When a person stops eating, the body enters a highly adaptive, programmed survival state that dramatically shifts its fuel sources. This metabolic transition is designed to conserve vital tissues, primarily protein, for as long as possible. Whether the cessation of eating is voluntary, such as during fasting, or involuntary due to illness or starvation, the physiological progression follows a predictable timeline focused on energy conservation. The body manages this change by sequentially depleting its available energy reserves to ensure the brain and other organs can continue to operate.
The Initial Metabolic Shift
The immediate reaction to the absence of food focuses on consuming the most readily available fuel: glucose. During the first 24 to 48 hours without caloric intake, the body relies heavily on stored glycogen, a complex carbohydrate found primarily in the liver and muscles. The liver breaks down this glycogen through glycogenolysis to release glucose directly into the bloodstream, maintaining stable blood sugar levels for the brain and red blood cells.
As glycogen reserves become depleted, typically within about a day, the body begins ramping up gluconeogenesis. This is the creation of new glucose, mainly from non-carbohydrate sources like the glycerol backbone of fat molecules and specific amino acids derived from protein breakdown. Falling insulin levels and rising counter-regulatory hormones, such as glucagon and cortisol, signal the body to initiate lipolysis, the breakdown of stored fat. This marks the transition from using sugar as the primary fuel to using fat.
Sustained Starvation and Energy Conservation
After the initial shift, often past the 72-hour mark, the body enters a phase of sustained fat utilization and protein conservation. The breakdown of fat into fatty acids becomes the dominant energy source for most tissues, including skeletal and cardiac muscle. The liver converts a portion of these fatty acids into ketone bodies, specifically acetoacetate and beta-hydroxybutyrate, which are released into the bloodstream.
This process, known as ketogenesis, is an adaptation because the brain cannot directly use fatty acids for fuel. The brain gradually begins to use ketones as a substitute for glucose, potentially providing up to 75% of its energy needs during prolonged periods without food. By supplying the brain with this alternate fuel source, the body significantly reduces its need to break down muscle protein for gluconeogenesis, conserving lean mass. The body also lowers its basal metabolic rate, or energy expenditure, to stretch the remaining fat reserves.
Severe Long-Term Systemic Consequences
Once the body’s fat reserves are exhausted, the metabolic strategy shifts from conservation to consumption of functional tissue. This late stage of starvation is marked by the accelerated breakdown of structural and functional proteins, including those in the heart, liver, and skeletal muscles. The body is forced to use these proteins as the primary source for gluconeogenesis to produce the minimal amount of glucose required by the central nervous system.
This consumption of lean tissue leads to profound muscle wasting, including the atrophy of the diaphragm, which compromises respiratory function. The heart muscle begins to shrink, resulting in starvation-induced cardiomyopathy, manifesting as a slow heart rate and reduced cardiac output. Electrolyte imbalances become severe, including low levels of potassium, magnesium, and phosphate, which can lead to fatal cardiac arrhythmias. The immune system is severely impaired due to the lack of necessary proteins, making the body vulnerable to infection.
Resuming Eating
When nutrition is abruptly reintroduced after a prolonged period of little or no intake, a potentially fatal condition known as Refeeding Syndrome can occur. The sudden influx of carbohydrates triggers a rapid surge in insulin secretion, an anabolic, or building, hormone. Insulin causes cells to quickly take up glucose, along with water, phosphate, potassium, and magnesium, to rapidly synthesize new glycogen, fat, and protein molecules.
Because the body’s electrolyte stores are already severely depleted during starvation, this sudden intracellular shift causes dangerously low levels of phosphate, potassium, and magnesium in the bloodstream. Hypophosphatemia, the hallmark of this syndrome, can impair cellular energy production, leading to respiratory failure, seizures, and cardiac arrest. Reintroducing food must be done gradually and carefully, often with close medical monitoring and proactive electrolyte supplementation, to prevent these complications.