In this battle I compare Breezy Packs to breast pads.
Why Breast Pads?
It may seem like a curious choice but there is method to it. In “Frio vs Breezy Packs” I mentioned that Breezy Packs use Phase Change Materials (PCMs) to maintain the internal temperature. For a rundown of the physics on how they work, head over to that post.
While the specific material used in Breezy Packs is a trade secret, one candidate substance is octadecane whose melting point is around 28C (82.5F). While not listed on the box, on eBay the listing for the breast pads had octadecane as one of the main ingredients. For $20 it was worth a shot.
Sure enough, on touching the pad there was a cooling sensation so things were promising.
The Setup
For Breezy Packs, I used their smallest size and put one of my Ozempic pens inside with a digital temperature sensor embedded within it.
For the breast pads, I used a mesh pencil case I had picked up and layered the breast pads inside with another pen with a sensor between them.
In the image you only see the pads on one side but I did put eight on one side and eight on the other for the experiment.
A third sensor was used to track the oven temperature.
With the two containers on a rack on an oven tray (I did not want the tray to be in direct contact with the containers) I placed them in the oven and took the temperature around every five minutes until one of the containers went past 30C (86F).
Prior to entering the oven, the breast pads consistently measured a lower temperature than the Breezy Pack. I assume this was because of the higher area of contact between the pads and the insulin pen. However, things changed when the oven became involved.
The Results
While the breast pads initially showed a lower temperature, this soon changed. Both were pretty stable but, at 17:15, the temperature of the oven was continuing to fall and was heading towards 30C so I increased the dial by a small amount. The different response can be seen with the breast pads increasing temperature much faster than the Breezy Pack and eventually hitting 30C. In fact, over 40 minutes, the breast pad temperature went up by 7C (12F) compared to 2C (3F) for the Breezy Pack.
Conclusions
Breezy Packs wins again although I suspect if we used a similar volume/weight of breast pad PCM the result may have been different. This being said, the amount of breast pads needed to achieve this would be excessively expensive. As with previous experiments, the components were fully funded by myself without commercial sponsorship of any kind.
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 😉
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.
ATTD 2021 was held 2-5 June, 2021 and, thanks to dedoc, I had the privilege to attend and live tweet the presentations. However, with many sessions running in parallel, it was not possible to attend every session and many sessions covered similar topics. To address this, I watched the recordings of the sessions I missed and brought them together under common themes. Where the presentation called out that the results were confidential and/or not yet published and not for distribution I left them out of my blog but I can confirm there was nothing presented under confidence which contradicted what I am presenting in these summaries.
This is my second “distillation” which is on pregnancy and gestational diabetes. For my first “distillation” covering looping go here. Firstly, let me be clear in my intent: I am a male and never been pregnant. My aim is to present the research, as I understand it, from ATTD 2021. I am not a medical professional and nothing here should be considered medical advice or me telling you what to do with your body. If something I have written is of interest, I strongly encourage you to discuss it with your medical team to determine the best course of action for you. I will also call out that this post discusses the possible adverse outcomes of pregnancy for the baby. Not all pregnancies go to plan and if this subject is distressing for you, you may be triggered by the contents of this post.
A common observation of women with diabetes is their menstrual cycle has a significant impact on their blood glucose level management. It is known in that the fluctuation of hormone levels in the body directly impacts insulin resistance. The same happens in pregnancy with the thinking being that hormone levels increase in a woman’s body to increase insulin resistance so more glucose reaches the baby for growth and development.
For women with diabetes this amplifies an existing health condition and, for women who do not have diabetes, given the stresses this puts the body under, it can trigger diabetes during pregnancy in what is called Gestational Diabetes. ATTD 2021 looked at some of the latest research on diabetes and pregnancy which I present here.
Specific questions covered in the presentations were:
As usual there is a TL;DR section at the end if you want to read the summary of results without the details.
If I am a Woman with Diabetes, What are the Health Risks to my Baby?
Dr. Helen Murphy presented on the risks to the baby for women with Type 1 and Type 2 diabetes. Both Dr. Murphy and other presenters made it clear that there has not been a lot of improvement in adverse outcomes for pregnant women with diabetes (congenital abnormalities and deaths), for decades. As we will see later, there is potential for this to change with tools like continuous glucose monitoring devices (CGMs).
A result which surprised me was the risks to women with Type 1 and Type 2 diabetes was about the same and slightly higher for neonatal death in women with Type 2 diabetes. While there appears to be a trend upwards in some of these graphs, Dr. Murphy pointed out the tending was not statistically significant.
A question I had was how this compares to the general population. Dr. Robert Lindsay, covered this with some earlier data. Assuming the risk level has remained the same for the general population, for stillbirth, women with diabetes have a risk somewhere between 2-4 times higher than the general population.
For adverse outcomes (death and congenital defects), we also see similar risk profiles for women with Type 1 and Type 2 diabetes. Literally 1 in 10 women with diabetes, who do not prepare for pregnancy, have a serious complication with their pregnancy. The good news is, with planning and preparation, this number goes down to 1 in 50 which is close to the rate for the general population.
Planning and preparation in this case means taking folic acid before and during pregnancy and controlling blood sugar levels as well as possible. The guideline is to have an HbA1c below 48mmol/mol (6.5%) which, for many, is easier said than done. Many factors affect a woman’s ability to control their blood sugars beyond the usual diet and exercise. For Type 1 is was shown that other factors include:
Age (younger Type 1s often struggle to control their average blood glucose levels compared to their older counterparts)
Social disadvantage (Deprivation)
Time since diagnosis (while older Type 1s typically have a lower HbA1c, those diagnosed 5 or more years ago typically have a higher HbA1c)
BMI (the higher the body mass index, the lower likelihood of a woman with Type 1 having an HbA1c below 6.5%)
For Type 2, social disadvantage was a factor although it does not seem to be as pronounced, time signce diagnosis was a factor, and also BMI.
The only one of these factors which can be easily addressed by a woman looking to get pregnant is BMI but, as many of us know, shifting the needle on weight is not a simple task.
While important before getting pregnant and in the first trimester, HbA1c is also predictive of adverse outcomes as late as the third trimester. For both women with Type 1 and Type 2 diabetes, the risks significantly increase for an HbA1c above 75 mmol/mol (9.0%). Dr. Murphy also pointed out that this result removed confounders (contributing factors such as weight, age etc.) In other words, HbA1c is very predictive of risk.
She also presented details of the relative risks for Neonatal Intensive Care (NICU) admission, preterm birth, and having a “big baby” (LGA: Large for Gestational Age) showing HbA1c also predicts for these events as well.
Dr. Robert Lindsay also presented on factors associated with still birth, including those with Gestational Diabetes.
Not surprisingly, blood glucose levels are a factor here as well even for those diagnosed and treated for gestational diabetes. Given there were different results for the diagnosed and undiagnosed, it suggests there is a factor beyond fasting blood glucose affecting outcomes which treatment is addressing. My assumption is it is the non-fasting glucose levels and their fluctuations.
While the results may seem depressing, there is hope. As we will see in the next two sections, there are new technologies and treatments which can positively impact pregnancy outcomes for women with diabetes of all Types.
Health Benefits of Using a CGM During Pregnancy
Dr. Jennifer Yamamoto presented on the performance and benefits of Continuous Glucose Monitoring (CGMs) for pregnant women with diabetes.
For sensor performance, she spoke of a study looking at placement on the body of the CGM sensor covering women of all Types.
Overall, regardless of placement the accuracy as measured by MARD (Mean Absolute Relative Difference), where a lower number indicates better accuracy, performance was good but the arm was the best area for placement achieving 8.7% accuracy.
In terms of the benefit of using a CGM device, Dr Helen Murphy, presented results specific to Type 1 showing, especially in the third trimester, significantly better results for pregnant women who used a CGM; they literally gained an additional 100 minutes per day in range.
As to be expected, this had a knock-on effect on neonatal outcomes with a statistically significant lowering of risk for a larger baby (LGA), hypoglycaemia, and neonatal ICU admission.
Dr. Claire Meek presented on the predictive power of CGMs for adverse outcomes, using CGM measures such as mean glucose levels (MEAN), Time in Range (TIR), Time Above Range (TAR), Time Below Range (TBR), the coefficient of variation (CV, a measure of variability of levels), and standard deviation (SD, another measure of variability). These were compared to the effectiveness of biomarkers in the blood and the traditional HbA1c.
Even for me these graphs are hard to read but the key takeaway is to look at the rows with an asterisk on the end as these are the measures which were significantly predictive. So, for preterm birth, for 12 weeks, CGM and one of the biomarkers fared well and for 24 weeks, CGM, a different biomarker, and HbA1c fared well.
Looking at predictors for a “big baby” (LGA), Neonatal ICU (NICU) admission, and Neonatal Hypoglycaemia (NH) we see CGM and HbA1c are the constant performers for prediction.
Looking at just Time in Range (TIR) and the HbA1c, we see, for early pregnancy a CGM offers good predictability and the opportunity for early intervention. Later in the pregnancy, HbA1c provides stronger predictability.
In conclusion, CGMs not only offer the ability to predict adverse outcomes early on in the pregnancy but their use can also improve them. Yet again we have compelling evidence that CGMs offer tremendous benefit to people with diabetes.
Should Women with Diabetes Take Metformin?
The final presentation I will talk about was a debate on the benefits and risks of using metformin during pregnancy. This was discussed between Professor Denice Feig who argued the “pro” case and Dr. Yariv Yogev who argued against. However, discussions in the question and answer session at the end showed both agreed on many of the key points with little debate between them.
Typically a “Type 2 drug”, metformin has many effects on the body but is broadly known as a drug which reduces insulin resistance. It is known to cross over the placenta into the baby but it is well established that it does not cause birth defects.
It is understandable that the issue of metformin use needs to be discussed/debated because international consensus on whether metformin or insulin should be used as a first line treatment is still mixed.
Professor Feig presented a meta-analysis study showing the benefit of metformin over insulin although it was clear in the discussion that many women with diabetes often used insulin as well as metformin to help control blood glucose levels.
Factors of potential concern were a lower gestational age i.e. babies were born slightly earlier and a slightly higher incidence of “small babies” or what is referred to as SGA (Small for Gestational Age).
Professor Feig presented other studies comparing metformin to insulin with similar results finding:
Metformin helped with glucose levels after meals
There were less cases of hypoglycaemia with metformin
Metformin reduced the amount of weight gain in mothers and the need for c-sections
For women with Type 2 we, again, saw similar results and the potential for a “small baby”.
There was discussion on the long term effects on the baby of exposure to metformin but both presenters agreed the results are mixed and no strong conclusions can yet be drawn that there are detrimental effects.
Dr. Yogev presented a great table showing how metformin compared to a placebo for outcomes (a p-value of 0.05 or less indicates statistical significance) indicating:
Lower birthweights with metformin
Reduction in the rate of extremely large babies
Increase in small babies
Dr. Yogev did point out that in his own studies he could not confirm the increased risk of small babies as a result of using metformin. Both agreed that where there was a risk of babies being born small, metformin may not be advisable e.g. in the case of twins. Professor Feig also made the point that, if a pregnant woman with diabetes was taking metformin and there was indications that her baby was undersized, metformin could be stopped during pregnancy to minimise any problems.
TL;DR
Health risks to the baby for women with diabetes are:
Higher risk of stillbirth and neonatal death (death in the first few weeks of birth) compared to the general population
Higher risk of congenital defects
These risks can be reduced through taking folic acid both before and during pregnancy and reducing HbA1c. However many factors affect the ability to reduce HbA1c such as age, social disadvantage, time since diagnosis, and weight. While difficult, HbA1c is a strong predictor of outcomes at all stages of pregnancy so any intervention which can help reduce HbA1c is of significant interest.
One intervention which shows promise are CGMs whose measures are predictive of outcomes (especially in early pregnancy while HbA1c is good at predicting outcomes later in pregnancy) and, therefore CGMs can be used to advise early intervention. It was also shown that the use of CGMs for women of all Types saw a reduction in adverse outcome risk. For pregnant women using a CGM while accuracy was good wherever the sensor was placed, placement on the arm showed the most accurate results.
A second intervention which shows promise is metformin, a drug which lowers insulin resistance. While reducing risk across most measures, there was potentially an increased risk in a smaller baby for gestational age (SGA). It was agreed that, in most cases, the risk could be managed through active monitoring of the pregnancy (and taking the pregnant woman off metformin if needed) but for cases where there was an existing known risk of SGA (twin birth, for example) metformin would not be advised.
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.
The Practical Diabetic 