If I Had Type 2 Diabetes

Dr Edward Leatham

Jul 11

13 min read

Updated: Sep 4

What I Would Do If I Had Type 2 Diabetes: A Personal Approach to Prevention and Management

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Patients often ask me, "If it were you, doctor — what would you actually do?" This is a fair question. The answer is often different from the printed guidelines. Let me answer plainly, in the order I would tackle it — with references attached.

Fix the Food First

I would start by fixing my diet. Then, I would focus on movement. After that, I would build muscle. Only then would I consider medication. This sequence aims to reduce visceral fat and stabilise blood sugar levels, rather than just meeting cost-effectiveness thresholds.

Why "Best Value" Is Not the Same as "Best Possible"

NICE does an extraordinary job of deciding how to spend a finite NHS budget. Their goal is to benefit the most people for each pound spent. This is the right question for a health system. However, it is a population question. It weighs cost-effectiveness alongside safety, access, and the average case.

Instead, I would ask, "What is the best I could do for my body, setting those constraints aside?" The answer can look different — earlier, more layered, and more aggressive in addressing the root cause of type 2 diabetes: visceral fat.

In fairness, the gap has narrowed. Since NICE NG28 was updated in February 2026, it recommends modified-release metformin along with an SGLT2 inhibitor as first-line therapy for most adults with type 2 diabetes. This approach continues to provide cardiovascular and renal protection, independent of glucose readings. It also brings GLP-1 agonists or tirzepatide forward for selected higher-risk groups.

The distinction I’m drawing is not that NICE is behind the science. They now explicitly balance individualised care, cardiorenal protection, obesity, and patient preference, not merely cost. However, a private, individualised strategy can act on the same evidence with fewer cost and eligibility constraints.

This is not a criticism of NICE. It's simply what I would choose if cost and eligibility thresholds were not part of the calculation.

Understanding Type 2 Diabetes

Type 2 diabetes is not a single disease; it exists on a spectrum. At one end is the metabolic-overload form — an insulin-resistant body, usually carrying excess visceral fat. This form is often pushed into remission once the load is reduced.

At the other end is the lean, insulin-deficient form. This includes type 1 diabetes, LADA (latent autoimmune diabetes in adults), or the insulin-deficient end of type 2 diabetes. Here, the pancreas genuinely fails to produce enough insulin. In this case, diet and exercise alone cannot solve the problem; insulin becomes essential.

Most people fall somewhere between these two extremes. The balance can shift over time. Years of overload can exhaust the beta cells, moving someone from the resistant end toward the deficient one. However, there is a window where shedding ectopic fat can still restore function.

A simple bedside check can help determine where you stand. A waist measurement greater than half your height indicates that visceral fat is likely the driver. This places you towards the modifiable, metabolic-overload end, where this plan is most effective.

Ethnicity can also shift the odds. For example, white European men with central fat are more likely to have visceral fat issues. South and East Asian backgrounds tend to have a greater innate limit on beta-cell reserve, leading to diabetes arriving younger and leaner. Hispanic and Latino backgrounds often exhibit strong insulin resistance and liver fat, making the visceral-fat strategy particularly relevant.

You don't need a diagnosis to apply most of this advice. It matters as much for those trying to avoid diabetes — anyone with a widening waist, a family history, or a "pre-diabetic" HbA1c — as for those who already have it. The biology is a continuum, and the early levers are identical. The main difference is the pharmacology, which decreases as you move from treatment toward prevention.

The Importance of Visceral Fat

I keep returning to visceral fat because it is more than just a proxy for insulin resistance. The fat packed around the organs is metabolically active and, frankly, hostile. It releases inflammatory cytokines linked to long-term risks, including dementia. It also drains free fatty acids into the portal vein feeding the liver. This leads to a shift toward small, dense LDL particles, which are more prone to oxidise and lodge in artery walls. This is why visceral fat is closely tied to coronary disease.

High visceral fat does not automatically mean diabetes. It is a principal driver of insulin resistance, but whether that leads to a raised HbA1c depends on the pancreas behind it. Someone with a generous beta-cell reserve may carry a large visceral load for years without abnormal glucose levels. However, someone closer to the insulin-deficient end may exhaust that reserve sooner.

The practical conclusion remains the same: high visceral fat challenges the entire system. Lowering it helps across the board. If the goal is to prevent pancreatic failure, it must be tackled early, long before glucose levels change. This is why a tape measure becomes an essential tool from the age of thirty. It is the cheapest diabetes-prevention tool we have.

Fixing the Food

If my HbA1c were creeping into pre-diabetic territory (42–47 mmol/mol, roughly 6.0–6.4%) or crossing the diabetic line (≥48 mmol/mol, 6.5%), the first step would be to fix my diet, not reach for a prescription.

I would cut back on carbohydrates, especially ultra-processed foods where sugar hides in plain sight. This includes sauces, breads, "healthy" cereals, and low-fat products that replace fat with starch. I would measure rather than guess. A continuous glucose sensor would help me keep my response to each meal as flat as possible.

The Lingo app logs meals and provides feedback on which foods and timings drive glucose excursions. This turns a vague sense of "I should eat better" into a personal, meal-by-meal map of how my body reacts to each food.

With that map in hand, I would either eliminate offending foods or defuse them. This means pairing them with fat, protein, and fibre, and eating them last in the meal. This approach helps produce a gentler glucose rise. Dietary fat provokes almost no insulin response, while protein only has a modest effect. Carbohydrates, especially refined ones, drive large glucose and insulin swings. By building meals around protein, fat, and fibre, and keeping starch small, I can maintain a flatter glucose curve.

To make this practical, I would use a food app alongside the sensor. SNAQ is my go-to choice. It allows me to photograph a meal and estimate its carbohydrate, protein, and fat content. It also lays that meal directly onto my glucose curve, making cause and effect impossible to miss. Crucially, it lets me set a protein target per meal and track whether I meet it. If I connect it to Apple Health, my steps and resistance-training sessions flow onto the same dashboard, bringing food, glucose, and exercise together.

The History of Carbohydrate Restriction

It's worth pausing to understand why cutting carbohydrates works. This idea is not new; it predates modern fads. Before insulin was discovered in 1921, carbohydrate restriction was the only treatment that provided any relief for people with diabetes. This "animal diet" consisted of fatty meat and green vegetables, with starch almost entirely eliminated. This lineage runs through the low-carbohydrate diet popularised by cardiologist Robert Atkins to today's ketogenic approaches.

There’s a mechanistic reason this idea endures. For most of the body, glucose is not the default fuel. The heart, for example, primarily runs on free fatty acids and ketones. One leading hypothesis for why SGLT2 inhibitors help failing hearts is that they produce a modest rise in ketones, providing a more oxygen-efficient fuel. This benefit is well established, even in people without diabetes.

Following this logic, glucose starts to look less like a staple and more like a specialist fuel. It is genuinely obligatory for only a few tissues — red blood cells, parts of the kidney and eye, and a portion of the brain. However, even the brain can run substantially on ketones once they are available. The liver can manufacture the small amount of glucose the body truly needs, meaning there is no dietary requirement for carbohydrates.

Moving More

Next, I would focus on aerobic activity. This doesn't have to be glamorous; it just needs to fit into a busy week. I would park further from work, take the stairs instead of the lift, and go for a short walk after meals to blunt glucose peaks. My target would be an average of 7,000–10,000 steps a day, not every single day, but averaged across the week.

If progress stalls, or if I prefer the idea of a home gym, I would invest in a machine I would actually use. A low-impact incline elliptical is gentle on the joints. In my experience, interactive, coached versions motivate better than "better" machines that gather dust. NordicTrack's incline ellipticals are a well-known example.

Building Muscle

Skeletal muscle is crucial for glucose disposal. Therefore, growing and maintaining muscle is vital. There are two levers here. First, I would focus on protein intake. I would aim for around 25–30 g of good-quality protein per meal to trigger muscle protein synthesis. Second, I would engage in progressive resistance training. Just fifteen minutes, five days a week, with weights or resistance bands can make a significant difference.

If it were me, and it were affordable, I would start with a personal trainer at a gym for as long as that was sustainable. This would help me learn proper form and build the habit. After that, I would transition to a simple home routine I could maintain for life. The maintenance phase is crucial; the initial push is just how I get there.

Protecting Sleep

Sleep is often the pillar people overlook, but it quietly undoes all the hard work. Short or broken sleep raises cortisol levels. Sustained cortisol worsens insulin resistance, nudges glucose higher, and increases appetite the following day. I would treat sleep as a measurable target rather than a luxury. A sleep-tracking ring makes it visible. The Oura ring is the best-known option, but there are now capable, subscription-free alternatives like the Ultrahuman Ring Air, RingConn, and Samsung Galaxy Ring. The key is that what gets measured tends to get managed.

The Role of Pharmacology

Now we come to medication. Notice how far down the page they sit. My trigger to escalate would be visceral fat, not the scales. A raised VAT reading on CT or DEXA, or simply a waist measurement greater than half my height, would prompt me to implement a monitoring system. This would allow me to see whether my food and exercise measures were effective. If the numbers improved, I would continue my current approach. If they did not, I would layer in pharmacology.

I would start with metformin at 500 mg twice daily, titrating up to 2 g/day. It effectively reduces the liver's glucose production and is well understood, inexpensive, and time-tested. This aligns closely with current guidance, which typically starts modified-release metformin and an SGLT2 inhibitor together from diagnosis.

If visceral fat did not decrease with lifestyle changes, I would consider a GLP-1 receptor agonist, gently dosed. This is where a private plan can move sooner than NHS eligibility allows. A low, carefully titrated dose (often referred to as "microdosing") can help reach waist targets. It's important to clarify that microdosing for this purpose is largely a private, off-licence approach.

Beyond private use, GLP-1 agonists are now recommended for all types of type 2 diabetes, regardless of whether the person is already on insulin. Adding one usually allows for a substantial reduction in insulin dosage, which is beneficial since less injected insulin means less weight gain. This is partly due to a direct insulin-sensitising effect, but I suspect the larger part is the drug's ability to reduce visceral and ectopic fat.

An SGLT2 inhibitor is another effective option. It blocks the sodium-glucose co-transporter in the kidney's proximal tubule, lowering the threshold for glucose retention. Above this threshold, glucose spills into the urine, reducing circulating glucose levels and providing heart and kidney protection. However, it comes with its own cautions, including a rare risk of ketoacidosis, particularly if you're eating low-carb.

A gliptin (DPP-4 inhibitor) is a gentler incretin option. Instead of flooding the system with a potent analogue, it simply slows the breakdown of your own GLP-1. I would treat it as an alternative to a GLP-1 receptor agonist, not something to stack on top.

Combining an SGLT2 inhibitor and a GLP-1 agonist is increasingly recommended for higher-risk patients. NICE now places semaglutide alongside metformin and an SGLT2 inhibitor as first-line triple therapy after established cardiovascular disease. This combination works on different organs and endpoints, allowing their benefits to add up rather than overlap.

The last two options I would consider are sulfonylureas and insulin. I believe that almost everything above is designed to lower the demand for insulin. A sulfonylurea like gliclazide does the opposite; it forces the beta cells to secrete more insulin, regardless of underlying resistance. This can lead to hypoglycaemia and weight gain, and over time, it can cause the fastest loss of glycaemic durability among common oral agents.

I view insulin as a last resort in type 2 diabetes. It should not be used early simply to make numbers look better. Current guidance prefers a GLP-1 receptor agonist to insulin when there is no true insulin deficiency. Adding insulin to an already insulin-resistant body tends to promote fat storage, counteracting the goal.

However, insulin is essential when genuinely needed — in cases of insulin deficiency, severe hyperglycaemia, or to protect against ketoacidosis and end-organ damage. Used briefly and deliberately, it can even rest an exhausted pancreas. The error I want to avoid is reaching for it first, before addressing the underlying workload.

Even where insulin is required, the strategies discussed here are not wasted. Building muscle, shedding visceral fat, and lowering carbohydrate intake all enhance insulin sensitivity. Many insulin-dependent patients report that both their insulin dose and weight decrease when they follow this approach.

Remember, carbohydrates are what drive significant insulin surges. By building meals around protein and fat, much of the pharmacology becomes a smaller task.

None of this is fringe. Contemporary programmes like Virta Health and Gary Taubes's Rethinking Diabetes make a similar case: fix the diet, reduce the load, and much of the medication can often be reduced under supervision. My emphasis simply adds another layer: focusing on visceral fat, muscle, and long-term healthspan rather than just glucose numbers.

How I Would Investigate and Keep Score

Cardiovascular disease is the leading cause of death in type 2 diabetes. Therefore, in a cardiologist's hands, the work-up focuses on defining arterial risk, not merely tracking glucose. NICE primarily defines the problem by glucose numbers; I would want to see the disease itself.

For cardiovascular risk, I would use CT coronary angiography (CTCA) to image the coronary arteries. This approach has been shown in trials to reduce heart attacks by changing subsequent treatment. I would also add the fat attenuation index (FAI), which provides insight into inflammation in the fat surrounding the coronary arteries.

For metabolic risk, I would quantify visceral fat using low-dose CT and track glucose patterns with a continuous glucose monitor (CGM) rather than relying solely on an annual HbA1c.

This is not abstract. If a scan showed soft plaque in my left main stem or proximal LAD, or an FAI indicating a twenty per cent eight-year mortality, a reassuring glucose level would not comfort me. I would want to measure the disease itself and take action to reduce it.

For day-to-day tracking, I would hand much of the responsibility to the patient. However, I would not present a flat dashboard of equal numbers, which often breeds anxiety. Instead, I would rank the measurements by their significance. At the top would be waist measurement (using a tape measure to keep the waist-to-height ratio under 0.5), which is the closest proxy for visceral fat and defines success. Next would be functional strength, measured with a simple grip dynamometer. Metabolic health and longevity correlate more closely with muscle strength than muscle mass, and strength protects you as weight decreases.

Following that would be the CGM, with SNAQ logging meals against the glucose curve. This is excellent for changing behaviour week to week. Bioimpedance scales would come last. While they can be engaging, a flattering correlation with a DEXA scan does not equate to agreement, so I would not let them drive decisions.

One measure I would not treat as diabetes-specific is blood pressure. It is the first of the four pillars of cardiometabolic health and matters for everyone. Averaging home readings over a week is more informative than any single clinic measurement. In diabetes, where cardiovascular and kidney risks are significant, I would track blood pressure closely. Each of these devices costs less than £100 and requires no prescription; I keep the current list on the VAT Trap toolkit page.

The foundation for treating plaque, both in diabetics and non-diabetics, is lowering LDL cholesterol and ApoB. For anyone with established disease, this comes first. I would not settle for a normal-looking LDL; I would aim to drive ApoB — the true count of atherogenic particles — to a stringent target of below 0.65 g/L (65 mg/dL). I would start with a statin, then add ezetimibe, and consider a PCSK9-inhibitor injection if the target remains unmet. This last step is a significant escalation, rightly reserved for high-risk cases. However, on the NHS, it is largely limited to individuals who have already experienced a cardiovascular event. The goal of defining my risk through imaging is to earn the right to use these more potent treatments before a first event, not only after it.

Once lipids are under control, I would turn to what the imaging reveals. Since the FAI measures coronary inflammation, it provides a target I cannot otherwise see. I would want to confirm that the inflammation driving much of the residual, modifiable risk is genuinely suppressed. If it were not, I would add an anti-inflammatory — low-dose colchicine has the strongest evidence in stable coronary disease.

For anyone flagged as high risk by CTCA and FAI, I would track whether the disease is regressing. This would involve a low-dose visceral-fat CT to monitor fat levels and a repeat CTCA every two to three years to ensure plaque is stabilising rather than advancing. Almost none of this falls within current NHS or NICE provisions; it is, unapologetically, what I would choose for myself.

One clarification the table cannot convey: the medicines are not interchangeable across the two columns. SGLT2 inhibitors are heart-failure, kidney, and diabetes drugs. Their proven role is in cardiorenal protection and glucose control, not diabetes prevention. I would not use one in simple prediabetes unless heart failure or kidney disease were already present, or if glucose levels were rising rapidly. A GLP-1 agonist is the more logical tool when visceral fat is the issue, and its cardiovascular benefits now extend to individuals with obesity and heart disease, even before diabetes manifests. This should be used alongside diet and strength training, not as a substitute.

Metformin also has a genuine evidence base for delaying progression in higher-risk prediabetes, although lifestyle changes have been shown to outperform it in head-to-head comparisons.

Key Takeaways

NICE optimises value across a population; a "money-no-object" plan for one person can be earlier and more layered.
Food first: cut carbs and hidden sugars, use a CGM to flatten your meal responses, and defuse spikes with fat, protein, fibre, and food order.
Move in the cracks of the day (7,000–10,000 steps average) and build muscle (~25–30 g protein/meal + resistance training) — muscle is a glucose sink.
Protect sleep — poor sleep raises cortisol and worsens insulin resistance. A sleep-tracking ring (Oura, or subscription-free options like Ultrahuman, RingConn, Samsung Galaxy Ring) makes it a target you can manage.
Escalate on visceral fat, not the scales. Start with metformin; then, if needed, consider a GLP-1 agonist and/or an SGLT2 inhibitor — with a gliptin as an alternative to (not an addition to) a GLP-1 drug.
Know which type of diabetes you have. This plan targets the visceral-fat-driven form; the lean, insulin-deficient form (type 1, LADA) still benefits from these strategies but cannot be managed without insulin.

Summary

Fix the food first, then move, then build muscle — and only then reach for drugs, in a sequence chosen to shrink visceral fat and flatten the glucose curve rather than simply to satisfy a cost-effectiveness threshold.

VAT Trap