DiabEasy as 123

07/02/2026

Some of you have asked me to explain how injected insulin works in my DiabEasyAs 123 way.
1: As you know, in diabetes, the body’s pancreas (insulin producing factory 🏭) either doesn’t make enough insulin anymore or can’t use it effectively (Type 2) OR doesn’t make any insulin at all (Type 1). It’s like the beta cells (factory workers 🧑‍🏭👩‍🏭) have gone “off sick with stress” or “died of exhaustion” (Type 2), or been “attacked and wiped out” (Type 1). So an alternative needs to be sourced - a bit like obtaining it from “another factory or key 🔑 supplier.” Remember without insulin the blood sugar cannot be regulated or reduced.
Insulin is a protein so has to be injected 🩼into body fat to be absorbed into the bloodstream via the capillaries. It cannot be taken orally as the stomach’s acid would destroy it before the body could use it. Injected insulin acts like the body’s natural insulin, giving cells the signal they need to take glucose out of the blood.
2: Insulin lowers blood glucose by moving sugar into cells working like a key, unlocking muscle and fat cells so glucose can move from the bloodstream into the cells, where it’s used for energy instead of building up in the blood.
3: Insulin stops the liver from releasing extra sugar by telling the liver to slow down glucose production. Without enough insulin, the liver would keep adding more sugar to the bloodstream — insulin injections help switch that off.
Remember blood glucose range should be no lower than 4 and ideally no higher than 7mmol/L.
Hope that helps - please comment if it does.
Explanation my own, image generated by AI.
My next post will be about the time profiles of different injected insulins.

03/02/2026

Reposting my SGLT2i DiabEasyAs 123 description using my analogy as I have created an AI generated infographic of it.
How do you explain SGLT2 Inhibitors to your patients?
These are the once daily tablets with the suffix “gliflozin” e.g. empagliflozin, dapagliflozin, canagliflozin, and these, especially dapagliflozin (as it’s the cheapest now) will be much more commonly used when the NICE Diabetes guidelines are updated in February.
My DiabEasyAs 123 way explaining the way they work for patients is like this. Think of these tablets as “Traffic Wardens”.
1. As you know, in diabetes there is too much sugar (glucose) travelling around in the bloodstream. The circulating blood is filtered by the kidneys, and normally the sugar is “transported” back into the blood to be used as fuel for the body by “special proteins” called Sodium-Glucose Linked Transporters (or “sugar trucks”).
2. The “traffic wardens” (or SGLT2 INHIBITORS) are stationed in the kidneys to REDIRECT the “sugar trucks traffic” by making them change “lanes”. So instead of the sugar going back into the bloodstream, the sugar trucks are redirected to the lane that leads to the urine, so they leave the body that route.
3. This redirection of the “sugar trucks traffic” means that blood sugar is reduced independently of the action of insulin, so these tablets won’t cause hypos (but could if prescribed alongside insulin or SU’s)
Obviously this process can have potential side effects, and these will need to be explained. I’ll save that for another post, but I always give or send a patient leaflet, to cover these and sick day rules.
Please comment if you find this helpful, or if you have a better analogy. Thanks

01/02/2026

Pioglitazone is the last of the oral therapies for Type 2 diabetes that appear in national and international guidelines. Please scroll down my page to see the other medications.
In my clinical experience this is not a drug we use a lot, but it might be something that is useful, especially in younger patients e.g. in Early Onset Type 2 diabetes. Here’s my DiabEasy As 123 way of explaining it, but as it’s quite complicated, I need to do a bit of a recap on “insulin resistance”. As you know, most people with Type 2 diabetes are still able to produce insulin but their bodies can’t use it properly, usually due to carrying too much central weight, (but not always).
Using an analogy again, if you think about fat being stored in cells, it is like a build up of “rust in the locks” making the “doors” of the cells to be stiff and hard to open as the insulin “keys” don’t fit or work in the lock properly anymore. This is what we mean by insulin resistance.
1: The main function of Pioglitazone is to reduce insulin resistance by improving insulin sensitivity - in other words making the cells more responsive to the insulin “keys” it still has by loosening or “oiling” the locks with a “Super Oil” (rather than the “WD40” in my metformin analogy), but this takes longer to “soak” into the cells in the muscles and the liver, but when it eventually does, it helps the insulin “keys” work properly again.
2: This next bit might sound too technical, (but I know some of you prefer this).
Pioglitazone works at the gene level by activating a special receptor called PPAR-gamma, which helps to increase glucose uptake in muscle and fat and also improves fat distribution, especially PUSHING it OUT of the liver, meaning less visceral fat and more subcutaneous fat, which as you know is less “dangerous”. Translation: It reprograms cells to behave more “insulin-friendly”.
3: By improving insulin sensitivity in the liver, this reduces unnecessary glucose output, especially overnight. It has a low hypoglycaemia risk (when used without insulin or SU’s) but as it has quite a slow onset of action, you won’t see quick results… it takes weeks to work well, not days. Doses start at 15mg once daily but can be increased to 30 or 45mg once daily.
The downsides of this class of treatment is that it can cause weight gain due to fluid + fat redistribution. It definitely needs to be avoided in heart failure due to fluid retention and risk of oedema, and there is a higher risk of bone fracture, especially in post-menopausal women.
It is safe in kidney decline so can be used with eGFR as low as 15mls/min (check BNF). AVOID if there is any history of bladder cancer.
One-line summary for patients: “Pioglitazone helps your own insulin work better by making your body less resistant to it, helping to preserve the function of your pancreas by not making it work so hard!”
Please comment if you find this helpful as it encourages me to keep the series of DiabEasyAs123 explanations going. There is so much more to managing diabetes than just medications.
Thanks🙏
Explanations my own.
Image generated by AI.

29/01/2026

Here is the next in my DiabEasyAs 123 series on diabetes medications.
How do you explain how “Gliptins’ or DPP4 inhibitors work? (examples: Linagliptin, sitagliptin)
1: First you have to understand what DPP4 is…..,DiPeptidyl Peptidase 4 is an enzyme that has a job to do to “switch off” incretin hormones in the gut. REMEMBER: the job of the incretins (GLP1 and GIP) is to stimulate the pancreas to release insulin after meals and suppress the release of stored glucose from the liver. If these hormones remained active all day, they could lead to incorrect blood sugar regulation. So DPP-4 ensures that incretins act only in response to food intake when glucose levels are rising or are high.
2: Because DPP-4 breaks down these beneficial hormones so fast, DPP-4 INHIBITORS known as “GLIPTINS” were developed by pharmaceutical companies to BLOCK this “interfering” enzyme. Useful in diabetes, this once daily oral “gliptin” tablet extends the action of GLP-1/GIP, allowing them to do their job for longer than usual, so helping with better control of blood sugar.
Examples are Sitagliptin 100mg once daily or Linagliptin 5mg once daily. Sitagliptin’s metabolites (waste products) are excreted via the kidneys, so dose reduction to 50mg and 25mg needs to be made dependent on the estimated filtration rate [eGFR] (check BNF.)
Whereas the dose of linagliptin 5mg does not have to be reduced as it is excreted via the bile (faecal route) so is a safer option if kidney decline is a factor. Safe down to eGFR 15mls/min.
3: In clinical trials, the effect on HbA1c reduction is only about 5-8 mmol/mol, so not really useful if it’s very high! They are weight neutral, don’t cause hypos when used without SU’s or insulin and other side effects are quite rare, (check BNF). Check for any history of pancreatitis as they should not be used if there is. Usually well tolerated, this class of therapy is often known as “a gentle drug for gentle people”.
In summary: They are a useful option for people who can’t tolerate metformin or where avoiding hypos is important (e.g. older adults). Do not use at same time as GLP1/GIP injections or Rybelsus as there is no extra benefit.
One-liner for patients:
“DPP-4 inhibitors keep the body’s own meal-time hormones working longer, helping insulin release only when glucose is high—without weight gain or hypos.”
Please comment if you find this useful - it encourages me to continue the series.
Explanation is my own.
Image is generated by AI.

28/01/2026

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DIabetes Facts Primary Care Collaborative DiabEasy as 123

24/01/2026

I’m often asked:
What are incretin hormones and what do they do? Here is my DiabEasyAs123 explanation.
1: Incretin hormones are located mainly in the gut (intestines) and are naturally occurring “messengers” triggered by the presence of food, that will send instructions to the insulin producing “factory” 🏭(pancreas) to tell the workers (beta cells) 👩‍🏭👨‍🏭to get busy because there is food coming in! There are two main types of incretin hormones called GLP-1 (Glucagon Like Peptide 1) and GIP (Gastric insulinotropic [or inhibitory] polypeptide.) They don’t always work normally like this, as there is an “interfering enzyme” called DPP4, that can sometimes stop them from working.
But when they do do their job properly, remember they nudge the “factory workers” 🧑‍🏭👨‍🏭(beta cells) to work a bit harder to produce more insulin “keys”, 🔑to help open the “locks” 🔐 to the cells so that glucose (sugar/ fuel⛽️) can be transported into them to provide the energy ⚡️needed for living, lowering blood glucose levels.
2: Our own natural incretin hormones, GLP1 and GIP, work well when we exercise 🏃‍♂️ regularly and eat a healthy diet. They have two other jobs, one is to send messages to the liver (warehouse that stores glucose) and tells it to stop ✋adding extra sugar to the bloodstream. (In other words, incretins reduce glucagon, the hormone that tells the liver to release glucose.) This helps prevent blood glucose rising too much after meals.
3: The third job of the incretin hormones is to slow down digestion of any food eaten, so they help to keep the feeling of fullness for longer, thereby reducing appetite! So, by stopping eating when full, people don’t eat as much, so they can help with weight maintenance or even weight loss.
As you all know, the pharmaceutical industry has been able to synthetically produce “incretin mimetics,” drugs that can “mimic” or act like these hormones.
When used as therapy for diabetes, the good thing about them is that they don’t cause hypos, because incretins only work when glucose is raised, and insulin release is reduced as glucose levels fall.
This makes the treatments that mimic the action of these hormones a low risk for hypoglycaemia. (e.g. Liraglutide, Semaglutide, Dulaglutide, Tirzepatide) - when used without insulin injections or SU’s.
Please comment if you find this helpful. It encourages me to keep the series going.
Image generated by AI.

21/01/2026

So, in a nutshell Semaglutide is the best GLP1 for Diabetes and CVD risk reduction! RCT’s prove! See link. I’ll be explaining these therapies a bit more in my DiabEasyAs123 series.

This month’s email includes news on results from the tirzepatide (Mounjaro; a dual GIP/GLP-1 receptor agonist) cardiovascular outcomes trial (CVOT), SURPASS-CVOT, which was conducted in people with type 2 diabetes and atherosclerotic cardiovascular disease.

20/01/2026

In my clinical experience, I often have to have “debates” with patients about the pros and cons of statin therapy, and to be honest, to ensure I’m working in a person-centred way, I don’t mind. Here is one of my DiabEasyAs123 ways of explaining the benefits of statins.
1: It’s important to remember that Statins don’t just reduce the LDL dumper truck production in the manufacturing plant (liver) they also make the roads (blood vessels) safer. There are many landmark studies that demonstrate that statins reduce LDL production, reduce inflammation (fewer triglycerides) so in effect make the roads more resilient to damage.
2: Statins also stabilise any existing cholesterol plaques making them less volatile (fewer crashes- so less likely to break). It’s when the plaques are bashed (for example high blood pressure) that they break and cause the cascade of events that leads to travelling blood clots.
3: If the blood clots get stuck in a narrow vessel that supplies the heart or the brain, this could cause deprivation of oxygen, which is the major cardiac event! Heart attack or stroke!

19/01/2026

These might be useful to some of you!

A unique digital reference tool for healthcare professionals to support the implementation of Continuous Glucose Monitoring (CGM) using the Freestyle Libre 2 system in the management of Type 2 Diabetes in Primary Care. Everything you need to know within this interactive card set.

17/01/2026

Don’t forget that if you’ve missed any of my DiabEasyAs123 explanations, just scroll down my page to find more. It will be an ongoing series. I’m very happy to share what I have learned over the years and how I remember things. If you have other ideas, or ways of explaining terms please add in comments. Thanks 🙏🤩

17/01/2026

Depending on the level of health literacy of your patients, you might need a few different ways to explain why cholesterol management is so important in diabetes. Before starting, always explore what they already know, and tailor the information you provide to their needs.
Here is one of my DiabEasyAs123 ways of helping them understand cholesterol.
1: “Imagine the bloodstream is like a motorway system, and blood fats (lipids) are the vehicles travelling on it. The dangerous vehicles are the “LDL dumper trucks.” These trucks dump lazy/ lousy/ lethal/ cholesterol INTO the artery walls crowding the roads, and causing traffic jams! What’s needed is more HDL cholesterol because these work like “road sweepers” (or I call them healthy, happy hoovers) because they clean up excess LDL cholesterol and take it back to the liver (clearing the roads of LDL trucks.)
Triglycerides are like big heavy lorries, which are fine in small numbers, but too many slow everything down and damage the ‘tarmac’ of roads (causing inflammation in the walls of the arteries or endothelium.)
2: Uncontrolled Diabetes is like “sugar spilling all over the roads.”High glucose also damages the road surface (endothelium) and damaged roads make it easier for LDL trucks to crash into and stick to it (furring up the arteries.)
3: In the presence of “Insulin resistance” (central weight/ large waist) the liver (which is the lorry manufacturer) will always make more LDL dumper trucks, and if people are inactive there will be fewer HDL sweepers being made. Additionally,if they have an unhealthy diet there will be more heavy lorries built (high triglycerides). These three factors result in FASTER and more dangerous traffic build-up, (accelerated atherosclerosis) meaning higher risk of cardiovascular events.
Hope that helps? Photo courtesy of Clare Jones- generated by AI.
Please comment if you find it useful.