Blood sugar, insulin and fat loss: what actually matters

9 min read

Somehow, “naked carbs” became a thing.

Women have been told to rearrange their eating around micromanaging blood sugar: never eat fruit on its own, have the apple with nut butter, save carbohydrates for around workouts, keep breakfast savoury because of cortisol. But then, insulin sensitivity is generally better earlier in the day, so carbohydrates should be eaten early and avoided in the evening.

Underneath most of it sits the same idea: insulin stops fat loss, and a large rise in blood glucose, often called a “spike”, ends in a crash, hunger and another craving.

Parts of that story are true. Whether they justify the effort of micromanaging every glucose rise in women without diabetes is another matter.

If you read nothing else, read this

One thing worth knowing: You don't need to keep insulin low or cut out carbohydrates to lose body fat or improve insulin sensitivity.

One thing to ponder: Adding butter or nut butter simply to dampen a glucose rise may lower the spike, but if those extra calories put you into a calorie surplus over time (considering how energy dense fat is), the smoother curve won’t move you closer to better health or your fat-loss goal.

One thing to experiment with: If you graze all day and have erratic meals, try more structure by eating more substantial meals at regular intervals for a week. Notice whether your hunger becomes more predictable, and whether you snack less without much effort.

Does insulin stop fat loss?

Not in the way it's usually described.

After a meal containing carbohydrate, blood glucose rises and the pancreas releases insulin. Insulin acts as a signal that helps move glucose out of the bloodstream and into tissues such as muscle, where it can be used for energy or stored for later. It also tells the liver to store rather than release more glucose.

At the same time, insulin temporarily slows the release of stored fat from fat cells, and the body shifts towards using more glucose for fuel. Across a normal day, the body moves back and forth between storing and releasing energy. Fat loss happens when, over time, more stored energy is used than replaced.

This has been tested directly. A review of 32 controlled feeding studies, where calories and protein were kept similar while carbohydrate and fat changed, found no meaningful fat-loss advantage from lowering carbohydrate and insulin. [1]

That doesn't mean low-carbohydrate diets don't work. They can work very well, often because some people find them easier for managing appetite. Others lose fat while eating bread, oats, potatoes, beans, fruit, rice and pasta.

Low insulin makes it easier to release and burn stored fat, but that is not the same as losing body fat over time: dietary fat can be stored without a large insulin rise, and a sustained energy surplus can still increase body fat.

Lower insulin changes which fuel you're burning; it doesn't abolish energy balance.

Fat loss still requires an energy deficit, but creating and sustaining one can be difficult because hunger and appetite, sleep, physical activity and the food environment all influence it.

Do blood sugar spikes and dips cause hunger and sugar cravings?

The “blood sugar rollercoaster” does not fully explain hunger and sugar cravings.

In the PREDICT study, larger dips in glucose two to three hours after eating were linked to modestly greater hunger and earlier eating. [2] But controlled studies that deliberately produced different glucose responses did not reliably change later intake. A meta-analysis of high versus low glycaemic-index breakfasts found no difference in how much people ate afterwards, and neither did a double-blind trial in 77 young adults despite clearly different glucose responses. [4,5]

In one small laboratory study, deliberately lowering blood glucose to mildly low levels increased desire for high-calorie foods. [3] So blood glucose dips can influence appetite, but that does not prove that an ordinary carbohydrate meal routinely triggers a sugar-craving cycle.

Hunger and craving are also not the same thing. Hunger is the general physiological drive to eat often building gradually. A craving is a stronger desire for one particular food, with or without underlying hunger. Previous meal size, protein and fibre content, sleep deprivation, habit and availability of hyperpalatable food can influence both hunger and cravings.

Can frequent insulin rises make you insulin resistant?

Insulin resistance means that tissues such as the liver and muscles respond less well to insulin, so the pancreas produces more insulin to compensate and keep blood glucose within its normal range. Blood glucose can stay normal for years while this is happening.

Researchers still debate whether high insulin levels is a result of insulin resistance or can also contribute to it. What hasn't been shown is that the ordinary rises after meals, even the large ones, simply add up to cause insulin resistance over time.

It's also worth knowing that a smoother glucose curve doesn't mean less insulin. Adding protein to carbohydrate lowers the glucose rise but increases the insulin response. [6]

Chasing a low glucose curve and chasing low insulin can pull in opposite directions.

What about grazing?

There's no evidence that you need a set number of hours between meals for insulin to “reset”.

But if eating has become almost continuous, some structure can help. If hunger creeps in soon after eating, the previous meal may not have been substantial enough. A proper, balanced meal may work better than repeatedly picking.

If grazing has become a matter of habit, boredom or simply happens because delicious food is within reach, get curious about the possible trigger. Sometimes “out of sight out of mind” works.

Regular meals can also make hunger easier to manage, as there is an anticipatory component to it.

For a closer look at how appetite, habits and our food environment influence eating, see Hunger Games: Why Restrictive Diets Can Backfire

So what drives insulin resistance?

Repeatedly consuming more energy than the body uses, and more than can be stored in the fat tissue under the skin. That storage capacity varies between people. When it is exceeded, more fat can accumulate around the organs and in the liver and muscle, where it interferes with insulin action. [7]

This is why two women of the same weight can have very different metabolic health.

Visceral fat, which accumulates around the organs, and ectopic fat within the liver and muscle are more strongly associated with insulin resistance than subcutaneous fat stored under the skin.

Not enough physical activity. Muscle is one of the body's main destinations for glucose after a meal. A week of strict bed rest reduced the body's response to insulin, mainly because the inactive leg muscles responded less. [8]

These studies do not mean that spending a couple of days in bed causes metabolic disease. They show how responsive muscle is to use and disuse.

Over time, less movement, declining fitness, muscle loss and increasing abdominal fat account for much of what gets blamed simply on ageing. [9]

The menopause transition. Menopause adds another layer to simply getting older.

Body composition can shift even when the scales barely move. In the long-running SWAN study, fat gain accelerated and lean mass began to fall during the transition. [10]

Declining oestrogen signalling may contribute directly, while changes in body composition, activity and muscle also matter.

Sleep disruption. In a six-week randomised trial in women, sleeping about 90 minutes less a night worsened insulin sensitivity, regardless of any change in body fat. [11]

Stress. Very high cortisol, as in Cushing's syndrome or with long-term steroid medication, directly causes insulin resistance. [12]

Everyday stress is harder to isolate because it is usually accompanied by changes in sleep, eating and movement.

Managing stress is not simple, and sometimes the load can't be removed. It can still help to cut unnecessary pressure where possible, protect time for recovery and build capacity through fitness, sleep, adequate nutrition, social support, healthy boundaries, planning and problem-solving.

What actually improves insulin sensitivity?

Lose some excess body fat, if relevant. Losing a moderate amount of weight can make a real difference.

In a controlled study of people with obesity, losing about 5% of body weight improved insulin sensitivity in the liver, muscle and fat tissue. [13] The weight loss came from a caloric deficit, not from a low-carb diet. Metabolic health can improve long before one reaches an “ideal” weight.

If there is no excess body fat to lose, then muscle health, overall physical activity and quality sleep become the focus instead.

Preserve and build more muscle, and stay physically active. Adequate protein intake and regular strength training provide the stimulus muscles need to stay strong and function well. It is also important to stay active throughout the day: take the stairs, get up from the desk, walk after a meal.

The point isn't to burn off food. It's to keep your muscles doing the job they're designed for.

In older adults with obesity at risk of type 2 diabetes, adding exercise to weight loss diet improved insulin sensitivity and fitness and helped preserve muscle and strength, while weight loss through diet alone led to more lean-mass loss. [14]

Strength training in midlife is metabolic care, not just for good looks.

Build meals around protein, fibre and overall energy needs. There is no need to cut carbohydrates. Start with enough protein, plenty of vegetables, fruit, beans, lentils and whole grains, and mostly unsaturated fats, then adjust portions to appetite, activity and goals.

Nut butter on an apple may lower the glucose rise. It also adds energy because fats are calorie dense. If those extra calories contribute to an energy surplus over time, they can work against a fat-loss goal even if the glucose curve looks smoother.

Look honestly at alcohol. Alcohol provides energy, can make a calorie deficit harder to maintain, can disrupt sleep, and higher intake can contribute to raised triglycerides and liver problems. [15]

Treat fasting as an option, not a requirement. Intermittent fasting can help if it suits the person and makes it easier to eat less. Across 28 randomised trials, intermittent and continuous calorie restriction produced broadly similar results, with no consistent advantage for insulin. [16]

There's no need to fast to give insulin “a break”.

Why not just test insulin for better prevention?

It is possible to be insulin resistant while blood glucose and HbA1c remain normal, because the pancreas can compensate for years. That has led to the argument that testing insulin, or wearing a CGM, might detect problems earlier and provide more useful data.

The important question is whether collecting more data actually improves decisions or health outcomes.

Current expert laboratory guidance doesn't recommend routine insulin testing for most people at risk of diabetes or cardiovascular disease. It describes these tests as mainly useful for research and notes that insulin assays still need better standardisation. [17]

A CGM measures glucose, not insulin resistance, and individual meal responses are less reproducible than they look. When adults without diabetes ate exactly the same meals a week apart, their glucose responses varied considerably. [18]

For people without diabetes, evidence that CGM use improves health or weight outcomes is still limited. [19]

More tests and metrics don't equal better prevention here.

More established health checks are blood pressure, blood lipids, and HbA1c or fasting glucose when a GP identifies a higher risk of type 2 diabetes. [20]

No one needs an insulin test or a CGM result before taking preventative measures and meaningful action to support metabolic health.

So, are carbohydrates good or bad?

Carbohydrates aren't unhealthy, and they aren't uniquely fattening.

A woman who spends most of the day sitting may choose a different amount from one who lifts weights, walks a lot or runs several times a week. Beyond meeting protein, fibre, essential fatty acid and micronutrient needs, the relative proportions of carbohydrate and fat can vary according to overall health, activity levels, appetite and preference.

The type of carbohydrates matters too. Lentils, oats, fruit, potatoes, biscuits and sugary drinks all contain carbohydrates, but they differ substantially in fibre content, nutritional value, satisfaction and how easy they are to overeat. There is no need to overthink about your choices if the main source of carbohydrates in your diet come from whole, minimally processed food.

The fundamentals of metabolic health aren't glamorous

And they don't require insulin testing or CGM monitoring.

Stay active, challenge your muscles, move regularly and sit less. Eat satisfying meals with enough protein and fibre, in amounts that fit your energy needs and goals.

If excess body fat is an issue, losing around 5% to 10% of body weight can meaningfully improve insulin sensitivity and several cardiometabolic markers.

Protect your sleep. Look honestly at alcohol and chronic stress. Keep up with appropriate health checks.

None of this requires keeping insulin as low as possible, refusing an apple unless it comes with nut butter, or engineering the smallest possible glucose rise after every meal.

The more practical goal is to look at the bigger picture and build a lifestyle that works for you now and supports your long-term health.


If you want help working out what's worth your effort and what isn't, get in touch. It's a friendly conversation, and you'll leave clearer on what actually drives results in midlife, whether or not we work together.

Next: Why knowing what to do isn’t enough (and what to do instead)

References

  1. Hall KD, Guo J. Obesity energetics: body weight regulation and the effects of diet composition. Gastroenterology. 2017;152:1718-1727.

  2. Wyatt P, Berry SE, Finlayson G, et al. Postprandial glycaemic dips predict appetite and energy intake in healthy individuals. Nature Metabolism. 2021;3:523-529.

  3. Page KA, Seo D, Belfort-DeAguiar R, et al. Circulating glucose levels modulate neural control of desire for high-calorie foods in humans. Journal of Clinical Investigation. 2011;121:4161-4169.

  4. Sun FH, Li C, Zhang YJ, Wong SHS, Wang L. Effect of glycemic index of breakfast on energy intake at subsequent meal among healthy people: a meta-analysis. Nutrients. 2016;8:37.

  5. Kendall FE, Marchand O, Haszard JJ, Venn BJ. The comparative effect on satiety and subsequent energy intake of ingesting sucrose or isomaltulose sweetened trifle: a randomized crossover trial. Nutrients. 2018;10:1504.

  6. Wolever TMS, Zurbau A, Koecher K, Au-Yeung F. The effect of adding protein to a carbohydrate meal on postprandial glucose and insulin responses: a systematic review and meta-analysis of acute controlled feeding trials. Journal of Nutrition. 2024;154:2640-2654.

  7. Virtue S, Vidal-Puig A. Adipose tissue expandability, lipotoxicity and the metabolic syndrome: an allostatic perspective. Biochimica et Biophysica Acta. 2010;1801:338-349.

  8. Mikines KJ, Richter EA, Dela F, Galbo H. Seven days of bed rest decrease insulin action on glucose uptake in leg and whole body. Journal of Applied Physiology. 1991;70:1245-1254.

  9. Coon PJ, Rogus EM, Drinkwater D, Muller DC, Goldberg AP. Role of body fat distribution in the decline in insulin sensitivity and glucose tolerance with age. Journal of Clinical Endocrinology & Metabolism. 1992;75:1125-1132.

  10. Greendale GA, Sternfeld B, Huang M, et al. Changes in body composition and weight during the menopause transition. JCI Insight. 2019;4:e124865.

  11. Zuraikat FM, Laferrère B, Cheng B, et al. Chronic insufficient sleep in women impairs insulin sensitivity independent of adiposity changes: results of a randomized trial. Diabetes Care. 2024;47:117-125.

  12. Beaupere C, Liboz A, Fève B, Blondeau B, Guillemain G. Molecular mechanisms of glucocorticoid-induced insulin resistance. International Journal of Molecular Sciences. 2021;22:623.

  13. Magkos F, Fraterrigo G, Yoshino J, et al. Effects of moderate and subsequent progressive weight loss on metabolic function and adipose tissue biology in humans with obesity. Cell Metabolism. 2016;23:591-601.

  14. Brennan AM, Standley RA, Anthony SJ, et al. Weight loss and exercise differentially affect insulin sensitivity, body composition, cardiorespiratory fitness, and muscle strength in older adults with obesity: a randomized controlled trial. Journals of Gerontology Series A. 2022;77:1088-1097.

  15. Klop B, Torres do Rego A, Castro Cabezas M. Alcohol and plasma triglycerides. Current Opinion in Lipidology. 2013;24:321-326.

  16. Schroor MM, Joris PJ, Plat J, Mensink RP. Effects of intermittent energy restriction compared with those of continuous energy restriction on body composition and cardiometabolic risk markers: a systematic review and meta-analysis of randomized controlled trials in adults. Advances in Nutrition. 2024;15:100130.

  17. Sacks DB, Arnold M, Bakris GL, et al. Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Diabetes Care. 2023;46:e151-e199.

  18. Hengist A, Ong JA, McNeel K, Guo J, Hall KD. Imprecision nutrition? Intraindividual variability of glucose responses to duplicate presented meals in adults without diabetes. American Journal of Clinical Nutrition. 2025;121:74-82.

  19. Liao X, Li Y, Tang S, et al. Continuous glucose monitoring in non-diabetic populations: a systematic review of observational and interventional studies with meta-analysis. European Journal of Medical Research. 2026;31:397.

  20. NICE. Type 2 diabetes: prevention in people at high risk. Public health guideline PH38.

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