A fasting girl was one of a number of young Victorian girls, usually pre-adolescent, who claimed to be able to survive over indefinitely long periods of time without consuming any food or other nourishment. In addition to refusing food, fasting girls claimed to have special religious or magical powers.

The ability to survive without nourishment was attributed to some saints during the Middle Ages, including Catherine of Siena and Lidwina of Schiedam, and regarded as a miracle and a sign of sanctity. Numerous cases of fasting girls were reported in the late 19th century. Believers regarded such cases as miraculous.

In some cases, the fasting girls also exhibited the appearance of stigmata. Doctors, however, such as William A. Hammond ascribed the phenomenon to fraud and hysteria on the part of the girl. Historian Joan Jacobs Brumberg believes the phenomenon to be an early example of anorexia nervosa.

Anorexia mirabilis literally means "miraculous lack of appetite". It refers almost exclusively to women and girls of the Middle Ages who would starve themselves, sometimes to the point of death, in the name of God. The phenomenon is also known by the name inedia prodigiosa ("prodigious fasting").

Obesity in Sweden has been increasingly cited as a major health issue in recent years. Sweden is the 90th fattest country in the world. In 2009, the number of people who are considered obese and overweight had not increased for the first time in 70 years. Claude Marcus, a leading Swedish nutrition expert from the Karolinska Institutet, stated that one solution is to introduce a fat tax. Folksam refused to insure a 5-year-old girl from Orust. The insurance company refused her insurance based on "serious overweight/obesity". A report showed that children whose parents were better educated had a lower chance of becoming fat.

Causes of hunger are related to poverty. There are inter-related issues causing hunger, which are related to economics and other factors that cause poverty. They include land rights and ownership, diversion of land use to non productive use, increasing emphasis on export oriented agriculture, inefficient agricultural practices, war, famine, drought, over fishing, poor crop yield, etc.

The basic cause of starvation is an imbalance between energy intake and energy expenditure. In other words, the body expends more energy than it takes in. This imbalance can arise from one or more medical conditions or circumstantial situations, which can include:

Medical reasons

- Anorexia nervosa

- Bulimia nervosa

- Eating disorder, not otherwise specified

- Celiac disease

- Coma

- Major depressive disorder

- Diabetes mellitus

- Digestive disease

- Constant vomiting

Circumstantial causes

- Child/ Elder/ Dependent Abuse

- Faminefor any reason, such as political strife and war

- Excessive fasting

- Poverty

The main causes of starvation are as follows:

- Economy; poor people sometimes cannot buy enough foodstuffs and thereby fail to fulfill the caloric demands of the body.

- Food scarcity in the society. This causes a decreased supply of food to the whole of the population, and thus mass starvation may occur.

- Diseases that can cause rapid weight loss either due to the nature of the disease or the inability of the person to either eat or eat enough due to symptoms including fatigue, nausea, and vomiting. The person may also be the host to a parasite such as an intestinal worm which may take a significant amount of the calories ingested by its host. This effect is exacerbated if the human host is already ingesting far less food than is required to meet their daily caloric intake needs.

- Clinical conditions, such as recovering from surgery or burns, etc., in which the person may be too fatigued or incapacitated to eat enough during their period of convalescence.

Early symptoms include impulsivity, irritability, and hyperactivity. Atrophy (wasting away) of the stomach weakens the perception of hunger, since the perception is controlled by the percentage of the stomach that is empty. Individuals experiencing starvation lose substantial fat (adipose tissue) and muscle mass as the body breaks down these tissues for energy. "Catabolysis" is the process of a body breaking down its own muscles and other tissues in order to keep vital systems such as the nervous system and heart muscle (myocardium) functioning. The energy deficiency inherent in starvation causes fatigue and renders the victim more apathetic over time. As the starving person becomes too weak to move or even eat, their interaction with the surrounding world diminishes. In females, menstruation ceases when the body fat percentage is too low to support a fetus.

Victims of starvation are often too weak to sense thirst, and therefore become dehydrated. All movements become painful due to muscle atrophy and dry, cracked skin that is caused by severe dehydration. With a weakened body, diseases are commonplace. Fungi, for example, often grow under the esophagus, making swallowing painful. Vitamin deficiency is also a common result of starvation, often leading to anemia, beriberi, pellagra, and scurvy. These diseases collectively can also cause diarrhea, skin rashes, edema, and heart failure. Individuals are often irritable and lethargic as a result.

There is insufficient scientific data on exactly how long people can live without food. Although the length of time varies with an individual's percentage of body fat and general health, one medical study estimates that in adults complete starvation leads to death within 8 to 12 weeks. There are isolated cases of individuals living up to 25 weeks without food. Starvation begins when an individual has lost about 30% of their normal body weight. Once the loss reaches 40% death is almost inevitable.

Lack of exercise along with sugar-sweetened foods and drinks have caused one out of six five-year-olds in Sweden to be overweight or obese. The breakdown is 12.9% of children are considered overweight and 4.3% are considered obese.

The symptoms include many of the symptoms associated with milder degrees of hypoglycemia, especially the adrenergic symptoms, but do not progress to objective impairment of brain function, seizures, coma, or brain damage.

- Shakiness

- Sense of weakness

- Altered or depressed mood

- Confusion

- Fatigue

- Anxiety

- Paleness

- Perspiration

- Increased pulse or respiratory rate

- Hunger

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.

People with this condition suffer from recurrent episodes of altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness. The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars.

Transmisogyny (sometimes trans-misogyny) is the intersection of transphobia and misogyny. Transphobia is defined as "the irrational fear of, aversion to, or discrimination against transgender or transsexual people". Misogyny is defined as "a hatred of women". Therefore, transmisogyny includes negative attitudes, hate, and discrimination of transgender or transsexual individuals who fall on the feminine side of the gender spectrum, particularly transgender women. The term was coined by Julia Serano in her 2007 book "Whipping Girl" and used to describe the unique discrimination faced by trans women because of "the assumption that femaleness and femininity are inferior to, and exist primarily for the benefit of, maleness and masculinity", and the way that transphobia intensifies the misogyny faced by trans women (and vice versa). It is said many trans women experience an additional layer of misogyny in the form of fetishization; Serano talks about how society views trans women in certain ways that sexualize them, such as them transitioning for sexual reasons, or ways where they’re seen as sexually promiscuous.Transmisogyny is a central concept in transfeminism and is commonly referenced in intersectional feminist theory. That trans women's femaleness (rather than only their femininity) is a source of transmisogyny is denied by certain radical feminists, who claim that trans women are not female.

Ketotic hypoglycemia is a medical term used in two ways: (1) broadly, to refer to any circumstance in which low blood glucose is accompanied by ketosis, and (2) in a much more restrictive way to refer to recurrent episodes of hypoglycemic symptoms with ketosis and, often, vomiting, in young children. The first usage refers to a pair of metabolic states (hypoglycemia plus ketosis) that can have many causes, while the second usage refers to a specific "disease" called ketotic hypoglycemia.

Ketotic hypoglycemia more commonly refers to a common but mysterious "disease" of recurrent hypoglycemic symptoms with ketosis in young children. The cause and the homogeneity of the condition remain uncertain, but a characteristic presentation, precipitating factors, diagnostic test results, treatment, and natural history can be described. It remains one of the more common causes of hypoglycemia in the age range.

Ketosis is a metabolic state in which some of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides energy. Ketosis is a result of metabolizing fat to provide energy.

Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose. It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate, and the levels of ketone bodies are regulated mainly by insulin and glucagon. Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder.

Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes. In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed. For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.

Ketosis and ketoacidosis are similar, but ketoacidosis is an acute life-threatening state requiring prompt medical intervention while ketosis can be physiological. However, there are situations (such as treatment-resistant epilepsy) where ketosis can be rather beneficial to health.

Signs and symptoms can include:

- hypoglycemia

- lethergy

- hepatomegaly

- muscle pain

- cardiomyopathy

Very long-chain acyl-coenzyme A dehydrogenase deficiency (VLCADD) is a fatty-acid metabolism disorder which prevents the body from converting certain fats to energy, particularly during periods without food.

Those affected by this disorder have inadequate levels of an enzyme that breaks down a group of fats called very long-chain fatty acids.

Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

- Shakiness, anxiety, nervousness

- Palpitations, tachycardia

- Sweating, feeling of warmth (sympathetic muscarinic rather than adrenergic)

- Pallor, coldness, clamminess

- Dilated pupils (mydriasis)

- Hunger, borborygmus

- Nausea, vomiting, abdominal discomfort

- Headache

Ketone bodies are acidic, but acid-base homeostasis in the blood is normally maintained through bicarbonate buffering, respiratory compensation to vary the amount of CO in the bloodstream, hydrogen ion absorption by tissue proteins and bone, and renal compensation through increased excretion of dihydrogen phosphate and ammonium ions. Prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, defined as acidosis if blood pH falls below 7.35.

There are two major causes of ketoacidosis:

- Most commonly, ketoacidosis is diabetic ketoacidosis (DKA), resulting from increased fat metabolism due to a shortage of insulin. It is associated primarily with type I diabetes, and may result in a diabetic coma if left untreated.

- Alcoholic ketoacidosis (AKA) presents infrequently, but can occur with acute alcohol intoxication, most often following a binge in alcoholics with acute or chronic liver or pancreatic disorders. Alcoholic ketoacidosis occurs more frequently following methanol or ethylene glycol intoxication than following intoxication with uncontaminated ethanol.

A mild acidosis may result from prolonged fasting or when following a ketogenic diet or a very low calorie diet.

Prediabetes typically has no distinct signs or symptoms except the sole sign of high blood sugar. Patients should monitor for signs and symptoms of type 2 diabetes mellitus. These include the following:

- Constant hunger

- Unexplained weight loss

- Weight gain

- Flu-like symptoms, including weakness and fatigue

- Blurred vision

- Slow healing of cuts or bruises

- Tingling or loss of feeling in hands or feet

- Recurring gum or skin infections

- Recurring vaginal or bladder infections

- A high BMI (Body Mass Index) result

Impaired fasting glucose is often without any signs or symptoms, other than higher than normal glucose levels being detected in an individual's fasting blood sample. There may be signs and symptoms associated with elevated blood glucose, though these are likely to be minor, with significant symptoms suggestive of complete progression to type 2 diabetes. Such symptoms include:

- Increased thirst

- Increased urination, especially waking up in the night to urinate

- Tiredness and fatigue

- Blurred vision

- Slow healing of wounds

- Altered sensation, such as numbness or tingling, particularly of the hands and feet

- Recurrent, and difficult to clear infections, particularly of the urinary tract

In fructose bisphosphatase deficiency, there is not enough fructose bisphosphatase for gluconeogenesis to occur correctly. Glycolysis (the breakdown of glucose) will still work, as it does not use this enzyme.

Typically, initial signs and symptoms of this disorder occur during infancy or early childhood and can include feeding difficulties, lethargy, hypoglycemia, hypotonia, liver problems, and abnormalities in the retina. Muscle pain, a breakdown of muscle tissue, and abnormalities in the nervous system that affect arms and legs (peripheral neuropathy) may occur later in childhood. There is also a risk for complications such as life-threatening heart and breathing problems, coma, and sudden unexpected death. Episodes of LCHAD deficiency can be triggered by periods of fasting or by illnesses such as viral infections.

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may also vary by age, by severity of the hypoglycemia and the speed of the decline. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, as well as previous incidents.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or "spells." Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed "hypoglycemia unawareness" and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Hypoglycemic symptoms can also occur when one is sleeping. Examples of symptoms during sleep can include damp bed sheets or clothes from perspiration. Having nightmares or the act of crying out can be a sign of hypoglycemia. Once the individual is awake they may feel tired, irritable, or confused and these may be signs of hypoglycemia as well.

In nearly all cases, hypoglycemia that is severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Research in healthy adults shows that mental efficiency declines slightly but measurably as blood glucose falls below 3.6 mM (65 mg/dL). Hormonal defense mechanisms (adrenaline and glucagon) are normally activated as it drops below a threshold level (about 55 mg/dL (3.0 mM) for most people), producing the typical hypoglycemic symptoms of shakiness and dysphoria. Obvious impairment may not occur until the glucose falls below 40 mg/dL (2.2 mM), and many healthy people may occasionally have glucose levels below 65 in the morning without apparent effects. Since the brain effects of hypoglycemia, termed neuroglycopenia, determine whether a given low glucose is a "problem" for that person, most doctors use the term "hypoglycemia" only when a moderately low glucose level is accompanied by symptoms or brain effects.

Determining the presence of both parts of this definition is not always straightforward, as hypoglycemic symptoms and effects are vague and can be produced by other conditions; people with recurrently low glucose levels can lose their threshold symptoms so that severe neuroglycopenic impairment can occur without much warning, and many measurement methods (especially glucose meters) are imprecise at low levels.

It may take longer to recover from severe hypoglycemia with unconsciousness or seizure even after restoration of normal blood glucose. When a person has not been unconscious, failure of carbohydrate to reverse the symptoms in 10–15 minutes increases the likelihood that hypoglycemia was not the cause of the symptoms. When severe hypoglycemia has persisted in a hospitalized person, the amount of glucose required to maintain satisfactory blood glucose levels becomes an important clue to the underlying etiology. Glucose requirements above 10 mg/kg/minute in infants, or 6 mg/kg/minute in children and adults are strong evidence for hyperinsulinism. In this context this is referred to as the "glucose infusion rate" (GIR). Finally, the blood glucose response to glucagon given when the glucose is low can also help distinguish among various types of hypoglycemia. A rise of blood glucose by more than 30 mg/dl (1.70 mmol/l) suggests insulin excess as the probable cause of the hypoglycemia.

Without effective gluconeogenesis (GNG), hypoglycaemia will set in after about 12 hours of fasting. This is the time when liver glycogen stores have been exhausted, and the body has to rely on GNG. When given a dose of glucagon (which would normally increase blood glucose) nothing will happen, as stores are depleted and GNG doesn't work. (In fact, the patient would already have high glucagon levels.)

There is no problem with the metabolism of glucose or galactose, but fructose and glycerol cannot be used by the liver to maintain blood glucose levels. If fructose or glycerol are given, there will be a buildup of phosphorylated three-carbon sugars. This leads to phosphate depletion within the cells, and also in the blood. Without phosphate, ATP cannot be made, and many cell processes cannot occur.

High levels of glucagon will tend to release fatty acids from adipose tissue, and this will combine with glycerol that cannot be used in the liver, to make triacylglycerides causing a fatty liver.

As three carbon molecules cannot be used to make glucose, they will instead be made into pyruvate and lactate. These acids cause a drop in the pH of the blood (a metabolic acidosis). Acetyl CoA (acetyl co-enzyme A) will also build up, leading to the creation of ketone bodies.

Mary J. "Mollie" Fancher (August 16, 1848 – February, 1916), otherwise known as the "Brooklyn Enigma", was extremely well known for her claim of not eating, or eating very little for extended periods of time. She attended a reputable school and, by all reports, was an excellent student. At age 16, she was diagnosed with dyspepsia. At around the age of 19, reports came out that she had abstained from eating for seven weeks.

It was after two accidents, in 1864 and 1865, that she became famous for her ability to abstain from food. As a result of the accidents, Mollie Fancher lost her ability to see, touch, taste, and smell. She claimed to have powers that involved her being able to predict events as well as to read without the ability of sight.

By the late 1870s, she was claiming to eat little or nothing at all for many months. Her claim to abstinence from food lasted for 14 years. Doctors and people in the public began to question her abilities and wished to perform tests to determine the truthfulness of her claims. The claims to abstinence were never verified, and she died in February 1916.

Impaired fasting glucose, or Impaired Fasting "Glycemia" (IFG) is a type of prediabetes, in which a person's blood sugar levels during fasting are consistently above the normal range, but below the diagnostic cut-off for a formal diagnosis of diabetes mellitus. Together with impaired glucose tolerance, it is a sign of insulin resistance. In this manner, it is also one of the conditions associated with Metabolic Syndrome.

Those with impaired fasting glucose are at an increased risk of vascular complications of diabetes, though to a lesser extent. The risks are cumulative, with both higher blood glucose levels, and the total amount of time it spends elevated, increasing the overall complication rate.

IFG can eventually progress to type 2 diabetes mellitus without intervention, which typically involves lifestyle modification. Those with impaired fasting glucose have a 1.5 fold increased risk of developing clinical diabetes within 10 years, when compared to the general population. Some studies suggest that without lifestyle changes, IFG will progress to clinically diagnosable diabetes in just under 3 years, on average.

Impaired fasting glucose is often, though not always, associated with impaired glucose tolerance, though it may occur in isolation, with such persons having a normal response to a glucose tolerance test.

The clinical presentation is similar to people with congenital lipodystrophy: the only difference is that AGL patients are born with normal fat distribution and symptoms develop in childhood and adolescence years and rarely begins after 30 years of age. Females are more often affected than males, with ratio being 3:1.

The hallmark characteristics are widespread loss of subcutaneous fat, ectopic fat deposition, leptin deficiency, and severe metabolic abnormalities such as insulin resistance. Subcutaneous fat loss in AGL patients are visible in all parts of the body. AGL mostly affects face and the extremities and may look sunken or swollen in the eyes. However, the degree and location of severity may vary by person. Especially, intra-abdominal fat loss is variable. As subcutaneous fat is lost, affected areas show prominent structures of veins and muscle. Those with panniculitis-associated AGL may present erythematous nodules.

Metabolic complications include insulin resistance, high metabolic rate, and uncontrolled lipid levels such as hypertriglyceridemia, low HDL, and high LDL. Patients may develop diabetes mellitus secondary to insulin resistance.

Recent case reports reveled that lymphoma is present in some patients but its prevalence is not known at this time.