#NDM – The Practical Diabetic

Insulin Cooling Battles: Frio vs Breezy Packs

December 19, 2021March 24, 2022leontribe7 Comments

My previous battle, Frio vs Gel, showed that while a gel pack slows down the transfer of heat, it has no power to stop that heat energy eventually reaching the contents of the pouch. In contrast, the evaporation of the water from the Frio pouch actively fights the heating of insulin by redirecting the heat energy to converting the water from a liquid to a gas.

In this battle, we have two related, but different technologies which both redirect the heat energy to perform other tasks than heating the pouch contents. As mentioned, for the Frio pouch, it is the conversion of water to steam and, for the Breezy Pack, it is the melting of a mysterious substance called a PCM (Phase Change Material).

What are PCMs?

We know from high school science that, in the everyday world, matter is in one of three states: solid, liquid, or gas. What we may not know is, to move from solid to liquid, or liquid to gas takes energy. The scientific term for the energy required to melt a substance is the “Heat of Fusion” or “Enthalpy of Fusion” and it is measured in energy per weight e.g. kJ/kg or energy per volume e.g. MJ/m^3.

The energy needed to evaporate a substance is called the “Heat of Vaporization”. It turns out the energy needed to evaporate water is really high. It literally takes five times the energy to get water to turn to steam once it reaches boiling temperature than it takes to take water from ice to that temperature. So, if you have a kettle or heater which can get your water to just under boiling temperature, and that serves your purposes, do so because you will save a LOT of money on energy bills.

So, in the case of our Frio pouch, the PCM at play is water going from a liquid to a gas. While water does boil at 100C (212F), even at 30-40C (86-104F) we get some cooling effect because the water molecules in the Frio pouch are at a range of energy levels so a little heat energy can tip some of these over to becoming a gas at these lower temperatures. This is why we may see a little steam, even before the water is boiling.

In the case of Breezy Packs, the makers do not reveal what the PCM substance is but we can make an educated guess.

What is the PCM in Breezy Packs?

This is what we know:

The substance is solid below 25C (77F) and turns to a liquid above this temperature. We know this from the instruction sheet.

From the Breezy Pack website, the substance begins to melt above 27C (80.6F)

Going to Wikipedia, we have a range of common PCMs. Assuming the manufacturers have gone for an inexpensive PCM whose melting point is somewhere above room temperature and below the fail temperature for insulin (around 30C/86F) the obvious choice is Sodium Sulfate, maybe with some salt added. At US5c/kg, it is the cheapest PCM in the table, after water. You will notice below that pure Sodium Sulfate melts at 32.4C (90.3F) but, adding a little salt brings this down to a lower temperature. I have bought some pure Sodium Sulfate to experiment with and see if I can replicate the Breezy Pack but that is for another post.

The Experiment

As with the Frio vs Gel experiment, I have enlisted the help of my oven to maintain an even temperature. While I used the middle shelf and the fan forced setting last time, I was finding the oven was going above 46C (115F) which I did not want so I put the Frio and Breezy pouches on the lower shelf with only the top element on. I also put a dishcloth on the middle shelf to act as a shield from the direct heat of the heating element. I also put the two pouches on two plastic cutting sheets to prevent contact with the metal bottom.

The wires were linked to digital sensors so I could monitor the temperature.

The blank one is the temperature of the oven.

The Breezy Packs, at the time of writing come in two versions: Breezy Basic and Breezy Plus. Both of these are the same physical size but the Breezy Plus contains more PCM so it can work for longer. This experiment used a Breezy Basic. The Frio pouch was the same one as I used in the Gel comparison and was soaked in water for the same amount of time prior to going into the oven i.e. 5 minutes. The only difference was the temperature of the water used which, in this case, was room temperature and not, as last time, from the cold tap.

The Results

So, for an oven where we the temperature is between 35-40C (95-104F), we see that the Frio took around 15 minutes to go from 25C (77F) to 30C (86F). In contrast, the Breezy Packs only moved 1.5 degrees Celsius over the same time period.

The rapid rise in the Frio surprised me as it took twice as long to move the temperature the same distance but, even if we use the Frio vs Gel pack results for considering the Frio pouch, we see that it is still out-performed by the Breezy Pack. My guess is the sensor in the Frio pouch was closer to the outside this time around and, therefore heated up quicker. An alternative explanation could be the difference in oven temperature from last time changing the performance of the Frio pouch i.e. the oven ran a little hotter, although more consistently this time around than last time.

Conclusions

To my initial surprise, the Breezy Pack strongly outperformed the Frio pouch. In hindsight, this makes sense. If we think about it considering the PCM in each case, for water, most of the water molecules are still too cold to transition to a gas state and, therefore the heat energy is simply used to warm the material. For the Breezy Pack though, the majority of the molecules are close to melting and will more heat energy can be redirected away from heating the pouch.

Given the Breezy Pack requires no soaking, is not damp and simply works and given the price point for both the Frio pouch and Breezy Pack are similar, it seems clear the Breezy Pack is the superior option between the two when carrying a couple of pens.

Please note: I bought all pouches with my own money and have received no financial benefit in this comparison. This being said, I am very, very open to receiving sample pouches if either Frio or Breezy Pack want me to compare different sized models in the future 😉

Insulin Cooling Battles: Frio vs Gel

November 28, 2021March 24, 2022leontribe3 Comments

David Burren recently put me on to Breezy Packs which, if their claims are to be believed, offer a new way to keep insulin cool in the field. I have ordered a couple of Breezy Packs to put them through their paces but, first, I thought I would try out the existing methods commonly employed to show how they work.

Gel

Gel packs contain gel (no surprise there) which holds its temperature well and acts as an insulator. There is no actual cooling mechanism here other than the gel slows heat passing from one side to the other. So, to use a gel pack, you cool it down in the fridge (not the freezer as insulin does not like to be frozen) and put your insulin inside it to protect it from outside fluctuations in temperature. Outside heat is slow to heat up the gel pack which means the insulin stays cold.

Frio

Frio is, arguably, the most popular brand name for evaporative cooling pouches for keeping insulin cool. There are other brands out there (I even sell a version in my Etsy store) so feel free to shop around. They all work in the same way though. You immerse the pouch in water for, say, five minutes and it puffs up. You take it out of the water, wipe it down and put your insulin inside.

Not only are the pouch contents (generally silica gel beads or similar) an insulator but they are spectacular at absorbing and holding on to water. How Frio bags work is, when exposed to a warm temperature, the water in the beads begins to evaporate but evaporating water molecules takes energy so, instead of the external heat being used to raise the temperature of the water, some of it is used to turn the water to steam. This means the water temperature stays reasonably stable and, in turn, so does the temperature of the insulin inside the pouch. Our bodies use the same trick to stay cool when we sweat.

Breezy Packs

Breezy Packs offer a new way to keep insulin cool, which is similar to Frio bags but, instead of absorbing energy, turning water from liquid to a gas, it converts its active material from a solid to a liquid. No need to soak and wipe down. The physics of Breezy Packs is actually very smart so I will save it for when the pouches arrive and I will write another blog on the subject.

The Cooling Battleground: My Oven

It turns out that I can get my fan-forced oven down to around 30-40 degrees Celsius (104 degrees Fahrenheit) so this was my “controlled environment”. The contestants were a small Frio pouch capable of holding two insulin pens and a massive pillow gel insert.

The insert is 30x40cm with three panels. Both pouches went onto an oven tray with baking paper underneath to try and insulate from the metal bottom.

The gel pad was folded into three with two of the panels at the bottom and both pouches had a temperature probe put in the middle of them. As indicated above, the gel pad had been stored in the fridge whereas the Frio was soaked in tap water.

Once in the oven, I monitored their temperature and the temperature of the oven.

Here the gel pack is 10.7 degrees Celsius, the Frio pouch is 23.8 degrees Celsius, and the oven is 35.5 degrees celsius.

The Results

Thanks to the magic of Excel we can see how the two pouches fared. The oven temperature, which had previously reached the target temperature, was slowly dropping but remained above 30 degrees for the whole time. The Frio pouch, with the oven’s heat being used to turn the Frio’s water to steam, was holding a reasonably even temperature. The gel pouch, with nothing but insulation, slowly increased in temperature, catching up to the Frio after about 30 minutes, despite the 15 degree head start.

To be honest I was not sure the Frio pouch would work as well as it did as the oven was closed and, therefore, once the air inside the oven was saturated with moisture, the Frio would no longer be able to cool but for the 30 minutes it continued to work.

Conclusions

First of all I was really impressed the results came out as well as they did, showing the characteristics of the two pouches. For my money, if I was expecting to carry insulin for an extended period of time in high heat, I would likely look to a pouch that uses evaporative cooling. I would also invest in a MedAngel so I could check the temperature inside the pouch at any time and be alerted if things were going astray. Gel is a much cheaper option, of course, so, for short excursions, it will work fine. You could also, if you had a large enough pouch, put a cooled gel pouch inside a Frio pouch and gain a double benefit. As long as the Frio pouch is on the outside this should work fine.

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.