Where your energy actually comes from — and why your body prefers carbohydrates over fat even when fat is available
The Krebs cycle is the engine at the centre of your metabolism. Understanding it explains why blood sugar spikes feel the way they do, why fat burning is slower, and what insulin is actually doing.
science
Every movement you make, every thought you have, every your body builds requires ATP — adenosine triphosphate. ATP is the universal energy currency of biology. You cannot store it in meaningful quantities; your cells produce and consume it continuously, turning over roughly your own body weight in ATP every day. The question of where that ATP comes from, and which fuel it comes from at any given moment, is the question at the centre of metabolic health.
The Krebs cycle — also known as the tricarboxylic acid cycle or citric acid cycle — is a closed loop of eight chemical reactions that takes place inside the mitochondria of every cell in your body. Its job is to take acetyl-CoA, a two-carbon molecule derived from the breakdown of fats or and extract the electrons stored in its chemical bonds. Those electrons are passed to carrier molecules called NADH and FADH2, which then carry them to the electron transport chain — the final stage where the vast majority of ATP is actually made. The Krebs cycle itself produces only a small amount of ATP directly; its primary role is to charge up these electron carriers.
enter the cycle via glycolysis — is broken down in the cytoplasm into pyruvate, which is converted to acetyl-CoA in the mitochondria. This process is fast, requires no oxygen in its early stages, and can produce ATP rapidly — which is why your muscles default to during high-intensity effort
Fats enter via beta-oxidation — fatty acids are broken down two carbons at a time into acetyl-CoA. This produces substantially more ATP per molecule than (a palmitic acid molecule yields roughly 129 ATP versus 32 for but the process is significantly slower. At rest, fat is the preferred fuel; under demand, takes over
Insulin is the hormone that clears from the bloodstream after a meal. When blood rises, the pancreas releases insulin, which signals cells to take up and either use it for energy or store it as in the liver and muscle. When stores are full, excess is converted to fat via de novo lipogenesis — a slower process that explains why consistently eating beyond energy needs leads to fat accumulation even on low-fat diets
The Krebs cycle is self-regulating — when ATP levels are high and the cell has sufficient energy, NADH accumulates and inhibits the enzymes that drive the cycle, slowing it down. When ATP is depleted and ADP accumulates, the cycle accelerates. The cell is continuously reading its own energy state and adjusting output accordingly
B vitamins are structural components of the electron carriers the Krebs cycle depends on — NAD+ is derived from (B3), FAD from (B2), and coenzyme A from pantothenic acid (B5). A deficiency in any of these impairs the cycle's ability to produce energy efficiently, which is part of why B vitamin deficiencies often present as persistent fatigue
The dominance of as a fuel source in modern diets is not just a consequence of what people eat — it is a consequence of the cycle's own kinetics. produces ATP faster than fat. After a carbohydrate-rich meal, blood rises, insulin rises, and the cell shifts toward oxidation and away from fat oxidation. Chronically elevated insulin — from chronically elevated blood from frequent intake — keeps fat burning suppressed for long periods of the day. This is not inherently harmful at normal metabolic health, but in the context of insulin resistance, it becomes a compounding problem.
Insulin resistance is a state in which cells stop responding normally to insulin's signal to take up The pancreas compensates by producing more insulin, which keeps blood roughly normal for years — while silently raising basal insulin levels, suppressing fat oxidation, driving more de novo lipogenesis, and loading the liver with fat. The Krebs cycle itself continues to run, but the substrates feeding it, and the hormonal environment controlling which substrates are used, shift in ways that progressively impair metabolic flexibility — the ability to switch efficiently between fat and as fuel.