Your metabolic system is how your body turns food into energy and decides what to do with the rest. Every time you eat, your body has to burn this food for fuel now, store it as glycogen (carbs) for short-term use, store it as fat for long-term reserves, or use it as building material for muscle, hormones, and tissue. Those decisions are made on a meal-by-meal basis by a handful of hormones and organs working in coordination, the pancreas, liver, fat tissue, muscle, gut, and brain all talking to each other constantly.
Energy production
The body runs on a single energy currency called ATP (adenosine triphosphate). Every muscle contraction, every thought, every cell division, every protein built, every signal sent, all of it is paid for in ATP.
The body has three fuels available:
- Glucose is the fastest. It can be burned with or without oxygen, keeping muscles at force during a sprint even when oxygen supply can't keep up. Glucose comes from the carbohydrates you eat, from glycogen broken down in the liver and muscles, or from gluconeogenesis (the liver manufacturing glucose from amino acids, glycerol, and lactate).
- Fat is the slowest but the densest. One gram of fat yields more than twice the ATP of one gram of glucose, but fat can only be burned with oxygen, making fat the dominant fuel during low-intensity activity and during long fasts. Fat comes from dietary fat or from triglycerides stored in adipose tissue.
- Protein is rarely a primary fuel. It's expensive to convert and the amino acids are usually doing more important jobs as building blocks for muscle, enzymes, and hormones. The body falls back on protein for fuel only when carbohydrates and fat are inadequate. When this happens, the liver converts amino acids to glucose, and the source of those amino acids is often muscle tissue.
At any given moment, the body is burning a mix of fuels, and the ratio depends on:
- Activity intensity. Low intensity (walking, resting, sleeping) favours fat oxidation. High intensity (sprinting, heavy lifting) demands glucose because it's the only fuel fast enough to keep up.
- Recent food intake. A high-carb meal pushes the body toward burning glucose for hours afterwards while insulin is elevated. A fasted state shifts toward fat oxidation
- Glycogen status. Full muscle and liver glycogen biases the body toward burning glucose. Depleted glycogen biases it toward burning fat and sparing remaining glucose for the brain.
The hormone running this whole decision tree most of the time is insulin. When insulin is high, the body is in storage and glucose-burning mode. When insulin is low, the body is in fat-burning mode.
Calories
Your body burns calories in four ways.
Basal metabolic rate (BMR) is what your body burns just keeping you alive. Heart pumping, lungs breathing, brain running, organs working, body temperature regulated, cells dividing and repairing. BMR accounts for roughly 60-75% of daily calorie burn for most people and by far the biggest line item. BMR is determined by body composition with muscle is more metabolically active.
Non-exercise activity thermogenesis (NEAT) is every calorie you burn moving outside of formal exercise. Walking, fidgeting, standing, taking the stairs, doing dishes, pacing on the phone. NEAT accounts for roughly 15-30% of daily burn (highly dependent on what you do for work etc). NEAT is also the variable that drops the hardest when you diet.
Thermic effect of food (TEF) is the energy cost of digesting and metabolising what you eat. Different macronutrients have wildly different TEFs:
- Protein: 20-30% of its calories spent on digestion
- Carbs: 5-10%
- Fat: 0-3%
Eating 200g of protein costs you roughly 200-300 calories just to process. Eating the same calories from fat costs almost nothing. TEF accounts for roughly 10% of daily burn for most people.
Activity (exercise) is the calories you burn during deliberate training. The frustrating truth is this is the smallest line item for most people, roughly 5-15% of daily burn. A hard hour-long lifting session burns 300-500 calories. A 5km run burns about 300. This is also why exercise alone is a weak fat loss lever.
Insulin and glucagon
Insulin and glucagon are the two hormones that manage blood sugar. Both are produced by the pancreas, and they work as a constant balancing pair.
Insulin is released when blood sugar rises (after eating). It tells cells throughout the body to pull glucose out of the bloodstream and store it. Insulin also activates mTOR (the master switch for muscle growth), prevents the breakdown of fat stores, and promotes cell growth and repair.
Glucagon is released when blood sugar drops too low (between meals, during exercise, during fasting). It signals the liver to break down its stored glycogen and release glucose back into the bloodstream. Glucagon is the release signal.
Left unchecked, high blood sugar is toxic to blood vessels, nerves, and organs. Too low and the brain, which runs almost entirely on glucose, starts to malfunction (shakiness, confusion, in severe cases unconsciousness, aka hypoglycemia). The constant push-pull between insulin and glucagon is what keeps blood sugar in the narrow range the body needs.
Decades of chronic high-carb intake, physical inactivity, visceral fat, and metabolic strain can wear this system down. The pancreas keeps producing insulin, but cells stop responding to it properly. This is insulin resistance, and it's where most modern metabolic disease starts. The pancreas compensates by pumping out more insulin, which works for a while, but over years the beta cells become exhausted from chronic overwork and their ability to fire strongly weakens. Blood sugar climbs higher after meals and stays elevated longer than it should. This progression, normal → insulin resistant → impaired insulin secretion → type 2 diabetes, can take 10-20 years and is largely invisible until late.
Carbohydrates
When you eat carbohydrates, the digestive system breaks them down into glucose. That glucose enters the bloodstream, and blood sugar rises. The pancreas detects this and releases insulin, which travels to cells throughout the body and binds to insulin receptors on their surface. This signals the cell to open special glucose transporters called GLUT4, essentially a door letting glucose enter the cell.
Blood from your intestines flows directly to the liver first through a dedicated vessel called the portal vein, so the liver sees all incoming glucose before the rest of the body does. From there, three things can happen:
1. The liver acts as the gatekeeper, taking up glucose and making a decision based on how full its glycogen stores already are. If stores are low (from exercise or fasting), it prioritises refilling them. The liver can hold roughly 100g.
2. Muscle cells pull glucose from the blood and store it as glycogen, but only if insulin is opening the GLUT4 door. Without a strong insulin signal the muscle glycogen tank stays empty even if there's plenty of glucose circulating right outside. Your muscles can hold roughly 400g of glycogen total, used purely as their own fuel for movement and recovery.
3. If liver and muscle glycogen are already full, the liver shifts to converting the excess glucose into fatty acids and shipping them out to fat tissue as triglycerides. This conversion process is called de novo lipogenesis.
If insulin signalling is too weak, glucose can't get into cells efficiently and just stays circulating in the blood. Chronically elevated blood sugar is corrosive over time, damaging the walls of blood vessels, the nerves, the kidneys, and the eyes. This is why uncontrolled diabetes causes blindness, kidney failure, and nerve damage in the extremities.
Gluconeogenesis
When glycogen stores run low and no dietary carbs are arriving the liver manufactures glucose from scratch pulling from three raw materials:
- Amino acids from protein, either from food or broken down from muscle tissue.
- Glycerol from fat tissue, released when stored fat gets broken down for energy.
- Lactate produced by muscles during intense exercise, recycled back to the liver and converted into glucose to be used again
This is why blood sugar stays relatively stable even during prolonged fasting or very low carb diets. The liver is continuously manufacturing glucose from whatever raw materials are available. And why, when dietary protein is insufficient, the liver increasingly raids muscle tissue to get the amino acids it needs.
Two routes into fat tissue
There are two completely independent ways the body stores fat.
Dietary fat (from meat, butter, oil, cheese) gets digested in the small intestine, packaged into particles called chylomicrons, and shipped directly into the lymphatic system and then the bloodstream. From there it goes straight to fat tissue. You get fat simply from eating fat.
Excess carbohydrates that the liver converts via de novo lipogenesis when glycogen stores are already full. This route only runs heavily when you're consistently eating far more carbohydrates than your body can store or burn.
GLP-1
GLP-1 (Glucagon-Like Peptide-1) is one of the primary signals in that system. It is produced by L-cells, specialized cells embedded in the lining of the small and large intestine. They sit with a tiny sensory tip facing into the intestinal cavity, essentially tasting what is passing through. When nutrients arrive, particularly fats, proteins, and fermented fiber byproducts, they release GLP-1 into the surrounding blood vessels.
GLP-1 starts rising in the blood within minutes of eating, before food has physically traveled down to those L-cells. Suggesting a neurological component.
What GLP-1 does
In the brain, GLP-1 receptors in the hypothalamus receive the signal a feeling of fullness, and reduced reward-driven eating (food becomes less compelling). This is why on GLP-1 drugs food stops being interesting.
In the stomach, GLP-1 slows gastric emptying, meaning food moves from your stomach into the small intestine more gradually. This blunts the spike in blood sugar after a meal and extends the feeling of fullness.
In the pancreas, GLP-1 tells beta cells to release insulin when blood sugar is actually elevated. When blood sugar is normal or low, the pancreas largely ignores the GLP-1 signal.
In the heart, GLP-1 receptors have protective effects, reducing inflammation, improving blood flow, and supporting cardiac function.
In the kidneys, GLP-1 reduces inflammation in kidney tissue and influences sodium reabsorption in a way that lowers blood pressure.
In the liver, GLP-1 helps reduce fat accumulation and decreases glucose production.
Protein
Protein is not a fuel source like carbs or fat. It's a building material. Your muscles, organs, enzymes, hormones, and immune cells are all made from protein, and the body uses huge quantities of it every day just to maintain itself.
Proteins are built from smaller units called amino acids. There are 20 in total. 9 of them are essential, meaning your body can't make them and they have to come from food. The other 11 your body can synthesise itself.
Unlike carbs, the body has no dedicated protein storage tank. There is a small free amino acid pool in the blood and tissues but it depletes quickly.
Where protein actually goes
- Replace worn-out tissue. The gut lining turns over every 3-5 days. Skin cells turn over every 4-6 weeks. Red blood cells every 4 months. All of this requires a continuous supply of amino acids.
- Build enzymes. Including every enzyme that runs digestion, energy production, hormone synthesis, and detoxification. Enzymes wear out and need constant replacement.
- Build peptide hormones. Insulin, GLP-1, growth hormone, all the pituitary hormones, and most of the gut hormones are proteins.
- Build immune cells and antibodies. Antibodies are proteins. T-cells and B-cells need amino acids to function. Poor protein status directly compromises immunity.
- Build muscle. The largest protein pool in the body, and the one that responds most dramatically to training and dietary protein
The body cycles through roughly 250-300g of protein per day across all of this, whether you train or not. Most of it is recycled internally, but a meaningful fraction is lost, in urine, in shed cells, in the breakdown that doesn't get perfectly recovered. Dietary protein is what makes up the deficit.
Muscle protein synthesis vs muscle protein breakdown
Your muscles are never in a static state. Two processes run simultaneously at all times:
- Muscle protein synthesis (MPS) is the building process. New muscle protein being assembled from amino acids.
- Muscle protein breakdown (MPB) is the demolition process. Old or damaged muscle protein being dismantled back into its amino acids.
The balance between the two is called net protein balance:
Net protein balance = Muscle protein synthesis − Muscle protein breakdown
When synthesis exceeds breakdown, you are net positive and building muscle. When breakdown exceeds synthesis, you are net negative and losing muscle. When equal, you are maintaining.
Training shifts the balance hard toward synthesis. Mechanical damage from lifting fires mTOR strongly, cranking MPS far above its resting level. MPB increases slightly from the cortisol response, but MPS increases dramatically more. The net result tips heavily toward building, provided amino acids are available. Training hard without eating enough protein fires a strong synthesis signal with nothing to build from, while breakdown runs in the background and wins the tug of war.
If you eat more protein than the body can use for synthesis, the excess doesn't get stored. The liver converts the surplus amino acids into glucose via gluconeogenesis, or into fat via de novo lipogenesis (the glucose conversion is far more common).
This is also why aggressive weight cuts cost muscle. When dietary carbs are too low and glycogen runs out, the liver increasingly raids muscle tissue for amino acids to convert into glucose.
Fats
Fats are essential in ways that carbs are not. Carbs are the one macronutrient the body can actually manufacture itself through gluconeogenesis when needed. There are essential fatty acids the body cannot make and must get from food.
The four fat types
All fats are chains of carbon atoms with hydrogen atoms attached, but they differ in how those carbons are bonded together. That structural difference is what makes one fat liquid at room temperature and another solid, and it's what determines how the body uses each type.
Saturated fat is fully "saturated" with hydrogen, no double bonds between the carbon atoms. This makes it stable, solid at room temperature, and resistant to oxidation. Found mostly in animal products (red meat, dairy, butter, egg yolks) and a few plant sources (coconut oil, palm oil). The body uses saturated fat as a primary building block for cell membranes and as the substrate for steroid hormone production. It also raises LDL cholesterol in most people, which is where the cardiovascular debate sits. The simple story of the 80s and 90s ("saturated fat causes heart disease") was overstated and based on weak evidence. The more nuanced current view is that saturated fat does raise LDL and ApoB, but the magnitude of the effect varies hugely between individuals, and the food source matters (a slice of cheese is not the same as a piece of ultra-processed sausage).
Monounsaturated fat has one double bond in its carbon chain, making it liquid at room temperature but still relatively stable. Found in olive oil, avocado, nuts, and most seed-based foods. This is the fat type with the strongest "safe and probably beneficial" evidence base. The Mediterranean diet research keeps converging on monounsaturated fat as a marker of cardiovascular protection. It supports cell membrane fluidity (better than saturated fat for membrane signalling) and doesn't raise LDL the way saturated fat does. If you're choosing a default fat to cook with or build meals around, this is the safest bet.
Polyunsaturated fat (PUFA) has multiple double bonds in its carbon chain. Those extra bonds make the molecule more flexible, which is why PUFAs get used in places where cell membranes need to bend and signal quickly, especially brain tissue, retina, sperm cells, and synapses. They're also where the body's inflammation signals are built from, every prostaglandin, leukotriene, and resolvin that regulates the inflammatory response comes from a PUFA cleaved out of a cell membrane.
PUFAs come in two forms the body can't produce itself: omega-6 and omega-3. Both are technically essential, but practically only omega-3 is worth worrying about, omega-6 is in almost everything in the modern diet and deficiency is essentially impossible. The two have opposite effects on inflammation, and the balance between them is what matters.
The tradeoff with PUFAs is stability. Those extra double bonds that make them flexible also make them chemically reactive, which means they break down when heated, exposed to light, or left open to air for too long. This process is called oxidation (the same reaction that turns cut apples brown or rusts metal), and oxidised fats are pro-inflammatory and directly damaging to cells. This is why repeatedly fried seed oils are a problem, the underlying oil might have started fine, but the high-heat cooking and reuse converts it into damaged compounds.
Trans fat is fat that's been industrially modified to be more shelf-stable, originally created by hydrogenating vegetable oils to mimic the texture of butter. It's the only fat type with no biological role and clear harm, raising LDL, lowering HDL, promoting inflammation, and directly linked to cardiovascular disease. Most developed countries have effectively banned industrial trans fats from the food supply over the last decade, but trace amounts still show up in some processed foods, baked goods, and fried foods cooked in old oil. Worth avoiding without exception.
Omega-3 vs omega-6
Polyunsaturated fats are the raw material the body uses to build inflammation signals. When the body encounters an inflammatory trigger (tissue damage, infection, intense training), enzymes called COX and LOX cleave fatty acids directly out of cell membranes and convert them into signalling molecules. Which signal gets produced depends on which fatty acid was sitting in the membrane.
From arachidonic acid (the dominant omega-6 in cell membranes), those enzymes produce strong pro-inflammatory mediators, the molecules that amplify pain, swelling, redness, and clotting. This is the acute inflammatory response, and in the right context (fighting infection, initiating wound healing) it's necessary.
From EPA and DHA (the two main omega-3s), the same enzymes produce much weaker inflammatory signals, plus a separate class of molecules called resolvins and protectins, which actively resolve inflammation rather than just dampening it. EPA and DHA aren't anti-inflammatory in the sense of blocking the response, they make the response weaker and shorter.
The critical point is that EPA and arachidonic acid compete for the same positions in cell membranes. When your diet is heavy in omega-6, your membranes are loaded with arachidonic acid and every inflammatory trigger produces a strong, prolonged cascade. When your diet includes adequate omega-3, EPA displaces some of that arachidonic acid, less substrate for inflammatory mediators, more substrate for resolution.
Inflammation has two phases, mounting the response (swelling, immune cells arriving, pain signals firing) and shutting it down (immune cells leaving, debris cleared, tissue repair starting). Both phases need their own signalling molecules. The mounting signals come from omega-6. The shutdown signals (resolvins and protectins) come from omega-3. A high omega-6 diet means the body is well-supplied with the molecules that start inflammation but undersupplied with the molecules that end it. The on-switch fires strongly, the off-switch is weak. The response drags on instead of resolving cleanly, and the result is chronic low-grade inflammation that shows up on bloodwork as persistently elevated CRP, IL-6, and TNF-α.
Humans evolved on an omega-6 to omega-3 ratio of roughly 1-4:1. The modern Western diet sits between 15:1 and 25:1. You can't meaningfully fix this by cutting omega-6 (it's in virtually everything), which is why consuming 
Omega-3 directly is the practical lever.
The best dietary sources are fatty fish: salmon, mackerel, sardines, anchovies, and herring. Plant sources like flaxseed and walnuts contain ALA (a different omega-3), but conversion to EPA is extremely low (2-10%) and to DHA is near zero, making plant omega-3s a poor substitute for marine sources.
Why we need fat
Fuel. Fat is the body's most energy-dense fuel and the dominant one during low-intensity activity, sleep, and any prolonged fast. One gram of fat yields more than twice the ATP of one gram of glucose, which is why the body stores excess energy as fat in the first place.
Fat-soluble vitamins. Vitamins A, D, E, and K can only be absorbed in the presence of dietary fat. 
Vitamin D specifically supports muscle function, immune health, and bone density. Low fat intake compromises absorption of all four regardless of how much you supplement.
Cell membrane structure. Every single cell in the body has a fat-based outer membrane. Membrane composition directly affects how well insulin receptors sit on the cell surface, how efficiently GLUT4 transporters function, and how well mTOR signalling propagates inside the cell. This matters everywhere but especially in the brain, which is roughly 60% fat by dry weight and depends on fatty acid composition for everything from neurotransmitter signalling to learning and memory.
Hormone production. Testosterone, oestrogen, cortisol, and every other steroid hormone are built from cholesterol, which is a fat. The body can synthesise cholesterol itself, but dietary fat intake regulates how much it makes and how it gets transported. Chronically low fat intake (below roughly 20% of total calories) noticeably compromises steroid hormone production.
Practical target
Fat intake should be roughly 20 to 35% of total calories. Going below 20% starts compromising hormone production and cell membrane health noticeably.
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