Tag: Knowledge recall

Your brain makes food decisions like an economist: weighing cost (effort, time) against expected reward. Research by Rangel shows the brain’s decision circuitry computes value based on effort and reward. Thaler and Sunstein’s “nudge” framework (a trade book’s case rather than a measurement) treats defaults as driving choices. Lower cost + higher reward = more likely to choose. This may be why convenient junk food so often wins. The solution: make healthy choices lower cost and unhealthy choices higher cost. This companion covers neural economics, why junk food wins, restructuring the equation, the environment lever, and defaults. (4 min read)

Health halos change how people judge food. Research by Schuldt found people rated organic Oreos as lower in calories than identical conventional ones, and judged it more acceptable for someone to skip exercise after an organic dessert. Whether halos make people eat more is disputed between reviews. This companion covers the health halo effect, the research, why it happens, and practical implications for awareness. (3 min read)

The liver is your metabolic command center: processing nutrients, regulating blood sugar, and managing fat storage. It is the primary site of fructose metabolism, extracting 50-70% of it on first pass. Research by Stanhope showed that fructose-sweetened beverages increased visceral fat while glucose-sweetened ones did not. When you consume fructose (from sugar, HFCS, or juice), the liver converts part of it to fat through de novo lipogenesis, a pathway fructose enters readily, because it bypasses the regulatory checkpoint that governs glucose. Excess fructose can overwhelm the liver, contributing to fatty liver disease and insulin resistance. This companion covers the liver’s…

On Jason Fung’s framing insulin is a switch, high meaning store fat and low meaning release it, though the transition is graded rather than a toggle. Ludwig’s carbohydrate-insulin model proposes that chronically elevated insulin keeps fat cells in storage mode; that is a proposal, not a demonstration. When you eat, insulin signals fat cells to take up fatty acids and blocks their release. During fasting, the brake lifts. This companion covers insulin’s dual role, the fasting state, why meal timing matters, and practical applications including creating insulin gaps. (4 min read)

Mostly because it doesn’t need to, though the reason usually given is argued rather than shown. During short-term fasting the body has ample fat stores to burn, and elevated growth hormone is often credited with sparing protein, though the one direct test found it mobilizing fat and not sparing protein. What the trials show is narrower: fasting cost no more lean mass than daily dieting, and neither preserved it. This companion explores the hormonal account, the research on fasting and muscle retention, when muscle loss does happen, and the myth’s origin. (4 min read)

Willpower’s limit is not that it runs out: it’s that it has to work every single time. Any arrangement depending on you to resist the same thing daily asks for an unbroken run of wins, and the food only has to win once. The familiar explanation is ego depletion, a resource drained by use; large preregistered replications have found effects indistinguishable from zero, though the question is unsettled rather than closed. The argument holds either way. This companion explores where that model now stands, why evenings are vulnerable, why willpower alone fails long-term, and what works better: environment design, habits,…

Every time you eat, insulin rises. On the carbohydrate-insulin account (a model that remains debated, with the underlying physiology undisputed and the human evidence for the model as a whole inconclusive), constant snacking keeps insulin elevated and the body never shifts toward stored fuel. One measured piece sits underneath it: people with mild blood sugar dips after a glucose challenge snack about six times more often than those without, though the absolute figures are modest at 0.9 occasions a day against 0.15. This companion explores the storage-burning switch, the snacking trap, what the “healthy snack” argument does and doesn’t establish,…

Table sugar is half glucose, half fructose, and your body handles them differently. Glucose goes everywhere, regulated by insulin. Fructose goes primarily to the liver, bypasses insulin, and readily converts to fat. Studies show fructose rapidly increases liver fat when substituted for other carbohydrates at equal calories. This companion explores what glucose does, what fructose does, why the combination may be worse than either alone, and why whole fruit is metabolically different from added sugar. (4 min read)

Your brain stem is a key hub for satiety signals. It receives real-time information from your gut (how much you’ve eaten, what you’ve eaten, how stretched your stomach is) and integrates all of this into the feeling of fullness that tells you to stop eating. This happens below conscious awareness. You don’t calculate when to stop; you feel full. That feeling is the brain stem’s output. This companion explores the two systems regulating eating, the gut-brain highway via the vagus nerve, why meal termination isn’t conscious, and what generates strong satiety signals. (4 min read)

Regular exercise may improve the body’s appetite regulation, not only burn calories. Habitual exercisers may have better-calibrated appetite systems, though over long periods people eat back most of what exercise burns. This companion explores the compensation problem, how exercise may improve leptin sensitivity, the time course of these changes, and why exercise may work better as a recalibration tool than as a calorie burner. (4 min read)