Looping/Automated Insulin Delivery: Does it Work? Commercial vs Open Source, Affordability, and How Professionals Can Support the Lived Experience

I recently presented at the Australian Diabetes Educators Association NSW Branch Conference and wrote an article for the Australian Diabetes Educator journal on looping and how diabetes educators can support people with type 1 diabetes (PWDs) using looping systems, both open source and commercial. This is not a verbatim reproduction of the presentation or the ADEA article but does cover some of the key points which may be useful to PWDs and Health Care Professionals (HCPs). While the focus of the article is the Australian experience, there is value for international audiences as well.

What is Looping?

There are many terms for technologies allowing a Continuous Glucose Monitor (CGM) and an insulin pump to make blood glucose management decisions without the intervention of the PWD. Originally, when such technologies were ‘hacked’ together on the internet, it was referred to as looping. Now, with both open source (internet) and commercial versions available, and recognition in the academic literature, the more formal term Automated Insulin Delivery systems (AIDs) is used. For the rest of the article, this is the term I will use. Similarly, for simplicity, open source/internet systems I will refer to as ‘Open Source’ and commercial systems as ‘Commercial’. There are nuances which are lost in this broad classification but, for the purposes of this article, they are not overly important.

For a brief history of how the internet made the first AID, you can go to my other blog. These days, there are a variety of options for PWDs. In Australia, there are now four main Open Source systems: 

For Commercial systems, at the time of writing, Australia has three commercial looping systems available: 

  • Medtronic 780G + Guardian 4 Sensor 
  • Tandem t:slim X2 with Control IQ + Dexcom G6 
  • YpsoPump with CamAPS FX + Dexcom G6 

Open Source vs Commercial Systems

These days, I use a Commercial system (Ypsopump with CamAPS FX + Dexcom G6) but my first loop was Android APS using both the Libre 2 and Dexcom G6 CGMs and Omnipod pumps. Neither is better than the other but each system has their own features which are more or less appealing to each PWD.

Open Source Commercial 
Built by the wearer/user Commercially available software 
(Generally) The code which it is based on is available for review Proprietary i.e. the code is not available and how it works is often a trade secret
Very ‘tweakable’ Less flexibility/features 
Not formally approved by a government bodyApproved by a government body i.e. the Therapeutic Goods Administration

There is nothing illegal about using an Open Source AID. The lack of government approval means while they cannot be sold commercially, the law in Australia allows the personal use of unapproved medical technologies and devices. This means, while the software code is usually openly available, it is the PWD who must compile it (not as technically challenging as it sounds these days). The advantage of Open Source is that, because it does not have to go through formal approval processes every time a change is made, innovation comes faster with Open Source AIDs.

The advantage of a Commercial system is that it is largely ‘plug and play’. While PWDs need formal training on the use of the CGM and pump, the commercial software is often simpler to use and administer. Some consumers prefer to be hands-on with their technology while others prefer simplicity.

Do AIDs Work and What Are Their Limitations?

AIDs continue to improve but they do have their limitations. While it is possible for a PWD to modify their diet e.g. eat a Low Carb or Very Low Carb diet, and minimise their intervention with the AID, most PWDs will need to bolus for meals and take care during exercise. For tips on dealing with AIDs in exercise, refer to my exercise article.

My experience has been, being a LADA with some residual pancreatic function, I can skip a lot of bolusing and the AID is very good at keeping me in range. These days I bolus for very carby meals (say 45g or more) but do not need to declare/bolus the rest. Everyone’s experience will vary. One thing I never do are bolus corrections. If I do not declare, the AID keeps adding insulin to manage the carbs and automatically manages the ‘landing’, preventing a hypo. If I manually bolus too much, the AID will suspend basal insulin to ‘soak up’ the excess. No corrections means no stacking and while it can be tempting to bring my levels down quicker after a meal, I always try to let the AID do the work. Similarly, whatever my levels are when I go to bed I can, almost without fail, be assured I will wake up in range. As long as my pump has enough insulin and my CGM does not expire, I can be assured a good night’s sleep.

The other great thing about AIDs is they do not stop you from pulling other ‘levers’ in managing diabetes. If you want to eat a very low carb diet with an AID you can. I touch on this in my “Practical Diabetic Solution” article. In short, when the PWD is asleep or otherwise occupied, the AID takes care of glucose management, ensuring superior results compared to relying exclusively on the PWD to make all decisions 24-7.

A criticism sometimes made of AIDs, especially in the Commercial systems, are their high blood glucose targets (the Tandem, for example, does not allow for a target below 6.1mmol/L (110mg/dL)). The truth is not all AIDs are equal. Broadly speaking the Open Source systems allow for a more aggressive target than the Commercial systems but the system with the lowest possible target is the CamAPS system whose target can be made to go as low as 4.4mmol/L (80mg/dL) although I generally set mine to 5.5mmol/L (99mg/dL) as this is the average resting glucose of a person without diabetes.

To the question of how well these systems work, there is now a strong body of evidence that they do and, from a clinical perspective, outperform any other alternative. For example, here are the times in range for the Medtronic system across various regions of the world. As we can see, it is typical to be at least 70% in range (70-180mg/dL) with minimal lows. These results are consistent across the variety of AID systems and, as mentioned before, do not prevent even better results through the use of adjunct therapies such as medications and diet.

How Do People Decide on the Right System for Them?

There are four key factors to consider when choosing an AID:

  • Availability: Are the pump, CGM, phone and related consumables available? 
  • Accessibility: Are the pump, CGM, and phone usable by the individual? 
  • Adaptability: Can the AID system be extended, as desired? 
  • Affordability: Is the AID system affordable? 

In terms of affordability, Australia is unique in being ‘half-pregnant’ with their AID subsidies. For people with type 1 diabetes, CGMs are funded with a small co-payment by the PWD whereas pumps are effectively unfunded. To get an insulin pump, the PWD must either get private health insurance or pay the, say, $8,000 for the pump out of their own pocket. There is a petition urging the Australian government to change this inequity which I encourage you to sign.

For the other factors, considerations include:

  • More choice of glucose targets.: As mentioned, different systems have different target ranges which may be important to some 
  • Readability: For a user with vision impairment, a high-contrast screen or management via a mobile phone may be desirable. 
  • Connectivity to other devices: Being able to access functions via a watch or the internet may be useful. 
  • Form factor: Device size, whether it is tubed or tubeless, and whether it has an IP rating for water resistance can be key decision factors for some wearers

The available combinations are also important as it is likely a PWD is already using a specific CGM and may want to stay with that CGM as part of their AID system. In fact, there are limited combinations available for AIDs.

 Tandem t:slim X2 YpsoPump Omnipod Dash Medtronic 780G 
Dexcom G6 Android/iPhone (CGM only) Android via CamAPS Android/iPhone  
Medtronic Guardian    Samsung/iPhone (Monitor only) 
Abbott Libre 2   Android  

Above we can see the available Open Source and Commercial combinations in the Australian market for pumps and CGMs approved for use in Australia (Green = Commercial, Blue = Open Source). As we can see, for someone using a Libre 2, the only option available is an Open Source one. Similarly, while the next version of the Omnipod has an AID system (approved in Australia but not widely available), the main Omnipod version available in Australia, at the time of writing, does not with the gap being filled, again, with Open Source.

How HCPs Can Help?

There is understandably some nervousness with HCPS about supporting or recommending Open Source systems to PWDs. These are, almost by definition, unofficial/unapproved systems. On the other hand, to stay relevant to a PWDs care, they cannot remove themselves completely and let the internet and social media be a PWD’s only source of information. Thankfully, there is some guidance for HCPs out there.

Locally, guidance is limited. Diabetes Australia has a position statement on “People with type 1 diabetes and Do It Yourself (DIY) technology solutions” but it is over five years old, light on specific guidance and, arguably, out of date. In its statements around commercial systems it suggests “(In Australia) there is no approved product that is a fully closed-loop system”, and “there is currently no subsidy for the CGM component for adults over the age of 21 years”. Both statements are no longer correct.

Internationally, there are three published documents providing guidance to HCPs and applicable to the Australian context. These are:

These documents are comprehensive in their guidance and freely available to view and download at the above links. Their main points are: 

  • While there are legal complications in recommending Open Source systems, users still require support. Therefore, it makes sense for the HCP to learn about these systems to provide effective guidance. 
  • If the HCP is unable to learn and provide guidance, they should collaborate with individuals who can. 

Conclusions

AIDs provide a lot of value to PWDs and both Commercial and Open Source systems are valid options, depending on the PWD’s needs. While they have their limitations, in terms of bolusing and exercise, AIDs are proven to provide benefit in all global settings in terms of time in range and overnight management.

While it can be daunting for an HCP to provide guidance to PWDs using AIDs, especially if it is Open Source, it is important to provide a voice of reason when there can be a variety of information sources which are less informed or reliable. Thankfully, there are multiple peer-reviewed international guides for the HCP to provide precisely the support PWDs need.

Thoughts on the Australian Government’s Inquiry into Diabetes

This week, on the 3rd July, 2024, the Australian government released the 23 recommendations resulting from their Inquiry into Diabetes. This blog will review each recommendation and consider its impact on people living with diabetes, and how the Australian government manages diabetes in general. The blog is quite long, so if you want the short version, head on over to the tl;dr section.

Details of the Inquiry

The Inquiry kicked off back in 24 May, 2023 when the Honorable Mark Butler MP called for a committee to investigate and report on diabetes. The Terms of Reference for the inquiry were, according to the committee’s chair, Doctor Mike Freelander, “very broad” with a view to “get as much information as we can so we can get a plan for the future”. Reading the article, the motivation for the inquiry seemed to be the incidence of obesity and type 2 diabetes in Australia and coincided with the release of a study from Deakin University confirming an increase in the rate of type 2 diabetes in Australia.

This was not an inquiry targeted at type 1 diabetes, but at diabetes in general, with obesity and risk factors also being considered. This is reflected directly in the formal Terms of Reference for the inquiry:

“The Committee will investigate:

  • The causes of diabetes (type 1, type 2 and gestational) in Australia, including risk factors such as genetics, family history, age, physical inactivity, other medical conditions and medications used;
  • New evidence-based advances in the prevention, diagnosis and management of diabetes, in Australia and internationally;
  • The broader impacts of diabetes on Australia’s health system and economy;
  • Any interrelated health issues between diabetes and obesity in Australia, including the relationship between type 2 and gestational diabetes and obesity, the causes of obesity and the evidence-base in the prevention, diagnosis and management of obesity; and
  • The effectiveness of current Australian Government policies and programs to prevent, diagnose and manage diabetes.”

The problem I have with investigating the “interrelated health issues between diabetes and obesity” and “risk factors such as genetics, family history, age, physical inactivity…” is these do not apply to all diabetes types equally, and also apply to other diseases, such as breast cancer. As can also be seen in this last link, risk factors are often conflated with causation. Correlation is not the same as causation and, in the case of diabetes, leads to a lot of unnecessary blame and stigma (there are plenty of skinny type 2s, chubby type 1s, and muggles of both sizes, so broad correlations have limited application at the level of the individual, especially when a proven chain of causality has not been established.)

As it was a public inquiry, submissions and public hearings were part of the process giving a voice, to any interest group who felt the inquiry Terms of Reference related to them, for consideration. So, from the start, there was potential for recommendations which may address broad health issues in the Australian population but not necessarily address prevention of diabetes, treatment of diabetes, or improvements for those living with diabetes. As you will see below, this lack of focus in the Terms of Reference led to a lack of focus in the Recommendations with some having tenuous links to diabetes, at best.

Let us review the recommendations and consider their implications.

The 23 Recommendations

Recommendation 1: The Committee recommends that the Australian Government undertakes a comprehensive economic analysis of the direct and indirect cost of all forms of diabetes mellitus in Australia.

This is an excellent idea. Approval for subsidised medications, equipment, and treatments rely on favourable economic consequences. Approval may require a measure of economic return e.g. spend $1 and return $2 worth of productivity within a specific time period, or an estimation of the cost for ‘Quality-Adjusted Life Years’ (QALYs.) In the case of the NDSS subsidy for CGMs, the cost came in at around $35,000 per QALY, below the unofficial approval threshold of $50,000 per QALY. Subsidies for things like Type 2 CGMs or Type 1 Loops will need to go through a similar exercise. Basically, accurate economic analysis will lower the barriers for smart decisions to be made.

Recommendation 2: The Committee recommends that the National Health and Medical Research Council expedites a review of the Australian Dietary Guidelines, and ensures that the revised guidelines include adequate information for Australians living with diabetes.

Here we see the broader terms of the inquiry coming into play. I do not see a lot coming out of this other than education programmes for ‘guides to healthy eating’. I do not believe information access is the problem. I think we all know we need to move more and eat less, preferably eating food with lower energy density. I can almost guarantee any “adequate information for Australians living with diabetes” will concentrate on type 2 diabetes and its risk factors and largely ignore any other type whose needs are different (people with type 1 are less concerned with glycaemic index/load and more concerned with total carbohydrate count, for example.) The cynic in me has no expectation this level of nuance will be captured in any revisions and expect the guidelines will not go much deeper than “fat bad, protein good, but remember to eat some carbs.”

Recommendation 3: The Committee recommends that the Australian Government implements food labelling reforms targeting added sugar to allow consumers to clearly identify the content of added sugar from front-of-pack labelling. This food labelling initiative should be separate from the information regarding added sugar potentially being included in the Nutrition Information Panel.

This one has little to do with people living with diabetes, whose concerns are carbohydrates in general, rather than just added sugar. I see this adding no value to me personally and see it causing a lot of confusion for people with type 1 diabetes. When bolusing, the need of a person using insulin is for clear carbohydrate labelling. This should not be sacrificed for ‘added sugar’ warnings.

The other concern I have is this recommendation will be seen as ‘proof’ that eating sugar causes diabetes. The causes of diabetes types 1 and 2 are unknown i.e. the reason the immune system starts attacking the pancreas in type 1 is still not understood. Even the proof that sugar causes obesity is limited so, given the Terms of Reference, I think sugar was over-represented in this inquiry.

Recommendation 4: The Committee recommends that the Australian Government implements a levy on sugar-sweetened beverages, such that the price is modelled on international best practice and the anticipated improvement of health outcomes. The levy should be graduated according to the sugar content.

Sugar levies in other countries have shown a decrease in sugar consumption and a slowing of obesity rates in children but that is all the evidence shows so far. While reductions in rates of type 2 diabetes are predicted, using the risk correlations, there has not been enough time to confirm the prediction. I am not against the idea of a sugar tax (my secret hope being it will increase the variety of sugar-free drinks on the supermarket shelves), I am simply uncertain of its place in this inquiry. The hypothesis that sugar consumption leads to weight gain which may lead to an increased rate of obesity which may lead to an increase in the rate of type 2 diabetes seems tenuous to me in its relevance for an inquiry into diabetes of all types.

Recommendation 5: The Committee recommends that the Australian Government considers regulating the marketing and advertising of unhealthy food to children, and that this regulation should:

  • Focus on children defined as those aged 16 and under
  • Be applied to television, radio, gaming and online
  • Use definition of unhealthy food that has been independently developed.

More recommendations relating to general population health with little consideration for diabetes specifically. At least Recommendation 2 threw diabetes in at the end. Again, I am not against lumping in unhealthy food in with cigarettes and alcohol, in terms of advertising, I am simply struggling to link the recommendation to diabetes and the Terms of Reference. My guess is the link is unhealthy food may lead to obesity which increases the risk of type 2 diabetes but I am surprised there were not recommendations raised with a more direct link to diabetes prevention and management. For example, Teplizumab is proven to delay stage 3 type 1 diabetes by literally years so why has it been left out of the recommendations, but an unproven sugar tax included?

Recommendation 6: The Committee recommends that the Australian Government provides its response to the Australian Food Story: Feeding the Nation and Beyond report and considers a dedicated resource within the Department of Health and Aged Care to support access to healthy food to all Australian communities.

For the curious, the referenced report can be found here. The report is focussed on food production and food security but was not about links between food and health. In fact, the word ‘health’ gets mentioned only three times throughout the report’s recommendations. Once in reference to the National Health and Medical Research Council and, of the other two references, the first calls for a National Food Council to advise the government of food matters of which ‘Health and Nutrition’ was one of ten factors to be considered. The second reference called for changes to funding research on ‘food, health and nutrition.’

As we can see, there is a theme here that food, and specifically, sugar is considered the culprit to Australia’s health issues and incidence of diabetes (diabetes type be damned). There is no doubt that access to healthy food is a good thing for Australia in general but, for me, these food recommendations miss the mark for an inquiry on diabetes of all types.

Recommendation 7: The Committee recommends that the Australian Government, in consultation and cooperation with state and territory governments, develops a best practice framework to tackle the problem of obesogenic environments, including through better urban planning and the development of physical activity initiatives and supports efforts to increase access to regular exercise in schools and neighbourhoods as a matter of urgency.

This is a recommendation exclusively considering obesity. The Term of Reference for obesity was “Any interrelated health issues between diabetes and obesity in Australia, including the relationship between type 2 and gestational diabetes and obesity, the causes of obesity and the evidence-base in the prevention, diagnosis and management of obesity.” The recommendation implies that lowering the barriers to physical exercise in urban areas will impact obesity levels. It is a reasonable hypothesis but I could not find a lot of evidence to prove it, similar to the case with sugar leading to obesity and type 2 diabetes. So, again, I question the relevance of this recommendation to this inquiry.

The recommendation is another nice idea for general health improvement but, for tackling how Australia manages diabetes? For me, it seems a poor foundation to build on. Perhaps funding research to work out the causes, rather than acting on the correlations and hoping for the best, would be a better use of money. To mix metaphors, we want to smash the causal chain, not throw stuff at the wall and see what sticks.

Recommendation 8: The Committee recommends that the Australian Government explores the potential for effective national screening programs for all forms of diabetes, particularly Type 2 diabetes.

I appreciate I have not been completely glowing in my appraisal of the recommendations so far but this one strikes me as really ill-conceived. Screening for every type of diabetes except type 2 diabetes makes more sense. For type 1, for example, we recently saw the approval for a national screening program in Italy. So why not type 2? Because there is no simple test to definitively diagnose type 2 diabetes. For type 1 we can test for auto-antibodies (which appear years before symptoms) and for MODY we can conduct genetic testing but, for type 2, the test is the symptoms i.e. elevated blood sugars and their effects on the body. There is literally no test we can conduct on a baby to determine if they are going to get type 2 diabetes and even in adults, diagnosis is a series of tests, not some simple screener.

The best we could do would be to implement regular testing of HbA1c which tells us the person may have some form of diabetes but is certainly not definitive for type 2. An elevated HbA1c, in the absence of a diagnosis of diabetes, is referred to as Pre-Diabetes and it is estimated over 1/3 of the US adult population is pre-diabetic. That is a lot of noise to filter out to find the true type 2 diabetics.

The idea of screening for MODY and type 1 diabetes makes sense to me, assuming it is cost effective (see commentary of Recommendation 1). Screening for MODY makes sense to reduce the widespread misdiagnosis and resulting mistreatment, and screening for type 1 makes sense because immune interventions can delay the onset of symptoms for years. It is clear though, screening only makes sense if something is going to be done with a positive test. Unless medical interventions are part of the overall strategy, screening is useless.

Recommendation 9: The Committee recommends that the Australian Government implements a national public health campaign to increase public awareness of the early signs of all forms of diabetes mellitus.

By the early signs for all forms of diabetes, I assume they mean the “Four T’s” which indicate an insufficient amount of insulin in the blood. Certainly, prior to diagnosis, I had enough awareness of two of the T’s (Toilet and Thirst) to know I needed to see a doctor when I was permanently thirsty and peeing every 30 minutes. Given awareness could prevent DKA death in an undiagnosed type 1, I do have some sympathy for this recommendation, assuming it is cost effective.

Recommendation 10: The Committee recommends that the Australian Government funds the development of education-based obesity screening information and resources.

More obesity recommendations which, again, speak to the health of the general population, rather than at diabetes. As with the screening in Recommendation 8, it only makes sense if there is a resulting intervention strategy for those positively identified. While ‘resources’ suggests some level of funded intervention, it is a bit nebulous.

Recommendation 11: The Committee recommends that the Australian Government implements a national public health campaign to increase awareness of the importance of prevention, identification of early signs, and good management of all forms of diabetes mellitus.

This is similar or, at least, related to Recommendation 9 regarding early signs. Prevention is an interesting one. Again, we are predicating our actions off of correlations, given the causes of diabetes in many of its forms (including type 1 and 2) are unknown. If the cause is unknown, how can we prevent it and raise awareness on what is needed to prevent it? As alluded to earlier, the usual suspects for ‘prevention’ equally apply to other diseases as they do to diabetes.

“Good management”, I assume, means eating less and moving more. I doubt this will include, for example, a national public health campaign on the correct use of insulin or on the importance of a well-rounded health care team.

What this is really recommending is a public health campaign to improve the overall health of Australians.

Recommendation 12: The Committee recommends that equitable access to health care for people living with all forms of diabetes be improved through:

  • Access to longer appointments with a health care provider subsidised by the MBS
  • Access to case conferencing models of health care, especially in rural and remote areas
  • Access to telehealth services
  • Increase in the number of item numbers for allied health consultation for those with diabetes for diabetes educators and dieticians and other allied health providers
  • Access to diabetes educators, including in high-risk outer metropolitan, rural and remote communities.

Finally! A recommendation which actually considers diabetes specifically, rather than being about general population health and issues of sugar consumption, a lack of exercise, and obesity. We are about halfway through the recommendations and, by my reckoning, maybe three of the 12 recommendations are specifically targeted at diabetes, rather than general population health.

Longer appointments are a nice idea if there is something to talk about. I would personally like to see more research and effort being put into structuring the conversations with health care providers so they are more relevant to the person with diabetes (PWD) and deliver real value, rather than being a doctor taking twice as long to tell their client they need to use insulin properly, eat ‘healthier’ carbs, lose weight, and do more exercise. How about a session where the concerns of the PWD are discussed BEFORE the blood results? How about a discussion around the various technologies available and why they may or may not be relevant/desirable to the PWD? How about a discussion of the various medications available which may be of benefit? I am hoping to construct a framework for such a discussion applying corporate motivation theory but this takes time. You can read details of my idea here.

I had to look up “case conferencing” but, from what I can tell, it is health care professional speed dating. Basically, you round up a team of health care professionals (Endo, Dietician, Exercise Physiologist etc.) and have people meet with them as part of a single session. Given the lack of health care professionals in rural areas the organised corralling of them in one spot, and the recommendation for telehealth services make a lot of sense.

Assuming it is done with cultural consideration, I see this having a huge impact in rural aboriginal communities. Aboriginal people are four times more likely to have diabetes/pre-diabetes than their non-indigenous counterparts. Anything that can be done to lower the barriers to health care and education access for these disproportionately affected communities is a good thing.

Then we move on to diabetes educators, a topic of particular interest for me. Firstly, fixing the ‘item numbers’ for allied health professionals is a great idea. A key reason why I do not see my diabetes educator is Medicare and my private health insurance do not recognise the visits. My Diabetes Educator has a Provider Number but, for whatever reason, the visits fall between the cracks. My hope would be that this recommendation would fix that.

Access to diabetes educators (DEs) is a problem in Australia whether it is in urban or rural areas although other HCPs seem to cover the shortfall so that the health of PWDs does not suffer. The online forums constantly buzz with people craving access to a DE but they either do not have one in their area or the DEs are booked out. The pathway to becoming a DE is quite narrow in that you must have a health-related qualification (dietician, nurse etc.) before you can become accredited as a DE.

My personal belief is a person who has lived with diabetes for, say, ten years, could offer tremendous value to someone newly diagnosed but the prospect of studying for three years to obtain a health degree so they can then study to be a DE is a barrier too high for many. A solution might be for a sub-accreditation for non-HCPs where PWDs can assist the newly diagnosed in a structured manner. The pool of available talent would increase and, if managed properly, would not compromise the quality of service given.

Recommendation 13: The Committee recommends that the Australian Government reviews the limits for accessing juvenile mental health and diabetes services, with a view to enabling young people to continue receiving support for longer.

I am unsure which specific programs this relates to, but it sounds like there are specific programs where the recipients ‘age out’, similar to what used to happen with the CGM subsidies when it was limited to people with type 1 diabetes who were 21 years and under. I can see this being particularly important in the case of mental health services where suddenly cutting off the services because of a birthday could be disastrous. This being said, the supply of mental health professionals, such as psychiatrists, is very limited with many having waiting lists stretching for months.

It may also be alluding to the largely useless Insulin Pump Program which subsidises insulin pumps for people with type 1 diabetes under the age of 21. To date, the program has not had a significant impact so broadening the pool of potential recipients would be good.

Recommendation 14: The Committee recommends the Australian Government work with the state and territory governments to develop education tools and resources to support all staff across the health care system to improve understanding of diabetes, its different forms, the early signs and management. The Diabetes in Schools program should be funded to allow all schools to access it.

A high-level but reasonable recommendation. In fact, the NDSS already have the National Diabetes Nursing Education Framework which would go a long way to achieving this goal. The workbook associated to the program is an outstanding resource to give this baseline understanding.

I had to look up the Diabetes in Schools program but it sounds like a great initiative.

Recommendation 15: The Committee recommends that subsidised access to Continuous Glucose Monitors (CGMs) be further expanded. In the first instance, all access limitations in relation to patients with Type 1 diabetes should be removed. Furthermore, individuals with insulin-dependent Type 3c diabetes and patients with gestational diabetes should be made eligible for subsidised CGMs and for those with Type 2 diabetes requiring regular insulin. The Committee recommends prioritising the removal of age limitations on access to subsidised access for Type 1 diabetes patients.

This is a great recommendation. Type 3c diabetes is diabetes caused by physical damage to the pancreas. This may be as a result of an accident, surgery, or perhaps cancer. People with type 3c diabetes often fall through the cracks and have a difficult time accessing subsidy programs despite often having similar needs as people with type 1 diabetes. Expanding access to people with gestational diabetes and insulin-dependent type 2 diabetes also makes sense. This may also open up the door to extending CGM subsidies to the wider type 2 diabetes cohort in the future if evidence shows it is economically viable.

Recommendation 16: The Australian Government should explore expanding subsidised access to insulin pumps for all Australians with Type 1 diabetes. A gradual increase, such as expanding access to those aged 40 and under, would be useful as an initial step.

This is another issue I have strong thoughts on, and I was a co-author on this petition which describes why the current model is broken. I was also a signatory to the recently released Consensus Statement on Automated Insulin Delivery for Type 1 Diabetes in Australia.

A gradual increase makes sense although why it would be based on being less than 40 years of age mystifies me. As far as I know, there is no medical evidence to suggest 40 years has significance in the efficacy of pump use. For me, it would make more sense to roll it out in a manner similar to how the CGM subsidy was rolled out e.g. ((type 1 diabetes AND (21 years and under OR indigenous OR concession card holder)) OR (insulin-dependent gestational diabetes). The rest of us would access a pump in the same way as we do today and, over time, the program could expend where the evidence supports the case.

Recommendation 17: The Committee recommends that the Australian Government undertakes a review of the price and choice of insulin pumps in Australia.

I have no idea where this one is coming from. We have a pretty good choice of pumps in Australia so why fix something which is not broken? I hope this is not suggesting we have too much choice and implies we should go down a path similar to, say, New Zealand where only two pumps are funded. Choice is not a luxury; it ensures people are getting the right technology to maximise their prospect of success. Their job may mean a tubeless pump is a better choice. They may have sight impairment which means a pump which connects to a phone or which has a high-contrast screen is the best option. A wider choice ensures a broader set of people’s needs can be met.

Recommendation 18: The Committee recommends that the Australian Government, subject to a positive recommendation from the Pharmaceutical Benefits Advisory Committee, expands the eligibility criteria for Glucagon-like Peptide-1 (GLP-1) receptor agonists, particularly for high-risk patients.

Yes! A great recommendation. I talked about GLP-1s and their benefits for all types of diabetes around four years ago, based on the results coming out from international conferences. These results are now filtering down to the government subsidy level and, hopefully, will soon lead to wider availability for these powerful tools although, historically, supply has been an issue.

The next generation of GLP-1s are now coming out with even more impressive results in terms of weight loss and glucose management. The most well-known is arguably Tirzepatide (Mounjaro) which is approved for people with type 2 diabetes but not type 1. Upcoming trials hope to show it is of benefit to both types of diabetes.

Recommendation 19: The Committee recommends that the Australian Government establishes mechanisms for securing supplies of Glucagon-like Peptide-1 (GLP-1) receptor agonists for disadvantaged and remote communities, including Aboriginal and Torres Strait Island communities.

As mentioned in Recommendation 18, supply of GLP-1s worldwide has been an issue. Given their benefit for both weight loss and for people with diabetes, it is a good suggestion although it is not clear to me how it is to be implemented. If those of us in the cities are struggling to get supply, and the issue is worldwide, this makes access a non-starter for remote communities whose logistics challenges will only add to the problems.

Recommendation 20: The Committee recommends that the Australian Government considers expanding access to bariatric surgery within the public system for eligible patients.

For people with type 2 diabetes and obesity, bariatric surgery has an impressive remission rate of around 50-95%. In Australia, to be eligible for the surgery you must have a Body-Mass Index (BMI) of over 40, or type 2 diabetes and a BMI of over 35. The recommendation is not clear in which direction access should be expanded (lower BMI? different types of diabetes?) Also, only so many surgeries can be conducted in Australia annually and the government would need to provide significant funding to keep up with the current demand, let alone increased demand.

Recommendation 21: The Committee recommends that the Australian Government takes steps to manage diabetes research efforts through the Australian Centre for Disease Control (CDC) by coordinating with the peak bodies such as JDRF and Diabetes Australia research priorities with an emphasis on equitable access and prevention. The Committee also recommends that the Australian Government considers increased funding for Type 1 diabetes research and clinical trials.

All sensible recommendations. I assume coordination between the relevant bodies is not as efficient as it could be and thus the call for improvement. If it means better use of money to help people with diabetes, I am all for it.

Recommendation 22: The Committee recommends that the Australian Government undertakes a survey of current diabetes-related data, with a view to developing strategies for establishing new and improving current data sources and for establishing a national diabetes mellitus register within the CDC.

This is an interesting one as I thought, until recently, that Australia had pretty good data because of the NDSS diabetes database. However, when the register was first established, ‘best guesses’ were made to the type of diabetes people had, based on the information available at the time. This summary covers the history of the NDSS register and some of the problems in the quality of its data.

To give an idea of how, even today, poor data are being captured, according to the NDSS database there are literally no people with type 1 diabetes in Australia who are insulin independent. This means LADAs who, by definition, do not require insulin for at least six months after diagnosis, are lost in the system. Why is this the case? Because it is really hard to change the details in the NDSS database once a person is registered. This means all LADAs, including myself, are told to register as insulin-dependent so that access to subsidised resources is not an issue later on. In short, there is no formal recognition of LADA in Australia and certainly no data to ascertain the prevalence and characteristics of this type 1 sub-type.

Recommendation 23: The Committee recommends that the Australian Centre for Evaluation in the Department of Treasury commits to the ongoing assessment of any actions taken in respect of Committee recommendations made in this report.

This sounds more like bookkeeping than a specific diabetes-related recommendation. Accountability is good though, so I appreciate the value of it.

tl;dr

The recommendations of the inquiry are a bit of a mixed bag, driven by overly broad Terms of Reference and, arguably, pre-conceived notions on the causes of diabetes and, specifically, type 2 diabetes.

The recommendations fall into the following categories (23 is generic and has been left off):

Sugar Recommendations (3, 4)

In short, added sugar is the devil and should be treated as such (change food labelling to call out sugar has been added and tax it). No argument from me on that front but, for type 1 diabetes, total carbohydrates is the key piece of information. As long as that is not sacrificed, all good. As for a sugar tax, if in encourages more variety in sugar-free drinks, I am all for it.

Why is sugar being mentioned in an inquiry into diabetes? No idea. Sugar is not mentioned in the Terms of Reference and its inclusion will feed misconceptions about diabetes being caused by sugar eating.

Obesity Recommendations (7, 10, 20)

The obesity recommendations (design cities for exercise, screen for obesity, and make bariatric surgery more accessible) do not talk at the links between diabetes and obesity, as outlined in the Terms of Reference and tenuously relate to “the causes of obesity and the evidence-base in the prevention, diagnosis and management of obesity”. I would argue they miss this mark given there is limited evidence that city design improves obesity rates. As for the final two recommendations, without investment in what happens after a positive screening and in bariatric services, all we are doing is creating demand for a system which is not set up to serve it.

General Health Recommendations (2, 5, 6)

In short, review dietary guidelines, regulate the advertising of unhealthy food to children, and ensure access to healthy food. All great ideas, and all as relevant to diabetes as they are to many other diseases where diet is considered a risk factor. Should they be in the recommendations for an inquiry into diabetes? Is there evidence that any of these measures will impact diabetes in the Australian population? Do they align to the specified Terms of Reference? No.

Diabetes Recommendations (1, 8, 9, 11-19, 21, 22)

The remaining two thirds of the recommendations actually relate to diabetes, which is good. Economic rigour around the cost of diabetes is a great idea (1) and provides a foundation for smart, economically responsible decisions. Screening for diabetes (I have no idea why they focus on type 2 diabetes here) and increasing overall awareness to enable ‘self-screening’ (8, 9, 11) makes a lot of sense. Catching diabetes early in all of its forms improves outcomes for the individual and the country.

Improved access to health care professionals (12, 13) for all Australians is a good idea but the shortage of these professionals is not considered in the recommendations and risks straining an already strained system further.

The call for improved education of health care professionals in their knowledge of diabetes (14) is a great idea. Many people with diabetes (especially people with type 1 diabetes) actively avoid engaging with the health system because they know they will need to educate the HCP themselves and, often, their knowledge and experience will not be respected and ignored for a lecture received back in medical school decades earlier. Improved education is a tide which will raise all boats and improve the system for all.

Improved and subsidised access to proven medications and technologies (15, 16, 18, 19) is a great idea although I am concerned about the suggestion to review the choice of pumps (17) unless this is aimed at getting the most recent pumps into the country as Australia is a version behind in many CGM and pump systems. The suggestion to use a cut-off of 40 years of age for pump subsidy confounds me and is misaligned to previous Australian subsidy schemes and pump subsidy schemes being rolled out internationally.

Improved research funding administration and access to data (21, 22), as with Recommendation 1, will only improve the decisions made in the future. We can only set our direction when we know where we are, where we are wanting to get to and the means we have to get there, and while many of the recommendations make good guesses to the direction we should head, Recommendations 1, 21, and 22 enable a foundation for much smarter navigation.

Conclusions

There are some good ideas here but there are also missed opportunities and half-solutions. Screening for different diabetes types and for obesity is well and good but what then? The emergence of immune intervention treatments for type 1 diabetes e.g. Teplizumab is also a missed opportunity and a great solution to the question of screening next steps. The lack of health care professionals to service the diabetes community is also absent from the recommendations despite calls to increase demand.

I look forward to seeing how these recommendations are implemented and hope, the ones which are truly focussed on diabetes get the attention they deserve. Diabetes is a costly disease for both the individual and the country so smart, evidence-based decisions, will make a big difference.

Getting Medical Interventions Approved By Government

Having played for a few years at the nexus of academia, big pharma, and government, it is interesting to watch how these three bodies orbit each other and interact (for those of you familiar with the Three-Body Problem you know such a system is often unstable, but I digress). It is often frustrating, being a person with type 1 diabetes, knowing there are, for example, medications out there with overwhelming evidence behind them but which are not funded by government national health programs. GLP-1s are a great example. These are well established to provide benefit to people with type 1 diabetes but are still, certainly in Australia, not covered and financially out of reach for those who would benefit.

So, what does it take to get something approved for government subsidy? I see four major factors which are necessary, and I thought I would write this article to describe them. For context, I will use the subsidy of continuous glucose monitors (CGMs) for people with type 1 diabetes (T1Ds) in Australia as a case example.

The ‘Ask’

The first step is a clearly articulated ask: “We would like the government to fund/subsidise <x>”. In the case of CGMs for T1Ds, the ask is “We would like the government to fund/subsidise CGMs for T1Ds”. In reality, the ask for was for a specific subset, and the program was expanded to all T1Ds over time (for reasons explained later), but I will keep things simple to illustrate the point.

It is, at this stage, where we can answer why GLP-1s are not available for T1Ds in Australia. The fact is, in the case of Ozempic, Novo Nordisk has not asked because they have no need to. Demand is outstripping supply such that Novo can set the price as they wish and run their factories at full speed. Asking will create a new audience which they cannot serve and force a negotiation on price. There is no motivation to do this until general demand abates or supply can be scaled up.

The Medical Benefit

The ‘Ask’ needs to be justified by a tangible benefit which can encompass quality of life measures and overall health measures. In the case of CGMs for T1D, subsidy would allow more people to access the technology and significantly reduce the need for finger pricking. Near-real-time tracking of glucose levels would reduce the risk of serious hypoglycaemia and hospitalisation. All good things and a great improvement for the lives of people living with type 1 diabetes.

The Medical Benefit provides the “So What?” element to the request and can be very emotive. A piece of wisdom often used in sales is people make decisions on how they feel about the purchase and justify it with logic after the fact. The Medical Benefit is the door to stirring the heart of government to act and, in turn, makes for an emotive tale for voters for justify the spend and show the government cares.

The Evidence

A good tale still needs evidence. Aristotle’s ‘Art of Rhetoric’ speaks of three key elements necessary to persuade:

  • Ethos: The argument should be from a credible body
  • Pathos: The argument should stir the emotions of the receiver
  • Logos: The argument should be based in reason

I have taken it as given that, if a request is being made, for it to get the ear of the government, it will need to be from a credible source (Ethos). The Medical Benefit is the key to providing Pathos and clinical/world evidence is the key to Logos. Without evidence, it is a stirring tale but an unjustified one. A government needs to back decisions on reason otherwise the opposition will exploit the weakness.

In the case of CGMs for T1Ds, there was a wealth of clinical evidence showing improved health outcomes with the use of CGMs. I gave an example of this back in 2021 in the context of PWD pregnancy and the use of CGMs.

The Economic Benefit

Governments are required to be fiscally responsible because of scarce resources. In short, if the government is to spend a dollar, it needs to do so on whatever yields the most benefit. For medical interventions, economic justification is usually measured in cost per QALY (Quality-Adjusted Life Years). Basically, a threshold needs to be met where the cost generates a minimum level of benefit which, in this case is a longer and better quality of life for the individual.

The threshold varies from country to country and, while there is no official limit in Australia, a general rule of thumb is government will consider a medical intervention which costs less than $50,000 per quality adjusted life year.

In the case of CGMs for T1D, the economic numbers came out at around $30-35k per QALY and the request was approved.

Case Example: Automatic Insulin Delivery for T1Ds

Let us consider a couple of items being discussed in the diabetes community at this time. The first is equitable access to insulin pumps and, by extension, looping (Automatic Insulin Delivery aka AID) for all Australians. In Australia, while CGMs are subsidised by the government for T1Ds, pumps are not and need to either be purchased directly or obtained through private health insurance. Given a pump costs literally thousands of dollars this puts it out of the reach of many Australians and I recently helped co-author a petition to help get this changed which I encourage you to sign (QR code below).

So, based on the four elements mentioned above, how would we expect the request to fare if raised by a credible body to government as part of, say, the Inquiry Into Diabetes?

The ‘Ask’: This is relatively straightforward i.e. “AID systems should be subsidized for T1Ds”

The Benefit: Lots of qualitative and quantitative benefits to AID systems such as better overnight control, improved HbA1c and Time in Range, and less manual intervention by the T1D.

The Evidence: Lots of clinical and real-world evidence to support this from companies such as Medtronic.

The Economic Benefit: While it would be great to subsidise AID systems for all T1Ds, to get the appropriate cost per QALY, it may be necessary to pick a sub-group e.g. children (who consistently have higher HbA1cs than their older counterparts in trials), T1Ds who are pregnant and so on. Generally, the cohort selection will be driven by The Evidence as this informs the economic modelling. In other words, if there are no studies of AID systems helping pregnant T1Ds, it will be harder to economically justify their inclusion.

Case Example: CGMs for People with Type 2 Diabetes (T2Ds)

On the back of the benefits seen in T1Ds with the use of CGMs it makes sense to expand the program to T2Ds.

The ‘Ask’: Again, this is relatively straightforward: “CGMs should be subsidised for T2Ds”

The Benefit: T2Ds being able to see how food affects them will inform eating habits and improve health outcomes.

The Evidence: There is some evidence of benefit for insulin dependent T2Ds but the body of evidence for general benefit is still being gathered with limited long-term studies to justify The ‘Ask’. To quote this last paper, literally written this year, “…few studies reported on important clinical outcomes, such as adverse events, emergency department use, or hospitalization. Longer term studies are needed to determine if the short-term improvements in glucose control leads to improvements in clinically important outcomes”

The Economic Benefit: Without evidence to act as a foundation for the modelling, it is harder (not impossible) to determine a cost per QALY. The best hope would be to exclusively focus on where there is evidence (insulin-dependent T2Ds) with the hope that, as more evidence is acquired, the program can be expanded to the wider T2D population.

Conclusions

It is easy for us to be frustrated with the glacial movement of governments to get behind the latest advances in technology and medicine when it is clear, for those of us at the coalface, there are benefits to many, many people. However, as we can see, with competing priorities, it is important government spending is used as effectively as possible.

The inclusion of medical interventions in national health programs requires collaboration of all three bodies (big pharma to provide the intervention, academia to show it works, and government to provide the funding) and the will by all of them to drive it. Without this willingness and the elements mentioned above it is hard, if not impossible, to achieve success.

ATTD2024: Analysing and Understanding Complex CGM Data for Informed Clinical Decision Making

I had the opportunity this weekend to catch up on some of the presentations I missed at ATTD2024. I struck gold with the first one I watched. Dr Pratik Choudhary spoke on interpreting CGM data and, as I am in the process of building a bot to do this, it was a talk of great interest. The tips and tricks he gave for reading Ambulatory Glucose Profiles (AGPs) and the rest of the CGM report, I believe, are useful to anyone running a CGM.

Structural vs Behavioral Factors

Dr Choudhary considers two broad levers to improve what he sees in the data: Structural and Behavioral Factors.

For Structural Factors, Dr Choudhary applies general formulae to give a guide on what the values should tend towards if there is an issue.

For people who bolus for meals, his general rule is a 50:50 split of daily units used for bolusing and daily units used for basal insulin. He mentioned exceptions to this rule such as people running hybrid loops and low-carbers who will have a much higher percentage of basal and those who micro-manage their glucose levels, giving themselves boluses many times a day, who will have a higher bolus percentage. In these cases, if it is working, he leaves it alone but if it is not, the 50:50 rule is his guide.

For his benchmark carbohydrate ratio he uses 350 / Total Daily Dose and for the correction factor, 120 / Total Daily Dose. He refers to these are rules but ‘guideline’ is probably a better term.

Dr Choudhary’s Flowchart

His position is, if the Bolus/Basal doses are as expected, the levers to pull are likely to be behavioral.

Showing an example, he presented a report for a person with diabetes (PWD) with top-heavy bolusing, based on the 50:50 rule. His experience is for top-heavy ratios, the PWD will often have a lot of variability. Considering the actual basal (32u/day) vs expected (39u/day) it suggests there is not enough basal, putting upward pressure on the CGM, rising between meals, which is confirmed in the graph.

The Insulin to Carb Ratio (ICR) was 5g/U whereas the predicted was 4.5 g/U suggesting a unit of insulin does not cover as much of a meal as the PWD thought. The Insulin Sensitivity Factor/Correction Factor was 2 mmol/L (1 unit of insulin drops blood glucose by 2mmol/L) whereas the predicted Correction Factor was 1.5 mmol/L suggesting insufficient insulin is being given corrections.

Sure enough, we see that the PWD is going high in the day and staying there, likely because they are not administering sufficient insulin due to bad factors/ratios, with the problem amplified by insufficient basal.

Behavioral Indicators

Dr Choudhary mentioned that for people without diabetes typical glucose variability is usually 15-20%. For PWDs between 20-35% they are generally looping or bolusing well. For people with a variability of 35-50% Dr Choudhary suggests this is a mismatch between food and bolus and so, in the case of high variability, he believes changing settings is not going to help. He also mentioned that any time a PWD can bolus 15 minutes before a meal is ‘free HbA1c/Time in Range and lower variability’.

The light blue area of the AGP relates to events which happen once every week or every fortnight, suggesting they are behavioral (or lifestyle driven e.g. an exercise day/Sunday roast/takeout night) more than systematic. Dark blue is more common and therefore more influenced by structural factors.

Where to Set the High Alarm

A great tip Dr Choudhary gave for setting the high alarm is at the top of the dark blue region on the AGP. When your blood sugar goes over this it is, by definition, an unusual event which may need intervention whereas anything below this is business as usual.

For low alarms, he warned setting them too high as it encourages the PWD to stay high, costing Time in Range. For myself, I set it to 3.3mmol/L (59mg/dL). For the five years post-diagnosis that I was insulin-independent, I wore a CGM and often dipped into the high 3s (high 60s) and got as low as 3.4mmol/L but never any lower. Therefore, below 3.4mmol/L, for me, is abnormal and worthy of attention.

Good Numbers but at What Cost?

Dr Choudhary also showed someone with excellent control due to frequent management. His recommendation for someone bolusing is to “scan, inject, eat and forget” meaning that once you have bolused and eaten, the trajectory of the blood glucose is set and there is very little which can change it. If the peak occurs around one hour after eating, you matched the bolus to the food. The level after two hours will indicate whether the bolus was enough to cover the food. After three hours may show rises influenced by protein and fats but he suggested there was little point in monitoring glucose movement around meals more frequently than this.

He also suggested that frequent management driven by fear of long-term complication may be ill-founded in some cases. From the DCCT study he cited that if a PWD has not had complication interventions in 20 years since diagnosis, their change of getting a life-changing complication for the rest of their life (loss of organ/sight/limb) is negligible. Therefore, if a person with this level of aggressive management is burning out after 20 years of micro-management the evidence supports the option of relaxing the regimen somewhat without significant consequence.

How Do I Fare?

As it happens I have just seen my Endo and my HbA1c has crept up to 5.9% so I am keen for suggestions on improvement (even though I am still well below the threshold for significant risk of complication ).

In terms of the structural settings, my Total Daily Dose for the last 3 months averaged 88U/day. However, as I run my CamAPS Ypsopump completely closed I do not bolus for meals and let the pump take care of it. Therefore, I cannot assess whether I am near the suggested 50:50 ratio. However, based on my profile numbers, informed by Autotune, I am a lot more ‘basal heavy’ than the 50:50 guideline would suggest, backing up Dr Choudhary’s position that it does not strongly apply to loops.

For 88U, the expected ICR is 4.0 g/U and the ISF is 1.4 mmol/L. Again, as CamAPS has automatically adjusted these values for me automatically as part of the loop I cannot check it directly but these values closely align to the default profile values in my pump which I determined using Android APS and Autotune, prior to switching to Ypso a couple of years ago.

My Glucose Variability is currently 31% which is in the typical range for someone looping but, as it is towards the higher end of the range suggests a slight mismatch between bolus and food. Given I let the algorithm do it all, this makes sense as I do not even declare I am eating, letting the loop figure it out for itself.

Looking at the dark blue, we can see a mismatch between insulin and dinner. As the family has roughly the same dinner on a given night of the week it would be interesting to see if the light blue is caused by “Lomo Saltado Lunes”, “Taco Tuesday”, or “Takeout Friday”. I will have to see if it is possible to generate AGPs for a given day of the week over a period on Nightscout…

My Endo has suggested providing some intervention to help the loop with dinner. CamAPS has a Boost function which I will activate at the start of dinner for two hours, giving the loop permission to be more aggressive, to see if this helps. Failing this there are plenty more levers to pull (restricting carb intake or, heaven forbid, giving a bolus).

As mentioned, my low alarm is set to 3.3mmol/L. You will see in the above stats that in the last 3 months it recorded 99 hypo values. These are, almost without exception, a new G6 sensor needing calibration. On the rare occasion I skip a meal and confuse the loop, I might skim the low alarm but it is nothing a few jelly beans cannot fix.

At the moment, my high alarm is set to 15 mmol/L (270mg/dL) but, based on Dr Choudhary’s advice, it should probably come down to 10mmil/L (180 mg/dL) if I was planning to intervene (at this stage I do not do correction doses either).

Where to Find Australian Clinical Trials

Ever since being diagnosed seven years ago, I have been keen to participate in trials of new treatments. Unfortunately, there are not a lot of trials for LADAs (at least, not in Australia). When I became insulin dependent, a couple of years ago, I thought things would change but either my age (I am 50) or my HbA1c excludes me (studies generally like higher HbA1cs and mine is too low). I do check for new studies every month or so and thought putting a list together of where people can go may be useful.

Diabetes Australia’s Research Opportunities

Current research opportunities | Diabetes Australia has a great list of research studies for all types across all of Australia

Disclosure: I am on the Diabetes Australia Community Advisory Council

JDRF’s Clinical Trials Archive

Clinical Trials Archive – JDRF lists trials specifically for type 1 diabetes all across Australia

Australia/New Zealand Clinical Trials Registry

ANZCTR search results | Australian Clinical Trials is an Australian Federal Government registry for many health conditions with filters to show only ones relating to diabetes. Despite the title it seemed to only show trials in Australia at the time of writing.

Baker Heart and Diabetes Institute Clinical Research Trials

Clinical research trials (baker.edu.au) covers all types of diabetes (or, at least, types 1 and 2). The Baker is based in Melbourne but my understanding is some of their trials do recruit outside of Melbourne.

Disclosure: I am a voluntary clinical affiliate with The Baker (basically I am on the books if they need Lived Experience input on a trial) and an Associate Investigator on their FAME-1 Eye trial.

Australasian Type 1 Diabetes Immunotherapy Collective (ATIC) Clinical Trials

Clinical Trials | ATIC (svi.edu.au) are studies focused on immune system mediation which means they generally relate to type 1 diabetes. Arguably this is the frontier of type 1 diabetes treatment and has recently seen exciting results with medications such as Teplizumab for delaying the onset of symptomatic type 1 diabetes. Recruitment is across Australia and, at the time of writing, there was even a study recruiting in New Zealand.

Disclosure: I am on the ATIC Community Engagement Panel.

Highlights from ATTD 2024

I have just returned from ATTD 2024 in Florence, Italy thanks to dedoc. ATTD (Advanced Technologies and Treatments for Diabetes) is one of the largest diabetes conferences in Europe. While the formal focus is on technology and new medications, the research coverage was quite broad. for example, I had a poster at the conference talking about motivation theory and its application in the doctor’s office.

I also presented on the petition to guarantee the humanitarian supply of medication, including insulin, to civilians in war-affected areas, in line with documents such as the Geneva Conventions. If you are interested in signing the petition, please go to https://www.change.org/insulinconsensus

Image care of https://twitter.com/1derfultype

So What Did I Learn?

In the spirit of Michelle Law’s Top Ten Takeaways and dedoc’s #PayItForward, I thought I would list the topics presented which piqued my interest.

Non-Invasive Glucose Measurement

In the expo area of the conference were a lot of companies looking to measure glucose in non-invasive ways, such as through saliva or with various electromagnetic waves scanning the skin. The measure of choice for determining accuracy for these systems is MARD (Mean Absolute Relative Difference). Generally speaking, a MARD less than 10% is considered accurate enough to inform insulin delivery i.e. be included in a bolus/looping system.

To understand how MARD can be manipulated look no further than Tim Street‘s excellent reviews of CGMs and how their accuracy is assessed, such as this one. However, even with the ability to artificially lower the numbers, the lowest MARDs being reported were in the low teens so, at least for now, finger-pricking and CGM insertion will need to continue.

TITR Gets More Coverage

At last year’s ATTD blog article, I mentioned Professor Thomas Danne pushing for Time in Tight Range (TITR, 3.9-7.8 mmol/L = 70-140mg/dL) rather than the usual Time in Range (TIR, 3.9-10 mmol/L = 70-180mg/dL) because it is a better predictor of the onset of Stage 3 diabetes and a better target for minimising the risk of long-term complications. In short, he suggested the evidence-based 50% TITR was a better goal than the consensus-based 70% TIR.

At this year’s ATTD, there was more talk of TITR and it is clear it is becoming an accepted standard in academic research. Some of the other dedoc voices expressed concern that a stricter range could lead to more pressure on people with diabetes (PWD) to ‘succeed’. While I am sympathetic to this concern, I would prefer my targets to be evidence-based but, to make sure people do not over-obsess on the numbers, perhaps a multi-target strategy should be considered with both quantitative and qualitative measures, aligned to the PWD’s goals.

Image care of https://twitter.com/Drhkakturk

Continuous Glucose Monitors (CGMs) and Looping for Type 2 Diabetes

Historically, CGMs and Looping technology has been considered a type 1 tool. However, there are people with type 2 diabetes who require insulin and, from a common-sense perspective, based on the type 1 evidence, it makes sense they would also benefit from the technology. ATTD 2024 presented a variety of studies which confirmed this. Given the type 2 diabetes market is literally ten times the size of the type 1 diabetes market, it makes sense that diabetes tech. companies would pursue it.

Continuous Ketone Monitoring

The idea of monitoring ketones continuously, as well as blood sugar was also presented. It was shown that rising ketones can be used to predict hyperglycemia spikes and potentially predict DKA before it becomes dangerous. Abbott even went as far as to talk about a future all-in-one sensor which would track both in the one unit. Where I see this being useful is providing additional information for looping systems, to predict exercise, better handle ketogenic diets and SLGT2i medications.

GLP1s for Obesity Management

Drugs like semaglutide (Ozempic/Wegovy) are “single agonist GLP1s”: they bind to cells and trigger the same response as GLP1s in the body. The next generation of these drugs are in trials, referred to as double or triple agonists i.e. they activate more receptor sites. The upshot is they are more effective than their single agonist predecessors. How effective? Trials are reporting people losing 20-30% of their weight on the drugs which is incredibly powerful.

LADA Confirmed as a Distinct Phenotype and “Curable”

Perhaps because ATTD was in Italy, the home of Professor Raffaella Buzzetti, one of the leading authorities on LADA, there was substantially more coverage of LADA than I had seen in previous conferences. Professor Buzzetti presented evidence showing LADA is a distinct phenotype of type 1 diabetes (a distinct disease that presented differently) and confirmed that, with immune intervention drugs such as Teplizumab, it may be possible to indefinitely hold off LADA from becoming insulin dependent i.e. a cure.

#LanguageMatters Becomes #DeliveryMatters

One presentation talked at, not so much the words we use in speaking with people with diabetes but, how we talk to them i.e. with empathy and respect. This is a shift in the #LanguageMatters movement but a welcome one.

Patient Reported Outcomes (PROs) and Measures (PROMs)

This had been touched upon in previous conferences but, again, seemed to have more prominence at ATTD 2024. In short, PROs are outcomes which are important to the person with diabetes, more than the clinician.

PROMs are the measures to assess them. At this stage, while there are PROM questionnaires being used in research, their efficacy is not strongly validated, and there is concern they are being used without a purpose in mind.

“Artificial Intelligence is not Ready for Primetime”

The use of artificial intelligence (AI) systems to provide guidance to people with diabetes in their daily management and in providing general advice on diabetes was discussed and considered not ready for general use because of ‘hallucinations’ (false facts incorrectly inferred by the AI engine which need to be verified by the user). Examples cited included mixing up mmol/L with mg/dL which could be disastrous in the context of giving insulin administration advice.

This being said, the potential was recognised once obstacles were addressed.

Tips and Tricks for People with Type 2 Diabetes

One study was presented which showed, even if the types of food a person with type 2 diabetes is eating does not change, intermittent fasting will still reduce their HbA1c. This is intuitively obvious, but it is good to have the evidence to back it up.

Another study showed 2.5-6.5 hours of exercise per week helps people with early stages of type 2 diabetes inproves beta cell function.

Type 1s have Insulin Resistance Too!

Rendering the term “double diabetes” somewhat redundant, it was shown that people with type 1 diabetes also have insulin resistance which, in their case, is driven by the insulin they inject and is independent of factors such as weight or glycemic control. Low carb was mentioned as one lever to pull in managing it.

Thank You dedoc!!

If you are interested in also attending these kinds of conferences, I highly recommend going to the dedoc web site and applying for one of their scholarships. They cover flights, accommodation, and conference registration. Am I one of these infamous “paid diabetes advocates” we hear so much about on social media? I do not think so. I still had to take leave from work and cover other expenses out of my own pocket. My bank account is no richer for the experience but my knowledge of where the research is heading certainly is and the friendships made with other diabetes advocates around the world are priceless. This is why I continue to apply for the scholarships for myself and for the communities I serve.

A Free AGP Reader, Driven By AI

One of the common reports generated by people with diabetes who use Continuous Glucose Monitors is the Ambulatory Glucose Profile (AGP) graph.

If you are unfamiliar with this graph, it is a “heat map” of your blood glucose level (BGL) sampled from multiple days and put over a 24 hour period. So, for example, in the above which is one of my AGPs from last year, the data were over three months (03/07/22 – 03/10/22) and there are clear spikes around 14:30 and 21:30. These, of course, related to meals (lunch and dinner). Why no breakfast spike? Because, generally, I do not eat breakfast.

What I set out to do (and achieved) is create a bot which can be fed an image like the one above and reply with observations to discuss with your health care team. It works via email and generates replies like this.

If you are interested in trying it out, send an email with a screenshot of an AGP (in JPG, PNG, or BMP format) to AGPReader@hotmail.com and you should get back a response in a minute or two. Do not worry if your AGP does not look exactly like mine, I have trained the bot to review graphs from a variety of software sources.

If you are interested in seeing how I put it together, check out my post on my technical blog here.

Next Steps

While reasonably reliable, I am keen to refine and improve it. To this extent, I am talking to medical academics and professionals to get their input on both the training and the analysis the bot generates. I expect, with their assistance, the bot will continue to improve.

Applying Motivation Theory to Diabetes Management

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

The 3C Model

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

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

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

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

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

Misalignment and Intervention

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

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

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

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

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

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

An Example of the Application of the Model

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

Application to Diabetes Management

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

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

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

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

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

How Can We Use This Model?

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

tl;dr

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

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

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

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

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

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

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

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

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

The Prevalence of Misdiagnosis

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

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

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

The Practical Diabetic’s Type Scorecard

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

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

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

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

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

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

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

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

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

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

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

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

Tests For a Definitive Diagnosis

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

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

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

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

tl;dr

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

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

The Types of Diabetes

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.