Starvation response in animals (including humans) is a set of adaptive biochemical and physiological changes, triggered by lack of food or extreme weight loss, in which the body seeks to conserve energy by reducing metabolic rate and/or non-resting energy expenditure to prolong survival and preserve body fat and lean mass. Equivalent or closely related terms include famine response, starvation mode, famine mode, starvation resistance, starvation tolerance, adapted starvation, adaptive thermogenesis, fat adaptation, and metabolic adaptation.
In humans Ordinarily, the body responds to reduced energy intake by firstly exhausting the contents of the digestive tract along with glycogen reserves present in both muscle and liver cells through glycogenolysis. After prolonged periods of starvation, this store of glycogen runs out, and the body then starts burning fat reserves and consuming muscle and other tissues. It uses the proteins within muscle tissue as a fuel source, which results in loss of muscle mass.
Magnitude and composition The magnitude and composition of the starvation response (metabolic adaptation) was estimated in a study of 8 individuals living in isolation in Biosphere 2 for two years. During their isolation, they gradually lost an average of 15% (range: 9–24%) of their body weight due to the harsh conditions. On emerging from isolation, the eight isolated individuals were compared with a 152-person control group that initially had similar physical characteristics. On average, the starvation response of the individuals after isolation was a 750-kilojoule (180-kilocalorie) reduction in daily total energy expenditure. 250 kJ (60 kcal) of the starvation response was explained by a reduction in fat-free mass and fat mass. An additional 270 kJ (65 kcal) was explained by a reduction in fidgeting. The remaining 230 kJ (55 kcal) was statistically insignificant.
General The energetic requirements of a body are composed of the basal metabolic rate (BMR) and the physical activity level (ERAT, exercise-related activity thermogenesis). This caloric requirement can be met with protein, fat, carbohydrates, or a mixture of those. Glucose is the general metabolic fuel, and can be metabolized by any cell. Fructose and some other nutrients can be metabolized only in the liver, where their metabolites transform into either glucose stored as glycogen in the liver and in muscles, or into fatty acids stored in adipose tissue. Because of the blood–brain barrier, getting nutrients to the human brain is especially dependent on molecules that can pass this barrier. The brain itself consumes about 18% of the basal metabolic rate; on a total daily intake of 7,500 kJ (1,800 kcal), this equates to 1,360 kJ (324 kcal), or about 80 g of glucose. About 25% of total body glucose consumption occurs in the brain. Glucose can be obtained directly from dietary sugars and by the breakdown of other carbohydrates. In the absence of dietary sugars and carbohydrates, glucose is obtained from the breakdown of stored glycogen. Glycogen is a readily-accessible storage form of glucose, stored in notable quantities in the liver and skeletal muscle. When the glycogen reserve is depleted, glucose can be obtained from the breakdown of fats from adipose tissue. Fats are broken down into glycerol and free fatty acids, with the glycerol being turned into glucose in the liver through the gluconeogenesis pathway. When even the glucose made from glycerol reserves start declining, the liver starts producing ketone bodies. Ketone bodies are short-chain derivatives of the free fatty acids mentioned in the previous paragraph, and can cross the blood–brain barrier, meaning they can be used by the brain as an alternative metabolic fuel. Fatty acids can be used directly as an energy source by most tissues in the body, but are themselves too ionized to cross the blood–brain barrier.
Timeline
After the exhaustion of the glycogen reserve, and for the next 2–3 days, fatty acids are the principal metabolic fuel. At first, the brain continues to use glucose, because if a non-brain tissue is using fatty acids as its metabolic fuel, the use of glucose in the same tissue is switched off. Thus, when fatty acids are being broken down for energy, all of the remaining glucose is made available for use by the brain. After 2 or 3 days of fasting, the liver begins to synthesize ketone bodies from precursors obtained from fatty acid breakdown. The brain uses these ketone bodies as fuel, thus cutting its requirement for glucose. After fasting for 3 days, the brain gets 30% of its energy from ketone bodies. After 4 days, this goes up to 75%. Thus, the production of ketone bodies cuts the brain's glucose requirement from 80 g per day to about 30 g per day. Of the remaining 30 g requirement, 20 g per day can be produced by the liver from glycerol (itself a product of fat breakdown). This still leaves a deficit of about 10 g of glucose per day that must come from some other source. This deficit is supplied via gluconeogenesis from amino acids from proteolysis of body proteins. After several days of fasting, all cells in the body begin to break down protein. This releases amino acids into the bloodstream, which can be converted into glucose by the liver. Since much of the human body's muscle mass is protein, this phenomenon is responsible for the wasting away of muscle mass seen in starvation. However, the body can selectively decide which cells break down protein and which do not. About 2–3 g of protein must be broken down to synthesize 1 g of glucose; about 20–30 g of protein is broken down each day to make 10 g of glucose to keep the brain alive. However, to conserve protein, this number may decrease the longer the fasting. Starvation ensues when the fat reserves are completely exhausted and protein is the only fuel source available to the body. Thus, after periods of starvation, the loss of body protein affects the function of important organs, and death results, even if there are still fat reserves left unused. (In a leaner person, the fat reserves are depleted earlier, the protein depletion occurs sooner, and therefore death occurs sooner.) The ultimate cause of death is, in general, cardiac arrhythmia or cardiac arrest brought on by tissue degradation and electrolyte imbalances. In the very obese, it has been shown that proteins can be depleted first. Accordingly, death from starvation is predicted to occur before fat reserves are used up.
… excerpt ends here. Continue reading the full article.
