A couple of months ago I went down a rabbit hole whilst researching diabetes. The studies mostly stated the obvious, that if you care about your blood sugars early, you’re less likely to have heart attacks and strokes.
But the surprising thing I found was if you looked after your sugars early, even if they became uncontrolled later, you’d preserve that protection [1, 4]. The opposite is also true, if you didn’t look after your sugars early in your life, even if you became very strict later, some of the damage would outlast the change and your risk of heart disease and stroke would remain higher.
This is not to say that treatment is futile, rather highlights what you do today matters.
And the more I read, the more it became clear that the idea of “early” starts well before anyone gets diagnosed with diabetes.
CARBS, SUGARS, AND GLUCOSE
Glucose is an important fuel source as it’s the main fuel for energy use, energy storage, and muscle and brain function. The main source of glucose in the diet is carbohydrates, a family of molecules ranging from:
- Simple sugars such as sucrose (table sugar, candy), just two molecules joined together
- Starches (potato, bread, pasta), which are long necklaces of glucose beads
- Fibre (vegetables, fruits, seeds, nuts) is a necklace bound in a way the gut can’t cut, so it passes through the intestine significant breakdown.
Our body also makes these necklaces from glucose to form Glycogen, to store spare energy in the liver and muscle. Digestion snips the dietary necklaces apart, step by step, until only single glucose beads remain, and those are absorbed through the wall of the small intestine and delivered by the portal vein directly to the liver.
Maintaining glucose concentration in the bloodstream is vital because the brain, which stores almost no fuel of its own, begins to fail within minutes without it. But persistent excess also causes issues, leading to increased fat storage, gradual development of resistance to insulin, ultimately leading to long-term vascular and tissue injury.
After a meal your body needs to distribute and store incoming fuel without allowing glucose to remain elevated for long periods of time. Between meals and overnight, it must keep supplying glucose even though nothing is arriving from the digestive system. The body therefore must maintain control of sugar levels and a failure of this dynamic control system over time is Type 2 diabetes.
INSULIN AND THE ORCHESTRA
In a well-regulated system, the small intestine, pancreas and liver work all together as an elaborate orchestra. As glucose is absorbed, the intestine releases hormones (GIP and GLP-1, you may have heard of these ones as there now drugs that target these specific molecules) that tell the pancreas that fuel is on its way. The pancreas senses the rising glucose, hears the signal from the gut, and releases insulin. The liver, sitting at the end of the portal vein, sees both the glucose and the insulin almost immediately.
Insulin is the coordinator that tells several organs at once that fuel has arrived and each does something different with the message.
- The liver stops manufacturing glucose and starts storing it
- Muscle moves more glucose transporters to its surface and takes up glucose molecules to burn or store.
- Fat tissue holds onto its stored fat rather than releasing it into the blood.
Between meals the whole system changes direction: insulin falls, glucagon rises, and the liver becomes the supplier, breaking down stored glycogen and generating glucose through a process called gluconeogenesis. The ability to switch smoothly between these states as supply and demand change is called metabolic flexibility, and it’s the thing that quietly erodes in the years before diabetes.
The part that erodes over time is that the organs stop responding to insulin the way they should. Muscle sends fewer transporters to its surface and takes up less glucose. The liver keeps manufacturing glucose even though a big delivery has just arrived from the gut. Fat tissue, which should be holding onto its stores, leaks fatty acids into the blood, and those fatty acids end up in the liver and muscle, where they make the resistance worse [7].
Genetics, ageing, inactivity, sleep disruption, some medicines and some hormone conditions all contribute. But the factor I’ve come to focus on most is where the body stores fat.
WHERE IS YOUR FAT?
Fat tissue can be thought of as a safe place for spare energy; think of it as a storage shed. The size of the shed is mostly genetic and varies enormously between people [8].
When its full, the spare energy needs to go somewhere and ends up getting dumped where it shouldn’t go, in the liver and inside muscle cells. This is called ectopic fat. A liver with high levels of ectopic fat, stops responding to insulin, keeps making glucose, and pumps out more cholesterol-carrying particles. Muscle with ectopic fat also stops responding to insulin and therefore cannot take up glucose [7]. Ectopic fat and visceral fat (fat around the abdominal organs) are interrelated, and often increase together.
Visceral fat is the measurement I focus most on when we review patients and perform a DEXA scan to look at their body composition.
This is the reason why BMI is a good rule of thumb but alone is a poor guide to metabolic risk. Two people with the same BMI can have very different amounts of visceral and ectopic fat and a very different capacity to store energy safely.
When insulin resistance starts to develop, the pancreas doesn’t give up quietly and instead it compensates by releasing more insulin. It therefore works overtime to hold blood glucose in the normal range for years meaning a normal glucose result on a routine blood test may be being maintained by an abnormal amount of insulin. But the number looks fine because the pancreas is working harder than it should. Eventually the insulin producing cells can’t sustain the output.
Glucose after meals rises first, then fasting glucose, then HbA1c, the three-month average. In one large British cohort followed for over a decade, insulin sensitivity was already falling and insulin output already climbing years before diagnosis, with the steep rise in glucose only appearing in the final three or so years [6]. By the time someone crosses the diagnostic line, the process may have been running for a decade which is why continuous glucose monitoring (CGM) can be so helpful in delving deeper into your metabolic risk. Looking at trends (CGM) to see what happens to glucose after a meal rather than a snapshot (a blood test or a finger prick) is much more insightful.
A normal glucose can hide an abnormal amount of insulin
GETTING STUCK INTO IT
Glucose is a sticky molecule and given time, it glues itself onto proteins. This is what the HbA1c test measures, glucose that is stuck to haemoglobin. The same thing happens throughout the body, glucose sticks to blood vessel walls, the kidney filtering system and nerve coverings, and together with oxidative stress and inflammation it damages the lining of the blood vessels [9].
A decade of rising glucose post meals is therefore not benign. The small vessels (eyes, kidneys, nerves) usually become damaged first, then the large blood vessels (heart, brain, legs) sustain damage. Some of the by-products persist in tissues for a very long time and some of the changes alter how genes are switched on and off inside cells.
The elevated sugars don’t care for a formal diagnosis and none of it resets the moment the glucose improves.
MY RABBIT HOLE
Which brings me back to the studies that sent me down the rabbit hole. The UK Prospective Diabetes Study enrolled just over 4,000 people newly diagnosed type 2 diabetics with approximately half randomly assigned a tightly controlled group and the other half following traditional treatment [2]. Whilst the tightly controlled group maintained lower HbA1c during the trial period, soon after the trial ended everyone went back to their own ways and both groups’ HbA1c had converged [3].
However, their outcomes never did. There was a follow-up 24 years post-trial, which found that the tightly controlled group still had sustained benefit, with roughly 10% fewer deaths, 17% fewer heart attacks and 26% less eye, kidney and nerve disease [1].
The same pattern appears in type 1 diabetes as in another trial, the tightly controlled group went on to have 57% fewer heart attacks, strokes and cardiovascular deaths [4] and a third lower mortality [5] years after the numbers had converged. Researchers call this the legacy effect.
This is due to the sticky by-products, the vessel damage and the altered gene settings hanging around after the glucose has improved. The best way to think of it is that years of heavy traffic leave potholes, and potholes don’t fill themselves in when the traffic eases. That doesn’t make later treatment futile as improving glucose at any stage reduces current exposure and slows complications. But earlier action does have disproportionate value.
The lasting benefits of early diabetes treatment reinforce the importance of acting early. Insulin resistance can develop years before type 2 diabetes is diagnosed, creating an opportunity to improve metabolic health before blood glucose rises into the diabetes range [1, 6].
Exercise is particularly useful because contracting muscles can move GLUT4 glucose transporters to the cell surface through a pathway that does not require insulin signalling. This allows working muscles to take up more glucose even when their response to insulin is reduced. Regular training also improves insulin sensitivity and can increase the amount of GLUT4 available in muscle [10].
In practice, the evidence supports some achievable targets:
- Walk for 10 minutes after each main meal. In a randomised crossover study involving 41 adults with type 2 diabetes, three 10-minute walks after meals reduced post-meal glucose exposure more effectively than one 30-minute daily walk without specified timing [11]. If three walks are difficult to fit in, starting after one meal is a practical first step.
- Build towards at least 150 minutes of moderate-intensity aerobic activity each week. Brisk walking, cycling or swimming all count. One way to achieve this is 30 minutes on five days each week. Spread activity across at least three days, avoiding more than two consecutive inactive days. Post-meal walks can contribute to this total when the pace is moderately demanding [12].
- Include resistance training two or three times a week, on non-consecutive days. Use weights, resistance bands or body-weight exercises that work the major muscle groups. Strength training helps preserve or build muscle and improves its ability to respond to insulin and handle glucose; its benefits extend beyond simply creating more storage space for glycogen, although this is also a factor [10, 12].
- Interrupt prolonged sitting at least every 30 minutes. Get up for a brief walk or some light movement. These breaks complement planned exercise and can help reduce post-meal glucose levels [12].
- If you have prediabetes and excess weight, consider an initial weight-loss target of 5–7%, with appropriate support. This degree of sustained weight loss can improve metabolic health and reduce progression to type 2 diabetes [13]. The Diabetes Prevention Program targeted 7% weight loss alongside 150 minutes of weekly activity; the combined programme reduced diabetes incidence by 58% over approximately three years. That benefit came from the programme as a whole, rather than weight loss alone [14].
- Aim for 7–9 hours of sleep each night, with consistent bed and waking times [15]. Experimental studies show that restricting sleep can impair insulin sensitivity, even without weight gain [16]. Adequate sleep supports metabolic regulation, although we cannot yet assign it a diabetes-prevention benefit comparable to that demonstrated in the lifestyle trials.
These are targets to build towards, adjusted to your health, fitness and circumstances. You can begin with a manageable change and build from there, even if your blood glucose is currently normal.
A normal result is reassuring, but understanding your metabolic health means looking beyond a single number. Changes over time, considered alongside your body composition, blood pressure, cholesterol and family history, provide a fuller picture and can help guide where to focus your efforts.
For selected people, additional assessment adds useful detail. A body composition scan can assess fat distribution and muscle mass, while continuous glucose monitoring over one to two weeks can show how glucose levels vary throughout the day and after meals. Understanding your metabolic dysfunction early provides the opportunity to act earlier, modify the ability of the body to handle fuel and prevent metabolic dysfunction from crossing the threshold into a diagnosis of type 2 Diabetes.