The plain English glossary.

Released by pancreatic beta cells. Insulin instructs muscle, liver, and fat cells to take up circulating glucose. After repeated high-sugar meals, cells become less responsive — the start of insulin resistance.

Years of chronic high insulin levels (hyperinsulinemia) precede measurable type 2 diabetes by a decade or more. Reversible in early stages through carbohydrate reduction and time-restricted eating.

High insulin sensitivity means your body needs less insulin to clear glucose from the blood. Improved by exercise, sleep, time-restricted eating, and sugar reduction. Insulin sensitivity declines naturally with age but is substantially modifiable through diet.

Can persist for 10–15 years before HbA1c is flagged. The Kraft 1975 protocol identified hyperinsulinemia decades before the diagnostic frameworks caught up.

Half of sucrose (table sugar) is glucose; half is fructose. Glucose triggers insulin; fructose largely does not.

Unlike glucose, fructose metabolism has no feedback brake. The liver converts excess fructose into fat (de novo lipogenesis) and uric acid. Foundational to the fructose-NAFLD-gout chain.

Distinct from hereditary fructose intolerance (HFI), which is a rare genetic disorder. Fructose malabsorption is more common and produces bloating, gas, and diarrhoea after high-fructose meals. Often co-occurs with IBS and improves on a low-FODMAP diet.

Cane sugar, beet sugar, brown sugar, caster sugar — all sucrose. Roughly 50% fructose by weight once digested.

Cheaper than sucrose; widely used in US-manufactured soft drinks. Slightly higher fructose ratio than sucrose, with similar metabolic consequences in most studies.

The mechanism behind non-alcoholic fatty liver disease (NAFLD). When fructose intake exceeds the liver's processing capacity, it shunts the excess into triglycerides and stores them in hepatocytes.

Elevated uric acid causes gout, contributes to NAFLD progression, and is associated with hypertension. The feedback loop: more fructose → more uric acid → upregulated fructokinase → more fructose metabolism.

A Pavlovian anticipatory response. The brain signals the pancreas via the vagus nerve within seconds of food cues. CPIR is blunted in type 2 diabetes but exaggerated in obesity — the insulin spike arrives before the glucose does.

GLUT4 is the insulin-responsive transporter in muscle and fat; it moves to the cell surface when insulin binds. GLUT2 is insulin-independent and found in the liver and pancreas. GLUT1 handles baseline glucose uptake in most tissues, including the brain.

Nutritional ketosis (blood ketones 0.5–3.0 mmol/L) is distinct from diabetic ketoacidosis. The brain can derive up to ~70% of its energy from ketones. Ketosis suppresses hunger via BHB signalling and reduces reactive oxygen species.

In obesity, the brain stops responding to leptin (leptin resistance). High-sugar diets accelerate leptin resistance within ~16 days.

Like insulin resistance but for satiety. Drives chronic hunger even with high body fat stores. Reversible with carbohydrate reduction and weight stabilization over months.

Normally drops after a meal. High-sugar diets blunt that post-meal drop, leaving you hungry even after eating.

GLP-1 receptor agonists like semaglutide (Ozempic) mimic this hormone pharmacologically. A high-sugar diet weakens natural GLP-1 secretion — quitting sugar restores it slowly.

Chronic stress elevates cortisol, which both raises blood glucose and stimulates cravings for high-energy foods. Box-breathing and parasympathetic-reset techniques drop cortisol measurably.

Chronic HPA axis activation (from psychological stress, sleep deprivation, or inflammation) elevates cortisol and drives sugar cravings independently of hunger. The stress→cortisol→sugar→dopamine loop is one of the strongest drivers of compulsive eating.

Amylin acts as insulin's partner: insulin clears glucose from blood; amylin slows the arrival of more glucose by delaying stomach emptying. Both are impaired in type 2 diabetes. Pramlintide (Symlin) is a synthetic amylin analogue used clinically.

Gut hormones GLP-1 and GIP are responsible for this ~50–70% amplification. The incretin effect is blunted in type 2 diabetes, which is why GLP-1 receptor agonists are effective pharmacologically — they restore what the gut should be doing naturally.

Sugar triggers dopamine release in the nucleus accumbens. With chronic exposure, the brain downregulates D2 receptors — requiring more sugar to feel the same.

Both food and drug addictions converge on the same nucleus accumbens dopamine pathway. Neuroimaging shows sugar-habituated and cocaine-habituated brains have remarkably similar receptor density patterns.

Johnson & Kenny 2010 showed striatal D2 receptor knockdown produced compulsive eating that persisted through 15 days of abstinence. The craving outlasts the sugar — and so does the recovery.

Dopamine spikes when a reward is better than expected, drops when it is worse, and flatlines when it is exactly predicted. Sugar exploits this: hyperpalatable foods produce a larger-than-expected dopamine signal that drives future craving even when hunger is absent.

Sugar withdrawal symptoms (headache, fatigue, irritability, intense craving) peak at days 3–5 and taper over 2–3 weeks. Mechanistically similar to mild opioid withdrawal.

Dependence refers to the body's adaptation: receptor changes, withdrawal symptoms on cessation, and tolerance (needing more for the same effect). Addiction adds the behavioural dimension of compulsive use despite harm. Most people with sugar dependence do not meet addiction criteria — but the dependence itself drives hard-to-resist craving.

Repeated pairing of sugar with specific contexts creates Pavlovian triggers: the 3pm office biscuit, the cinema popcorn, the post-dinner chocolate. The cue itself triggers dopamine anticipation, making the behaviour feel automatic. Breaking these conditioning loops is central to sugar-quit success.

Useful in isolation but misleading in practice — a high-GI food in a small portion can have a lower real-world impact than a moderate-GI food in a large portion. Use Glycemic Load instead.

GL = (GI × grams of carbohydrate per serving) / 100. A watermelon has GI of 72 but a serving has GL of only 5. What you eat matters; how much you eat matters more.

WHO recommends ≤25g/day of added sugar for meaningful health benefit. The average UK adult consumes 60–80g/day; the average American consumes 71g/day.

Crucially includes fruit juice (even 100% pure) because the fibre matrix has been removed. Whole fruit is excluded.

Class 1: unprocessed (apple). Class 2: cooking ingredients (oil, butter). Class 3: processed (bread, cheese). Class 4: ultra-processed (most packaged supermarket food). Class 4 is the primary delivery vehicle for added sugar.

Studies consistently show UPF consumption correlates with weight gain, cardiometabolic disease, and all-cause mortality. The mechanism likely combines hyperpalatability, low satiety, and additive effects.

Improves insulin sensitivity independently of what you eat. Compresses the period of insulin elevation, allowing longer windows of low-insulin metabolic repair.

The same meal eaten at 8am produces a smaller glucose excursion than at 8pm — insulin sensitivity follows a circadian rhythm. Late-night eating, especially of sugar, works against the body's natural metabolic clock and is independently associated with weight gain and insulin resistance.

Originally developed for type 1 diabetes management, CGMs are now marketed to the general wellness market (Levels, Veri, Nutrisense). They reveal individual glucose responses to foods that differ substantially from published GI values — the same banana can spike one person and barely move another's glucose.

US incidence rose 15-fold between 1990 and 2024. People with metabolic syndrome carry 5× the T2D risk.

Driven largely by fructose-induced de novo lipogenesis. The first quiet domino in the metabolic disease cascade — often present for years before diagnosis.

Affects ~35% of UK adults. Carries 5× T2D risk and 4× dementia risk.

Emerging research framework suggesting chronic hyperinsulinemia drives neuroinflammation and amyloid accumulation. Not a formal diagnostic category — but increasingly cited.

Tightly linked to fructose intake — fructose metabolism generates uric acid. Modern gout prevalence tracks the rise in HFCS consumption in soft drinks.

Hyperinsulinemia drives ovarian androgen production. Carbohydrate reduction is a first-line lifestyle intervention.

Sheiham & James 2014 showed a dose-response relationship: each 1% reduction in sugar-energy reduces caries risk roughly proportionally. The single most preventable disease in modern dentistry.

Caused by an exaggerated insulin response overshooting the glucose load. The resulting low blood sugar triggers adrenaline and cortisol — the 'hangry' state. Clinically defined as blood glucose <3.9 mmol/L with symptoms that resolve on eating. Common in early insulin resistance.

Originally developed for type 2 diabetes; now widely prescribed for weight loss (Ozempic, Wegovy, Mounjaro). They slow gastric emptying, increase insulin secretion, and reduce appetite via brain GLP-1 receptors. Their effectiveness indirectly demonstrates how powerful the gut-brain satiety axis is.

HbA1c ≥ 48 mmol/mol (6.5%) is diagnostic for type 2 diabetes. 42–47 mmol/mol indicates prediabetes. Unlike a finger-prick glucose reading, HbA1c cannot be gamed by fasting the night before — it shows the real long-term picture.

AGEs form when sugar molecules bind irreversibly to proteins, cross-linking them and impairing function. They accumulate in skin (wrinkling), arteries (stiffening), kidneys, and the lens of the eye (cataracts). AGE formation accelerates when blood glucose is chronically elevated.

The popular '21 days to form a habit' is folklore. Real-world habit research shows wide individual variation. Simpler habits form faster; behaviour change involving substance withdrawal sits at the longer end.

Most full relapses begin as lapses that shame turns into spirals. Reframing 'I broke my streak' as 'tomorrow is day one again' is the single most protective behavioural move.

Gollwitzer's research showed implementation intentions roughly double the rate at which goals translate into action — by removing the in-the-moment decision burden.

'I'm trying not to drink soda' vs 'I'm not someone who drinks soda' — the identity framing reduces in-the-moment willpower demand because the decision is already made.

Marlatt-derived technique. Most cravings peak at 5–8 minutes and resolve naturally. The 10-minute rule is the most evidence-backed sub-pharmaceutical intervention for any craving.

In operant conditioning, when a previously rewarded behaviour stops being rewarded, the organism often tries harder before giving up. For sugar quitting, this means cravings may intensify around days 3–7 before tapering. Knowing it is coming — and that it signals the habit is dying — reduces the risk of relapse.

Two-tier (above 5g/100ml and above 8g/100ml). Reformulation has reduced UK sugar intake from soft drinks by an estimated 30%. A rare modern public-health intervention with measurable impact.

The conditional recommendation for meaningful health benefit. The unconditional recommendation is ≤50g/day.

SSBs account for ~25% of UK added-sugar intake in adolescents. Unlike solid food sugar, liquid sugar bypasses satiety signals, produces a rapid glucose+ fructose spike, and contributes to weight gain independently of total calorie intake. The UK Soft Drinks Industry Levy specifically targets SSBs.