Sugar: the reward that never has to wait

Why sweetness gains value in your brain so quickly, what free sugars actually do inside your body, and which choices genuinely make a difference. Reading time about 15 minutes.

---

Stand in front of a bakery window for a moment. Not long. Two seconds is enough.

Within those two seconds you already know what you want. You weighed nothing up. You counted no calories. Your body chose before your mind arrived.

I know that feeling well. For one large raspberry macaron I would skip a meal. Not because I don’t know better. Precisely because I do.

Then comes the second part, the one fewer people talk about. Afterwards I turn strict with myself. Often too strict. The craving and the correction live in the same day.

Why does a brain that understands everything still give priority to a slice of cake, over moving or learning? And how harmful is sugar really, once you set aside the noise of social media?

There is no list of forbidden foods here. There is a way of looking at doors. Which door you choose now. How many doors your body opens afterwards. And what happens when the room behind them fills up.

First: which sugar do I mean?

Without this agreement we talk past each other.

By sugar I mean free sugars throughout this article. The World Health Organization describes these as all sugars added to food and drink by the manufacturer, cook or consumer, plus the sugars naturally present in honey, syrups, fruit juices and fruit juice concentrates.¹

That is different from the sugars locked inside whole fruit, vegetables and unsweetened milk. Those do not count.

And it is different from carbohydrates, which also include bread, rice, potatoes and pulses.

One thing stands out in that recommendation: the World Health Organization names only an upper limit. There is no recommended minimum for free sugars.¹

Sweetness was once a promise, not a threat

Children like sweetness more than adults do. Not slightly more. Measurably more.

Researchers at the Monell Chemical Senses Center in Philadelphia summarised the basic research on this. Children find a stronger sweet taste pleasant than adults do. That preference only drops to adult levels in the mid to late teenage years, and that moment coincides with the end of physical growth. In newborns, sweetness can also dampen pain.²

Coincides, note. Whether growth is the cause, we do not know. Researchers suspect a link, nothing more.

None of this makes a craving for sweetness a character flaw. A strong sweet preference is, at the very least, a normal part of childhood.

History tells the same story on a larger scale. We often assume sugar has always been here. It has not. Sugarcane does not come from Europe. Genetic research from 2025 shows that the species we eat was domesticated in the New Guinea region, from a wild relative. From there the plant travelled with people.³

So sweetness was, for a very long time, something that grew far away.

And how it arrived here cannot be told honestly without the plantations. On the British Museum blog, food historian Tasha Marks puts it plainly: sugar was a driving force and a catalyst to the slave trade, and the image of sugar between the sixteenth and nineteenth centuries is not one of luxury but of the horrors of slavery.⁴

Idealised depiction of enslaved women, men and children cutting sugar cane in the British colony of Antigua. William Clark, “Slaves cutting the sugar cane”, from Ten Views in the Island of Antigua, plate IV (London, 1823). Source: Wikimedia Commons, via the British Library. Licence: CC0 1.0. Resized and converted to WebP.

So what is new is not the craving. It is the availability. Concentrated sweetness was expensive and rare for centuries. Now it sits beside every till.

Your brain has no scale for health

There is no “addiction centre” that sugar switches on. That picture is everywhere, and it is wrong.

Reward does not sit in one place in your head. It is a collaboration between regions that assign value, adjust expectations and remember behaviour.

Researchers Oscar Bartra, Joseph McGuire and Joseph Kable mapped this in 2013. They placed 206 brain imaging studies on a single pile. Such a pile is called a meta-analysis: not a new experiment, but existing studies laid side by side to see which pattern survives.

What they found can be said simply. Two places in your head keep a kind of scoreboard.

The first sits low behind your forehead (the ventromedial prefrontal cortex). The second sits deep in the middle of your brain, towards the front (the anterior ventral striatum). Together they signal how much something is worth to you right now. Researchers call this subjective value.⁵

The remarkable part is that everything lands on the same scoreboard. Money, food, music, a compliment, a walk that feels good.

Your brain converts everything into the same currency.

That is a beautiful system. Without a shared currency you could never choose between two things that have nothing in common. Try comparing an apple with phoning your mother. You do it all day anyway.

Health does make it onto that scoreboard. It simply lands there weakly. Its reward lies far away, it is uncertain, and it asks something of you today.

Seen that way, your brain does not weigh what is good for you. It weighs what is worth something now.

The same applies to dopamine. Dopamine is not a simple happiness hormone. It plays a role in craving, expectation, motivation and learning from surprises, among other things. It moves you towards something.

Wanting and enjoying are not the same. You notice that the moment a packet of biscuits is empty without you having tasted a single one.

Why the macaron beats the walk

If moving, learning and eating all use the same scoreboard, why does the cake win so often?

Not because sugar is stronger. Because the sum works out differently.

Two things weigh heavily in that sum: how long you have to wait and how much effort it takes.

A research group around Andrew Westbrook mapped this. Participants with higher dopamine production in the striatum (the deep middle region that helps determine how much effort you will spend) were on average willing to invest more mental effort. Two medicines shifted that trade-off between benefit and cost, and they did so mainly in participants whose dopamine production was lower.⁶

The task did not become more enjoyable. The expected benefit simply came to weigh more heavily against the effort.

Dopamine is not a pleasure meter. It is a weighting factor between benefit and effort.

Even so, speed does not explain everything. Music rewards just as quickly as sugar does.

Valorie Salimpoor and colleagues showed that music which moves you deeply releases measurable dopamine in that same middle region. Just before the most beautiful moment one part became active, during the peak itself another.⁷

Three differences remain, and this is my reading of these studies rather than a complete explanation.

• Certainty. You know exactly what that macaron will do. An hour of studying offers no such promise.
• No start-up cost. Unwrap and bite. A walk asks first for shoes, a coat and the decision to stand up.
• The reward arrives before the effort. With movement the good feeling comes afterwards. With sweetness it comes first.

Your brain is not a saboteur. It is an excellent employee working from a hopelessly outdated job description.

And underneath that lies something quieter.

You are not choosing between cake and health. You are choosing between yourself right now and someone who does not exist yet.

The person who benefits from that walk is a future version of you. They are not at the table. They have no hunger, no voice and no opinion.

This is not a battle between good and bad. It is a conversation in which one of the two is always absent.

Sugar is not cocaine. And that is no reassurance

The claim that sugar is more addictive than cocaine comes from animal experiments.

Researchers in Cambridge placed those animal studies and the human studies side by side. Their conclusion: in humans there is little evidence that sugar is addictive in its own right. In rats, addiction-like behaviour such as bingeing appeared almost only when the animals were given sugar intermittently.⁸

First denied. Then allowed. Then denied again.

That is an indication that the interruption did more than the sugar. It is not proof. Rats are not people, and whether a strict ban produces the same pattern in humans has not been demonstrated. I do notice it in myself, and I cannot make more of it than that. Being strict works against me.

The fact that sugar alone is not addictive does not mean nothing is going on.

Kevin Hall and his team had twenty adults live in a research centre for four weeks. For two weeks they were served ultra-processed food, for two weeks unprocessed food. What was offered was carefully matched, down to the sugar and the fibre. They could decide for themselves how much to eat.

During the ultra-processed weeks they ate on average 508 kcal per day more. They gained roughly 0.9 kg in two weeks. During the unprocessed weeks they lost about the same.⁹

Read the wording carefully. What was offered was equal, not what was eaten. Why people ate more has not been proven. Eating faster, softer texture and more energy per bite are the explanations most often given.

The cracks belong in the story. It was twenty people, two weeks per phase. And scientists still disagree about where “ultra-processed” actually begins.

The lesson holds, though. With ultra-processed food the question is not only how much sugar it contains, but also how easily you eat too much of it.

Your body pushes doors outwards

Table sugar is called sucrose. In your small intestine it is cut in two: glucose and fructose. Glucose enters the blood. Fructose is processed mainly in your gut and liver.

Your gut notices the arrival and sends a signal ahead to your pancreas. The pancreas responds by making insulin.

Insulin is often called “the key” that lets glucose into the cell. That picture is not quite right.

In your skeletal muscle and fat tissue sit small passages that work like doors. At rest many of those doors are stored inside the cell. Insulin is not the key. Insulin is the message that makes the cell decide to push those doors to the surface. More doors on the outside means more glucose coming in.¹⁰

There is a second route, and it is too good to leave out here. A contracting muscle pushes those same doors outwards. Without insulin. That is why people with type 2 diabetes take up glucose normally during exercise, even though their cells respond poorly to insulin at rest.¹¹

So the walk from the previous section is not only a moral choice. It activates a second route to the same doors.

_{A deliberately simplified diagram, made for this article. It shows the idea, not the molecular reality: inside the cell the doors are stored in small vesicles, and the liver works through a different mechanism.}

After that, glucose goes three ways. Burned. Stored as fuel in muscle and liver. Or, when too much keeps arriving, towards fat.

Remember this, because it is almost never said: an insulin peak after eating is not a disease. It is exactly what should happen. A body that makes no insulin after a meal is a sick body.

The problem is not the peak. It is the pattern.

The storeroom that talks back

Fat is not the enemy. Fat is the storeroom your body built when nobody knew what a supermarket was. Under your skin it does useful work: reserve, insulation, a cushion around your joints.

It goes wrong when fat settles where it does not belong. In your liver cells, and between and within your muscle fibres. This is called ectopic fat, which literally means “in the wrong place”.¹⁰

So where fat sits says more than what percentage it makes up. And even the place is not the whole story. When researchers in Pittsburgh looked at the muscle fat of trained endurance athletes, it turned out to be high. Yet they were highly sensitive to insulin. What set them apart was their muscles’ capacity to burn that fat.¹²

For a long time fat tissue was seen as a passive storeroom. Bags of reserve, otherwise silent. That turns out to be wrong. Fat cells continuously release signalling substances into your blood that influence your hunger, your immune system and your metabolism.¹⁰

As long as the fat cells are not overfull, that stream of messages is calm and helpful. Once they do become overfull, the tone changes. The mix shifts towards inflammation. And precisely those substances disturb the route along which insulin delivers its message.¹⁰

A quiet storeroom becomes a room that talks back. And not kindly.

Insulin resistance, in five sentences

Social media loves this word. It is simpler than it sounds.

1. You eat. Energy arrives.
2. Insulin asks your cells to open doors.
3. Behind those doors it is already full, because for years more came in than went out.
4. The cell therefore responds more slowly to the request.
5. Your pancreas notices this and does the only thing it can: shout louder. More insulin.

The signal arrives, but there is no room left to act on it, so the shouting gets louder. An important caveat: this is one model, not the model. The mechanisms differ per organ, and genetics, liver fat, inflammation and energy balance all play a part.¹⁰

Now the part people rarely hear. Your blood sugar can stay perfectly normal for years while your body works harder and harder to keep it there. That is the silent phase. A good result does not always mean a calm system.

The danger does not lie in insulin itself. It lies in the price of that louder shouting. Eventually the cells that make insulin cannot keep up the pace. Then blood sugar does rise, and type 2 diabetes becomes visible.¹⁰

One warning belongs here immediately. You do not diagnose insulin resistance in yourself. Not with a single home measurement, not with a spike on a glucose sensor, and certainly not with a checklist from social media. That is work for your GP, with blood tests and context.

And it is not on or off. Insulin sensitivity is a dial, not a switch. It is not fixed at birth, and it does not depend on your plate alone.

And then the question that really matters

Is it reversible? For some people, yes.

In the DiRECT trial almost three hundred people with type 2 diabetes received, through their GP practice, either usual care or a closely supervised programme with a period of liquid nutrition and long-term support. After two years, 36 per cent of the programme group were in remission, against 3 per cent in the control group.¹³

Notice what is not said. It does not say that cutting sugar did this. What predicted remission was sustained weight loss. Of the 45 participants who had held on to at least ten kilograms, 64 per cent were in remission.¹³

And the cracks are here too. This was a supervised programme, not a tip. The participants were selected, and two thirds were not in remission after two years. Remission is also not a cure: diabetes can return.

Why drinks stand apart

With sugary drinks two very different consequences come together.

The first is your teeth. The World Health Organization calls the relationship between free sugars and caries clear and causal. Caries is also the most common noncommunicable disease in the world, affecting roughly 2.5 billion people.¹

This is the best-established direct effect of free sugars, and it is almost always forgotten in the debate about weight. The mechanism is simple: plaque converts free sugars into acid, and that acid slowly destroys the tooth.¹

The second is metabolic disease. A 2024 overview placed 47 meta-analyses side by side, together covering more than 22 million observations. In 79 per cent of the associations examined, more sugary drink went together with a less favourable outcome.

The strongest level of evidence applied to depression, cardiovascular disease, kidney stones, type 2 diabetes and higher uric acid. Slightly weaker, but still clear, was the link with liver fat and with caries.¹⁴

Strictness belongs here too. This is observational research. Researchers watched, they did not intervene. People who drink a lot of soft drinks often differ in other ways from people who do not.

Such studies therefore prove no cause. But the direction is strikingly consistent.

If you change one thing, change what is in the glass.

What “sugar-free” actually does

Cutting sugar has been compared with other ways of eating less. The outcome makes you read every nutrition video differently.

In 2024 a British research group divided sixty healthy adults into three groups for twelve weeks. The first ate less than 5 per cent of their energy as free sugars. The second carried on as usual, around 18 per cent. The third followed a ketogenic diet with almost no carbohydrate. Nobody was given a calorie target.

Even so, energy intake fell on its own in both restricting groups: by about 250 kcal per day with sugar restriction, and about 400 kcal on the ketogenic diet. Both groups lost fat mass, without any change in energy expenditure. Sugar restriction also lowered LDL cholesterol. On the ketogenic diet this did not happen.¹⁵

A meta-analysis then gathered all the experiments and long-running population studies on this question. Three numbers tell the story.

When people ate freely and reduced their sugar, they lost on average 0.80 kg. When they increased their sugar, they gained on average 0.75 kg. But when sugar was replaced by the same number of calories from other carbohydrates, the difference was 0.04 kg. Practically nothing.¹⁶

That same analysis also included cohort studies in children. Children with the highest intake of sugary drinks were more than one and a half times as likely to be overweight as children with the lowest intake.¹⁶

For body weight, extra energy therefore appears to be the main route by which higher sugar intake leads to weight gain. And extra energy is remarkably easy to take in through sugar, especially when you drink it.

But weight is not the whole story. For your teeth that reasoning does not apply. There, sugar causes damage that has nothing to do with calories.

The World Health Organization advises keeping free sugars below 10 per cent of your daily energy. That recommendation is strong. Going further, below 5 per cent, is a conditional recommendation, intended mainly as extra protection for your teeth.¹⁷

Made concrete: at 2,000 kcal a day, 10 per cent is about 50 grams, which the WHO converts to roughly twelve level teaspoons.¹⁸ The stricter limit of 5 per cent then works out at about 25 grams, or six teaspoons. For an entire day, including everything hidden in sauce, bread, yoghurt and biscuits.

The greatest gain sits in four places, in this order.

1. What you drink. Sugary drinks are among the best-evidenced and most influential places to start, and they are an immediate win for your teeth.
2. How processed it is. Not only because of the sugar itself, but because ultra-processed food is easier to overeat.
3. Whether you eat it or drink it. An apple and a glass of apple juice are not the same. The juice counts as free sugar, the whole apple does not.
4. Whether you choose it, or it happens to you. A chosen macaron on a Sunday is something other than a packet of biscuits emptying while you do something else.

In closing

I will go on wanting that macaron.

That craving is not a flaw in my character. It is a human response to a fast and reliable reward.

What has changed is not my hunger. It is the distance. Sweetness used to sit at the end of a long search. Now it sits on the route home.

Almost two thousand years ago Epictetus separated what is ours from what is not. Our judgement and our actions are. Our property, our reputation and the world around us are not.¹⁹

There are things which are within our power, and there are things which are beyond our power.

Epictetus

The bakery is not mine. Nor is the industry that supplies it. What is mine is what I make of it and what I do with it.

That is less than I would like. And it is enough.

What sits within arm’s reach in your home that you never consciously put there? And when did you last solve something not by trying harder, but by moving something?

This article provides general information and is not medical or psychological advice. If you have questions about your own health or wellbeing, please speak with your GP or a treating specialist. If you use blood-glucose-lowering medication or insulin, do not make large changes to your carbohydrate intake without consulting your own clinician.

---

Related reading

• The body is not a calculator
• Diet: what really works?
• Honey: superfood or just sugar?

---

Sources

The numbers in the text refer to this list.

1. World Health Organization. (2025, August 14). Sugars and dental caries [Fact sheet]. https://www.who.int/news-room/fact-sheets/detail/sugars-and-dental-caries
2. Mennella, J. A., & Bobowski, N. K. (2015). The sweetness and bitterness of childhood: Insights from basic research on taste preferences. Physiology & Behavior, 152(Pt B), 502–507. https://doi.org/10.1016/j.physbeh.2015.05.015
3. Garsmeur, O., Rio, S., Pompidor, N., Lipzen, A., Hervouet, C., Durand, T., Daum, C., Yoshinaga, Y., Butterfield, M., Sanchez, A., Piperidis, G., Lincoln, N., Hale, A., Hoarau, J. Y., Terajima, Y., Lakshmanan, P., Sacks, E., Sharma, S., Vitrac, M., … D’Hont, A. (2025). The genomic footprints of wild Saccharum species trace domestication, diversification, and modern breeding of sugarcane. Cell, 188(25), 7252–7266.e15. https://doi.org/10.1016/j.cell.2025.09.017
4. Marks, T. (2018, June 13). The story of sugar in 5 objects [Blog post]. British Museum. https://www.britishmuseum.org/blog/story-sugar-5-objects
5. Bartra, O., McGuire, J. T., & Kable, J. W. (2013). The valuation system: A coordinate-based meta-analysis of BOLD fMRI experiments examining neural correlates of subjective value. NeuroImage, 76, 412–427. https://doi.org/10.1016/j.neuroimage.2013.02.063
6. Westbrook, A., van den Bosch, R., Määttä, J. I., Hofmans, L., Papadopetraki, D., Cools, R., & Frank, M. J. (2020). Dopamine promotes cognitive effort by biasing the benefits versus costs of cognitive work. Science, 367(6484), 1362–1366. https://doi.org/10.1126/science.aaz5891
7. Salimpoor, V. N., Benovoy, M., Larcher, K., Dagher, A., & Zatorre, R. J. (2011). Anatomically distinct dopamine release during anticipation and experience of peak emotion to music. Nature Neuroscience, 14(2), 257–262. https://doi.org/10.1038/nn.2726
8. Westwater, M. L., Fletcher, P. C., & Ziauddeen, H. (2016). Sugar addiction: The state of the science. European Journal of Nutrition, 55(Suppl. 2), 55–69. https://doi.org/10.1007/s00394-016-1229-6
9. Hall, K. D., Ayuketah, A., Brychta, R., Cai, H., Cassimatis, T., Chen, K. Y., Chung, S. T., Costa, E., Courville, A., Darcey, V., Fletcher, L. A., Forde, C. G., Gharib, A. M., Guo, J., Howard, R., Joseph, P. V., McGehee, S., Ouwerkerk, R., Raisinger, K., … Zhou, M. (2019). Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism, 30(1), 67–77.e3. https://doi.org/10.1016/j.cmet.2019.05.008
10. Petersen, M. C., & Shulman, G. I. (2018). Mechanisms of insulin action and insulin resistance. Physiological Reviews, 98(4), 2133–2223. https://doi.org/10.1152/physrev.00063.2017
11. Alvim, R. O., Cheuhen, M. R., Machado, S. R., Sousa, A. G. P., & Santos, P. C. J. L. (2015). General aspects of muscle glucose uptake. Anais da Academia Brasileira de Ciências, 87(1), 351–368. https://doi.org/10.1590/0001-3765201520140225
12. Goodpaster, B. H., He, J., Watkins, S., & Kelley, D. E. (2001). Skeletal muscle lipid content and insulin resistance: Evidence for a paradox in endurance-trained athletes. The Journal of Clinical Endocrinology & Metabolism, 86(12), 5755–5761. https://doi.org/10.1210/jcem.86.12.8075
13. Lean, M. E. J., Leslie, W. S., Barnes, A. C., Brosnahan, N., Thom, G., McCombie, L., Peters, C., Zhyzhneuskaya, S., Al-Mrabeh, A., Hollingsworth, K. G., Rodrigues, A. M., Rehackova, L., Adamson, A. J., Sniehotta, F. F., Mathers, J. C., Ross, H. M., McIlvenna, Y., Welsh, P., Kean, S., … Taylor, R. (2019). Durability of a primary care-led weight-management intervention for remission of type 2 diabetes: 2-year results of the DiRECT open-label, cluster-randomised trial. The Lancet Diabetes & Endocrinology, 7(5), 344–355. https://doi.org/10.1016/S2213-8587(19)30068-3
14. Lane, M. M., Travica, N., Gamage, E., Marshall, S., Trakman, G. L., Young, C., Teasdale, S. B., Dissanayaka, T., Dawson, S. L., Orr, R., Jacka, F. N., O’Neil, A., Lawrence, M., Baker, P., Rebholz, C. M., Du, S., & Marx, W. (2024). Sugar-sweetened beverages and adverse human health outcomes: An umbrella review of meta-analyses of observational studies. Annual Review of Nutrition, 44(1), 383–404. https://doi.org/10.1146/annurev-nutr-062322-020650
15. Hengist, A., Davies, R. G., Walhin, J.-P., Buniam, J., Merrell, L. H., Rogers, L., Bradshaw, L., Moreno-Cabañas, A., Rogers, P. J., Brunstrom, J. M., Hodson, L., van Loon, L. J. C., Barton, W., O’Donovan, C., Crispie, F., O’Sullivan, O., Cotter, P. D., Proctor, K., Betts, J. A., … Gonzalez, J. T. (2024). Ketogenic diet but not free-sugar restriction alters glucose tolerance, lipid metabolism, peripheral tissue phenotype, and gut microbiome: RCT. Cell Reports Medicine, 5(8), Article 101667. https://doi.org/10.1016/j.xcrm.2024.101667
16. Te Morenga, L., Mallard, S., & Mann, J. (2013). Dietary sugars and body weight: Systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ, 346, Article e7492. https://doi.org/10.1136/bmj.e7492
17. World Health Organization. (2015). Guideline: Sugars intake for adults and children. https://www.who.int/publications/i/item/9789241549028
18. World Health Organization. (2026, January 26). Healthy diet [Fact sheet]. https://www.who.int/news-room/fact-sheets/detail/healthy-diet
19. Epictetus. (2014). The Enchiridion (T. W. Higginson, Trans.). Project Gutenberg. https://www.gutenberg.org/ebooks/45109

Sources on this site are cited in APA style, with a DOI wherever one exists. Why I made that choice →