Keeping A Sensor On For Weeks

I often see posts asking how to keep continuous and flash glucose sensors on for more than a week. As I pay full retail price for my CGM (it is not easy to get a CGM subsidy in Australia), I try to get every last bit of performance out of them before throwing them away.

My record so far for a Dexcom G5 was seven weeks and I gave up at that point because the sensor wound had healed enough that it was no longer registering the spikes; the line just slowly rose and fell in a dampened response to the glucose levels.

These days I change the sensor in the first weekend of the month, getting around four weeks per sensor.

Here is how I do it.

Skin Tac

I bought a bottle of this on eBay but you can also buy wipes with the same name that do the job. The very first thing I do is apply it, using the sponge applicator, to the area where the sensor is going to sit.

To wipe off any excess, simply use Methylated Spirits (Denatured Alcohol).

Prepare the Sensor, Rocktape and Opsite

While the Skin Tac dries and gets sticky, I prepare the other components. Firstly, I take sensor out of its packet ready for application, then I prepare the RockTape.


I use the Rocktape to keep the sensor’s sticky material in place. The white gauze that comes with the Dexcom is good for about one week so the Skin Tac and Rocktape help extend this.

I cut a little rectangle out of the Rocktape for the transmitter to fit through and keep the rectangle for later.

I also cut off the corners of the main piece of Rocktape and this stops it from peeling away from the skin as readily.

With the Skin Tac now nice and sticky, I apply the sensor, attach the transmitter, and start the soak-in period on the receiving app.

If the transmitter looks a little unusual, I use a modified G5 transmitter with a rechargeable battery attached to replace the embedded batteries. It is a little experimental but it has saved me a fortune in new transmitters.

Next I put on the RockTape on top of the gauze.

Opsite Flexifix

This is a transparent, breathable covering which sits on the skin. There are cheaper alternatives in the market though so do shop around. The idea is to cover the sensor and Rocktape completely to help prevent the sensor getting knocked out by leaning or bumping into things.

The rectangle of Rocktape we reserved sits in the middle of the Opsite to stop the Opsite getting stuck to the transmitter. The adhesive attaches very strongly to the resin on the transmitter making it difficult to remove when we want to change the dressing.

We now apply the Opsite to the sensor, keeping the backing on the Rocktape rectangle and we have a secure sensor with its own Rocktape camouflage. With the backing on the Rocktape still in place, the dressing comes away easily when we want to replace it.


Once a week I check for peeling and, if it is coming away, I reapply the Rocktape and Opsite, removing the old dressing by peeling sidways to or away from the transmitter to minimize the risk of dislodging.

Hacking the Amazon Echo Spot for Blood Sugar

In my last blog I showed how you can link a Dexcom CGM to an Amazon Echo via the SugarMate Skill. This time I have taken it a little further to see what can be done with the Echo Spot. The Echo Spot is like the Echo (a voice-enabled speaker) only it also has a screen. This means if we open up the SugarMate skill, we not only get told our blood sugar, but we also get to see the graph of latest results.

SugarMate Skill on the Echo Spot

Unfortunately, in the middle of the night, when you are sleepy and potentially have low blood sugar, remembering to say “Alexa, ask SugarMate for my latest reading” is a little too much. I was hoping to create a custom voice command but this proved impossible at this point. While there are custom ‘Routines’, these cannot be linked to skills and neither could Amazon Blueprints.

I did find a way to invoke the Skill without speaking though through “Tap to Alexa”. Tap to Alexa is activated through the Accessibility areas in Settings and is then configured through the Home screen by swiping until you get to Tap to Alexa and touching ‘Manage’.

Once there you can pick a command and link it to a named icon. It took me a while to get this set up right because it turns out Alexa has big problems with the word ‘SugarMate’ (one word). It works fine with ‘Sugar Mate’ (two words) though. So, by linking the command “Open Sugar Mate and get latest reading” to an icon, I could invoke SugarMate with nothing more than a swipe left and a tap.

Swiping Left and Tapping with the Echo Spot.

Linking xDrip+ to Amazon Alexa

I managed to link my Dexcom to Amazon Alexa today via xDrip+ so I thought I would step through how it works so others can do the same. As usual, a summary is at the end in the tl;dr section.

Why Would You Do This?

I can think of a few reasons why you might want to set this up:

  • Anyone in my home can now ask Alexa what my blood glucose level (BGL) is, regardless of where I am.
  • If I have a Spot or Dot by my bed I can ask Alexa my BGL without having to move anything more than my mouth
  • If looking at screens is problematic, this provides an alternative way to know your levels

My Setup

As if often the case with diabetic hacks, there are a few links in the chain. Let us go through the applications and devices.

  • The Dexcom G5 (although any CGM/Flash Monitor will work which is compatible with xDrip+). The Dexcom G5 has a Bluetooth connection to my Android phone running:
  • xDrip+: An Android app which displays the Dexcom results and uploads them to the:
  • Dexcom Share Server: An online repository of your BGLs. This is accessed by:
  • SugarMate: An online report generation app, similar to which has a Skill in:
  • Amazon Alexa: Invoke the SugarMate app and you have your BGL and when it was last checked

Dexcom G5

Not much to do here. Attach it to your arm.

My slightly hacked Dexcom G5


Install the app, go to the Settings and connect your Dexcom.

You will know if it is working because you will get a pretty graph of results when they come in.

Dexcom Share Server

To get the data from xDrip+ to the Dexcom Share Server we first need an account on the Dexcom site.

Once we have this we go to the xDrip+ Cloud Upload Settings, choose Dexcom Share Server Upload and give it the Dexcom account details.

As I am in Australia I am not using the US servers. If you are in the USA, your setting may be different. Also, as I am not using a Dexcom Receiver, I left the 10 Character Serial Number blank.

Amazon Alexa

I will work backwards from here (it just makes life a little easier). Firstly, enable the SugarMate skill through the Alexa app on your phone. This will give you the option of signing up for SugarMate and it will also give you an email address to add as a follower.

Once signed up and linked to Dexcom, go back to xDrip+ and add the email address as a Follower (the other name fields do not matter so make them something friendly for you).

That is it. With all that in place you can simply say “Alexa, ask Sugarmate for my latest reading” and it will tell you your reading and when it was last checked.

Using Routines

I was hoping I could use a Routine to modify the invocation command to something more ‘middle of the night’ friendly such as “Alexa, what is my BGL?” but at this stage it is not possible to invoke a Skill from a Routine.


Using xDrip+ with your preferred CGM/Flash Monitor, uploading to the Dexcon Share Servers, linking it to SugarMate and enabling the SugarMate Alexa skill, anyone in your household can ask Alexa what your blood glucose is.

This is useful in the middle of the night or if a loved one is at home and concerned. It is also useful if sight impairment is an issue.

Unfortunately I have found no way to simply the invocation phrase “Alexa, ask Sugarmate for my latest reading” but if I do I will add it to the article.

What Do Those Blood Tests Mean?

Diabetics get a lot of blood tests done and sometimes we should ask for others. Here they are broken down so you know what you are getting done and what you should ask for.

Summary at the end for those who find the article tl;dr.

‘Sugariness’ And Insulin Measures


Practically every diabetic knows their HbA1c (Hemoglobin A1c). This is a measure of the number of hemoglobin proteins in the blood with glucose attached. This gives an indication of how sugary a person’s blood has been for the last three months.

Why three months? Hemoglobin is part of your blood’s red blood cells. In a healthy human, red blood cells survive for around three months in the blood before dying.

This has a few implications. Firstly, if you have a disease which affects the life of your red blood cells, such as anemia, this will throw off your HbA1c measure, shortening the time over which the HbA1c is a representative average. Also, the measure is not a linear average; the result is biased to the more recent ‘sugariness’ because not every red blood cell lives for exactly three months. Not all of those ‘born’ three months ago will be around but most of the one born a month ago will.

It should be noted that there is around a 10% relative error in this test so if you have, say, an HbA1c of 7% and it moves on your next test by less than 0.7%, this could be nothing more than measurement error.

Finally, while a lot of emphasis is put on the HbA1c, it is only a number to indicate your average blood glucose level (BGL); it says nothing of the fluctuations. Some doctors will get nervous at lower HbA1c results because they have no visibility of the fluctuations. If you have excellent blood glucose control do not be afraid of lower HbA1c results.


When beta cells produce insulin they actually produce a thing called proinsulin which is two halves of the insulin molecule and a ‘connecting peptide’ (c-peptide) which joins them. Through the magic of biology this eventually transforms into insulin and a residual c-peptide molecule.

By measuring the amount of c-peptide in the blood we can get an indication of how much insulin the pancreas is producing (injected insulin is not in the form of proinsulin so there is no c-peptide residue).

A typical Type 2 will have a high c-peptide reading because their pancreas is trying to overcome their insulin resistance. A typical Type 1 will have a low c-peptide because the immune system has destroyed their beta cells and with it the ability to produce proinsulin. I say typical because for a LADA like me with insulin resistance, my c-peptide is normal/high even though I am Type 1.

Fasting Insulin

This measures the level of insulin in the blood for a fasting individual. Unlike c-peptide this cannot distinguish between insulin made by the body and injected insulin.

Fasting Glucose

The blood sugar level when fasting. For an individual producing enough insulin to keep their liver in check, this should be normal.


The ‘Homeostatic Model Assessment of Insulin Resistance’ (HOMA-IR) and the ‘Homeostasis Model Assessment of β-Cell Function’ (HOMA-β) are mathematical formulae using the blood’s (fasting) insulin and glucose levels to give an indication of the individual’s insulin resistance and beta cell function.

In other words, for someone not using insulin, their fasting insulin and glucose results can be used to determine how much insulin resistance they have and how much beta cell function they still have.

Vitamin D

Linked to insulin sensitivity, this may be useful to see if you are low (many of us office workers are).

Vitamin B12/Active B12

If you are taking Metformin/Diabex/Glucophage (different names for the same thing), you should check your B12 levels as Metformin can affect the body’s ability of absorb vitamin B12 from food. The difference between ‘B12’ and ‘Active B12’ is that, while different forms of B12 are circulating in the blood only the ‘active’ form can be used by cells in the body.

Autoantibodies Against Islet Cells (ICA), GAD, IA2, ZnT8, and Insulin

This is the definitive test for determining if someone is a Type 1 diabetic as it proves the immune system is attacking the body’s insulin production machinery.

If this test is positive, you are Type 1, by definition. However, there are people with all the hallmarks of Type 1 diabetes who do not get a positive result on autoantibody tests. Possible reasons for this include:

  • The person has had Type 1 diabetes for so long that there are no longer any beta cells left to provoke an immune response
  • Their Type 1 diabetes is caused by an as yet unknown autoantibody

Whether these ‘idiopathic’ Type 1s should be classified as Type 1, given the lack of autoimmunity evidence, is a matter of debate but, from a treatment perspective, it makes sense to align them to ‘classic’ Type 1s.

Body Mass Index and Waist Measurement

While not blood tests, the Body Mass Index (BMI) and a person’s waist measurement give a general indication of obesity. Obesity is linked to insulin resistance so, in an ideal world, diabetics of any Type would stay within a healthy weight range.

Oral Glucose Tolerance Test (OGTT)

Although I never had one of these myself (presenting with mild DKA at diagnosis was enough to establish I had diabetes), it is something often used to determine if a person has diabetes.

The test is relatively simple: the patient, who has fasted, is given a fixed measure of glucose syrup and blood is taken at the one, two, and maybe the three hour mark to measure the patient’s glucose response. If the patient cannot bring the blood glucose levels down fast enough and they go too high, the patient is diabetic.

Heart and Kidney Disease

Diabetics, due to damage from high BGLs, are prone to kidney disease and have a higher rate of heart disease, compared to the general population

Blood Pressure

Not a blood test, but the test the doctor does with the arm band and an air pump. A high blood pressure can be a risk factor for kidney and heart disease.

Albumin/Creatinine Ratio

This is a urine test and, for healthy functioning kidneys, there should be little to no albumin in the urine. It is measured as a ratio because creatinine is generated at a reasonably constant rate in the body so, if creatinine fluctuates in urine, this is likely due to relative levels of hydration in the body. So, by measuring the ratio, we get a stable indicator of albumin in the urine, independent of hydration levels.

Cholesterol (LDL/HDL/Triglycerides)

The prevailing thinking in conventional medicine is that the different types of cholesterol play a role in a person’s risk of heart disease. A metastudy (review/compilation of multiple actual studies) in 2016 found the evidence for this was not strong. I am not going to settle this debate in this blog article so discuss this with your health care team and do your own research if it is important to you.

For myself, I eat a lowish carbohydrate diet which means I have moved to eating more proteins and fats. My thinking is that, even if there is an increased risk of long term heart disease, this is outweighed by my short term desire to preserve my beta cells and remain insulin free for as long as I can, while keeping my BGLs in a healthy range.

Assuming cholesterol measures are relevant to a person’s heart health, here are the measures on interest:

  • Total cholesterol: ideally low
  • LDL: ideally low
  • HDL: ideally high
  • Triglycerides: ideally low
  • Cholesterol/HDL ratio: ideally low i.e. you want relatively low cholesterol or high HDL with the absolute amount being less important (useful for diets higher in fat)
  • LDL/HDL ratio: ideally low based on the above and again, talks at relative levels, rather than absolute levels


High levels of sodium can indicate kidney dysfunction.


This is a measure of how acidic your blood is (low levels suggest more acidic blood). Again, this can be an indicator of kidney health but, be warned, if you are engaging in a low carbohydrate diet and producing ketones, these are acidic and may throw off the test. I have seen this in my test results on occasion.

The idea that one blood test can be the result of one of many causes speaks to the need to get multiple tests done to confirm something like kidney disease. While my blood may sometimes be slightly acidic, my albumin/creatinine ratio is always within range, confirming it is my keto-like diet that is the cause and not organ damage.


Like the bicarbonate test, urea can be indicative of a number of things. Most importantly it can indicate kidney damage or heart failure. Urea in the blood is a result of protein breakdown so, again, if you are engaging in a low carbohydrate diet and eating more protein, a higher urea level may be the cause. It is no coincidence that on those blood tests where my bicarbonate was low, my urea was also high and was indicative of nothing more than me being a little more keto than usual.

Liver Disease

The other organ that gets a battering from diabetes is the liver. We have a raft of tests available to us to ensure our liver is doing its job and keeping us healthy.

Gamma Glutamyltransferase (GGT)/ Lactate Dehydrogenase (LD, LDH)/ Aspartate Aminotransferase (AST)/ Alanine Transaminase (ALT)

These are enzymes found in the liver and usually only in small amounts in the blood. An elevated level of them in the blood can indicate kidney damage. It can also indicate a bumpy ride on a motorcycle leading up to the test so always regard blood test results with caution until confirmation tests have been conducted.

Total Protein

This is related to the Albumin/Creatinine test as Albumin is a protein. Abnormal total protein levels in the blood can indicate kidney damage but can also indicate liver disease. A high protein diet has no effect on protein in the blood.


Total Protein = Albumin + Globulin so, again this is a protein test where abnormal results can indicate kidney or liver disease, among other things.


Another protein test which can test for severe liver disorders in non-pregnant people.

Infection Markers

White Cell Count/ Lymphocytes/ Eosinophils/ Monocytes

Lymphocytes, Eosinophils, and Monocytes are all types of white blood cells. All of these can be tested to get an idea of infections, allergies, and other disorders which may be affecting the body.

While I occasionally have elevated levels of these, it generally settles down by the time of my next quarterly/biannual blood test. If it did not, it could be indicative of an undiagnosed prevailing condition e.g. cancer or infection and would warrant further investigation.


Here is the list of common blood (and other) tests done for diabetics and their meaning.

  • ‘Sugariness’ and Insulin Measures
    • HbA1c: An average of your last three months of blood sugars
    • C-Peptide: A measure of how much insulin your body is still producing
    • Fasting Insulin: How much insulin is in your blood to keep your liver in check
    • Fasting Glucose: How sugary you are without food
    • HOMA-IR/HOMA-β: Mathematical formulae using the fasting insulin and glucose used to determine insulin resistance levels and beta cell function
    • Vitamin D: Low levels can contribute to insulin resistance
    • Vitamin B12/Active B12: B12 absorption can be hindered by diabetic medications such as metformin
    • Autoantibodies Against Islet Cells (ICA), GAD, IA2, ZnT8, and Insulin: Tests whether diabetes is caused by an autoimmune response and is therefore Type 1 diabetes
    • Body Mass Index and Waist Measurement: Body measurement tests to give an indication of obesity and potential insulin resistance
    • Oral Glucose Tolerance Test (OGTT): A test involving the drinking of glucose syrup to assess whether a person is a diabetic
  • Heart and Kidney Disease
    • Blood Pressure: The test with the armband and pump. This can indicate an increased risk of heart and kidney disease
    • Albumin/Creatinine Ratio: A urine test for kidney health
    • Cholesterol (LDL/HDL/Triglycerides): Measures of fatty acids and fatty acid transporters in the blood. Abnormal levels are traditionally considered a risk factor for heart disease
    • Sodium: High levels can indicate kidney disease
    • Bicarbonate: Low levels can indicate kidney disease but can also result from a ketogenic diet
    • Urea: Used as an indicator for heart or kidney disease but can also be indicative of a high protein diet
  • Liver Disease
    • Gamma Glutamyltransferase (GGT)/ Lactate Dehydrogenase (LD, LDH)/ Aspartate Aminotransferase (AST)/ Alanine Transaminase (ALT): Liver enzymes not usually found in the blood which can indicate liver damage
    • Total Protein: Abnormal levels can indicate liver or kidney damage. Not affected by dietary protein intake
    • Globulin: Abnormal levels can indicate liver or kidney disease
    • Alpha-Fetoprotein: Can indicate severe liver damage/disease
  • Infection Markers
    • White Cell Count/ Lymphocytes/ Eosinophils/ Monocytes: White cell tests which can indicate infection, allergy or disease.

You Are A Newly Diagnosed Type 1! What Next?

Welcome to the club no one wants to join. If you are reading this it is likely you, or someone close to you, has just been diagnosed as having Type 1 diabetes. This is the guide I would have loved when I first got diagnosed. Do not have the time to read? Go to tl;dr.

Everything Is Going To Be OK

First of all, while it may feel overwhelming, everything is going to be fine. There are Type 1 diabetics in most walks of life from elite athletes to pilots. Around 1% of people in the UK, USA, and Australia (1 in 100) have Type 1 diabetes. That is one in three or four school classrooms. Type 1 diabetes affects both genders roughly equally, people of all ages, and people from all walks of life. You are not alone.

You may not know someone with Type 1 but they are out there and dealing with it every day. For me, it was 11 months from diagnosis before I met another Type 1 diabetic in the flesh. There were plenty of resources along the way to help me though.

Quick Reads

Two excellent online documents my endocrinologist pointed me to was the Australia JDRF Guides, and the Australian Type 1 diabetes Starter Kit.

In the USA there is the US JDRF, and in Canada there is Diabetes Canada. If you live somewhere else Google: ‘diabetes “type 1” <your country>’ for local resources.

Longer Reads

There are some really great resources for Type 1s in book form, written by Type 1 diabetics. Some of the ones I rate or which other Type 1s I know have rated are:

  • Dr Bernstein’s Diabetes Solution: Even if you do not subscribe to Dr Bernstein’s very strict low carbohydrate diet, the book is full of information about diabetes and tips for managing it.
  • Think Like a Pancreas: Great advice on how to manage diabetes with insulin as well as covering the essentials of what diabetes is.
  • Bright Spots and Landmines: This is a more general guide for Type 1s and Type 2s. I have not read it, I hear good things.
  • Sugar Surfing: While books such as Dr Bernstein focus on the more traditional basal + mealtime bolus insulin regimen, Sugar Surfing incorporates the use of a continuous glucose monitor (CGM) to do regular micro-adjustments of insulin. The people I know who do multiple daily injections (MDI), all rate this book strongly as a guide for keeping blood sugars within range

Online Communities

By far it was the online communities that helped me the most in the first 11 months. Practically every form of social media has some kind of diabetes group in it. While I do not ask a lot of questions on social media, it is great to listen to the questions and answers of others. Ones which I found (and continue to find) useful are:

  • Facebook: So many diabetes communities here; some friendlier than others. Embrace the ones which work for you
  • Twitter: Around the world are Twitter chats for diabetics. Basically, each week, diabetics gather to converse on a topic of the week. The format is a series of questions, thrown out to the group and people answer with the relevant hashtag. Ones I have participated in are:
    • #OzDOC: The Australian Diabetic Online Community, this group is, sadly, all but wound up.
    • #ADEAChat: A gathering of the Australian Diabetes Educators Association but diabetics are also welcome. The weekly chat is at 7:30pm AEST on Tuesdays
    • #DSMA: The US-based Diabetes Social Media Advocacy meet at 9:00pm EST on Wednesdays
    • #GBDOC: The UK-based chat which runs weekly at 9:00pm UTC on Wednesdays
  • Reddit: A relatively new medium for me, Reddit has two Type 1 channels and the karma system ensures people are, mostly, on their best behavior.
  • YouTube: Arguably the best diabetes resource on YouTube is Dr Bernstein’s YouTube channel. If his book is too expensive or you want to try before you buy, watch his hundred or so free videos.

A Good Health Care Team

At diagnosis it surprised me to learn it would take a team to help me manage diabetes but it is absolutely true. The best advice I can give is do not accept anyone into your health care team you are not comfortable with. You are paying good money for their expertise and service but this does not give them the right to make you feel bad about yourself. Diabetes is stressful enough without a health care professional exacerbating the problem. Get a good health care team and it will make managing diabetes so much easier. People you have on the team might include:

  • An Endocrinologist (endo) for specific disease-related advice
  • A Diabetes Educator to give you more practical day-to-day advice for managing the disease
  • A General Practitioner (GP) for general medical advice (and generally cheaper than the endo)
  • A Podiatrist for regular feet checks (diabetes-related damage often reveals itself in the feet)
  • An Optometrist/Ophthalmologist for regular eye checks (diabetes-related eye damage can often be prevented through an eye check and early intervention)
  • A Nutritionist to assist, if required, with food and nutritional advice. Try to make it one who specializes in Type 1 diabetics otherwise you will likely be told advice which may be useful for muggles (non-diabetic folk) but of limited value to someone who cannot process carbohydrates well.
  • An Audiologist for regular hearing exams (or benchmark yourself with an online test list like this one and get the specialists involved when there is a measurable change)
  • A Dentist for regular teeth checks (a diabetic’s sugary nature makes their teeth more susceptible to problems).
  • A Cardiologist for regular heart health checks (diabetics have a higher risk of heart problems than muggles)
  • An Exercise Physiologist if you are looking to get into shape to help manage the disease

Get Educated

With the internet you have the ability to go into as much detail as you like on any topic you desire. You are the best advocate for your health and well-being so be the strongest advocate you can be.

Topics worth researching include:

  • Food and nutrition. Understanding which foods have low carbohydrate levels, which foods are low GI (glycemic index), and how you can ‘hack’ the GI of foods can be very beneficial in managing blood glucose levels
  • What those blood tests actually mean (and do not be afraid to suggest additional tests if you think they will help inform your management. In my experience endos and doctors are happy to add other measures to their list of blood tests if you ask)
  • What do your medications do and how to avoid the side effects e.g. taking Metformin in the middle of my meal helps me to avoid embarrassing side effects
  • How does diabetes work. Understanding how Type 1 works means you can effectively assess the relevancy of information you come across. It might be information useful exclusively for Type 2s or it could be complete nonsense. With a good knowledge of Type 1, you will be able to discern the difference.
  • What is the latest medical research? An excellent source of information is NCBI which contains a vast repository of the latest medical research. I try to review this at least once a month for new findings to help inform my management. For example it was through NCBI that I found the growing evidence that DPP-4 inhibitors help preserve beta cell function in newly diagnosed Type 1s. With this evidence I then convinced my endo to prescribe me saxagliptin to help extend my honeymoon

Another way to get educated is through courses set up by diabetes groups in your local area. Often these are free and provide a great foundation for the newly diagnosed. Your endo or Diabetes Educator should be able to point you in the right direction.

If you are venturing onto the internet for information, you will need to be discerning about the quality of the sites you visit. As mentioned, NCBI is an excellent source of information but there are plenty of junk sites out there promoting their own snake oil products and feeding fearful diabetics a lot of nonsense.

Similarly, do not take medical advice from strangers online, me included. Some self-important bloggers and Facebook pundits take it upon themselves to insist, for example, that every newly diagnosed Type 1 should go onto insulin as soon as they are diagnosed. While this may be true for many Type 1 diabetics, it is far from a blanket rule (I am a prime example of this as I am still in insulin-free honeymoon as I write this, two and a half years after diagnosis, with well-managed blood glucose levels). If someone online is telling you to start or stop a medication, especially one as serious as insulin, walk away. This is a decision for you and your health team with careful consideration of your specific symptoms and medical history.

Get To Know Your Blood Better

What I mean by this is start keeping track of your blood glucose levels. I initially started with a glucometer (the machine with the strips). Using an app like MySugr I was able to record my blood glucose readings before, during, and after meals, and understand which foods were ‘friendlier’ than others. This allowed me to make smarter food choices and bring my HbA1c under control. These days I use a CGM which provides a wealth of information about the things that affect my sugariness.


While Type 1 diabetes may seem daunting and overwhelming when first diagnosed, it is manageable and the proof are the millions of Type 1 diabetics out in the wild doing it every day.

By educating yourself with quality information and getting involved with online and offline diabetes groups, you can get through this and thrive as a Type 1.

Online Resouces

PDFs and Pages:

Online communities:

  • Facebook groups
  • Twitter chats:
    • #ADEAChat: 7:30pm AEST on Tuesdays
    • #DSMA: 9:00pm EST on Wednesdays
    • #GBDOC: 9:00pm UTC on Wednesdays
  • Reddit Type 1 channels
  • Dr Bernstein’s YouTube channel

Medical Research:

Offline Resources

Books written by Type 1 diabetics:

A good health care team:

  • An Endocrinologist (endo)
  • A Diabetes Educator
  • A General Practitioner (GP)
  • A Podiatrist
  • An Optometrist/Ophthalmologist
  • A Nutritionist
  • An Audiologist (or an online test list like this one until there is a measurable change)
  • A Dentist
  • A Cardiologist
  • An Exercise Physiologist

Online courses run by local diabetes organisations.

A glucometer and an app like MySugr, or a CGM to help you understand how your body reacts to different foods.

You Do Not Need To Eat Carbohydrates!

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)


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.


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?

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:

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.


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.


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:

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


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

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
First degree relative0+100+1
Insulin resistance0+1+100

(*) 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
First degree relative0+100+1
Insulin resistance0+1+100

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.


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

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 (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?


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.


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.