.

If you are interested in my diabetes story keep reading. If you would prefer to cut to the chase and see what this blog is about, jump to here.

Where It All Began

My diabetic journey started near the beginning of 2017. I had been feeling exhausted for months, which I attributed to poor sleeping habits. My hair was falling out in small round patches (alopecia areata) but it ran in the family so I just accepted it. My ankles ached, making it hard to go up and down stairs, which I had no explanation for, other than being middle aged and not particularly health conscious. I had a rash in places one should not have a rash and this also had no valid explanation. Finally, my eyesight was acting up. I had worn contact lenses for shortsightedness since adolescence but it seemed my prescription was on the move again.

Then things started to get a bit more specific to something I could self-diagnose. I was at a conference away from home and found myself permanently thirsty. This was strange because I rarely got thirsty. I was also needing the bathroom every half hour or so and emptied a full bladder each time. This was a problem because I was supposed to be doing an hour presentation at the conference and one does not normally hop off stage for a quick bio-break.

A heavier, thirstier, and overall sicker me on stage

I got through the presentation and flew home. Pretty much the only thing I knew about diabetes was it made you permanently thirsty and pee a lot so I headed to the doctor.

(Mis)Diagnosis

Sure enough my fasting blood sugar was three times what it should have been and I had ketones. For the uninitiated this meant I had the early stages of Diabetic Ketoacidosis (DKA). In short, my body had a shortage of insulin and was out of control because of it. My blood was slowly going acidic which is a very bad thing. It also confirmed to the doctor that I had some form of diabetes. The doctor recommended I immediately go to hospital, now, right now, like immediately.

Sure enough I headed directly to hospital where they put me on a drip to re-hydrate me and start a bunch of blood tests. The re-hydration stabilised me and given I was a guy with a few extra pounds in his early 40s with diabetes they came to the (wrong) conclusion I was a Type 2 diabetic.

Misdiagnosis of diabetes happens a LOT with many people being thrown into the Type 2 bucket incorrectly. It was my doctor (a generalist with an interest in diabetes but no formal specialization) who had the sense to test my blood for the tell-tale auto-antibodies which confirmed a Type 1 diagnosis; something the ‘experts’ in the hospital had failed to do. I was a middle-aged man with ‘Juvenile Diabetes’.

Since Diagnosis

Type 1 is a relatively rare disease; roughly one in 200 people have it or, 0.5% of the population. For the first 11 months I met no one with Type 1. This was quite isolating so I started up a monthly meetup to meet others and to learn from them. If you live in Sydney, feel free to come along to our monthly gathering.

While I did not need insulin to keep myself healthy, I was taking pills (Metformin at first, and now also Saxagliptin). However, the pill boxes in the market were dull so I created my own out of a pocket watch. Thinking others may also feel the same way, I now sell them on Etsy.

All this time I have also been learning as much as I possibly can about this disease. My training as a physicist means I can absorb quite a large amount of information quickly, which has proved very useful. This blog is a vehicle to share some of the things I have discovered on the way and, hopefully, help others manage this chronic disease (‘chronic’ just means long term).

Why Read This Blog?

There is a lot of complex information and a lot of nonsense out there. My aim is to reduce the noise and provide simple explanations and practical advice (non-medical, of course) for diabetics of all Types. If you have questions about how diabetes works and how to manage it effectively, my sincere hope is that my blog helps you in some way.

What Is In It For Me?

Perhaps one day I will convert this blog to a book (publishers feel free to contact me :P) but until then this is simply a vehicle for me to clarify my ideas and get them in a format I can refer back to. That is it. There are no paid endorsements and I am not yet in the pocket of Big Pharma.

If you have made it this far, well done and welcome aboard. Thank you for taking the first step with me on a journey of 1,000 miles.