Overnutrition or hyperalimentation is a form of malnutrition in which the intake of nutrients is oversupplied. The amount of nutrients exceeds the amount required for normal growth, development, and metabolism.

The term can also refer to:

- Obesity, which "usually" occurs by overeating, as well as:

- Oversupplying a "specific" nutrient, such as dietary minerals or vitamin poisoning. This is due to an excessive intake or a nutritional imbalance caused by fad diets.

For mineral excess, see:

- Iron poisoning, and

- Low sodium diet (a response to excess sodium).

Overnutrition may also refers to greater food consumption than appropriate, as well as other feeding procedures such as parenteral nutrition.

Snakes that consume a diet largely composed of goldfish and feeder minnows are susceptible to developing thiamine deficiency. This is often a problem observed in captivity when keeping garter and ribbon snakes that are fed a goldfish-exclusive diet, as these fish contain thiaminase, an enzyme that breaks down thiamine.

Polioencephalomalacia (PEM) is the most common thiamine deficiency disorder in young ruminant and nonruminant animals. Symptoms of PEM include a profuse, but transient, diarrhea, listlessness, circling movements, star gazing or opisthotonus (head drawn back over neck), and muscle tremors. The most common cause is high-carbohydrate feeds, leading to the overgrowth of thiaminase-producing bacteria, but dietary ingestion of thiaminase (e.g., in bracken fern), or inhibition of thiamine absorption by high sulfur intake are also possible. Another cause of PEM is "Clostridium sporogenes" or "Bacillus aneurinolyticus" infection. These bacteria produce thiaminases that will cause an acute thiamine deficiency in the affected animal.

The effects of HG on the fetus are mainly due to electrolyte imbalances caused by HG in the mother. Infants of women with severe hyperemesis who gain less than 7 kg (15.4 lb) during pregnancy tend to be of lower birth weight, small for gestational age, and born before 37 weeks gestation. In contrast, infants of women with hyperemesis who have a pregnancy weight gain of more than 7 kg appear similar to infants from uncomplicated pregnancies. There is no significant difference in the neonatal death rate in infants born to mothers with HG compared to infants born to mothers who do not have HG. Children born to mothers with undertreated Hyperemesis have a fourfold increase in neurobehavioral diagnoses.

Vomiting is a common condition affecting about 50% of pregnant women, with another 25% having nausea. However, the incidence of HG is only 0.3–1.5%. After preterm labor, hyperemesis gravidarum is the second most common reason for hospital admission during the first half of pregnancy. Factors such as infection with "Helicobacter pylori", a rise in thyroid hormone production, low age, low body mass index prior to pregnancy, multiple pregnancies, molar pregnancies, and a past history of hyperemesis gravidarum have been associated with the development of HG.

Overeating is the excess food in relation to the energy that an organism expends (or expels via excretion), leading to weight gaining

and often obesity. It may be regarded as an eating disorder.

This term may also be used to refer to specific episodes of over-consumption. For example, many people overeat during festivals or while on holiday.

Overeating can sometimes be a symptom of binge eating disorder or bulimia.

Compulsive over eaters depend on food to comfort themselves when they are stressed, suffering bouts of depression, and have feelings of helplessness.

In a broader sense, hyperalimentation includes excessive food administration through other means than eating, e.g. through parenteral nutrition.

Cognitive behavioural therapy, individual therapy, and group therapy are often beneficial in helping people keep track of their eating habits and changing the way they cope with difficult situations.

There are several 12-step programs that helps overeaters, such as Overeaters Anonymous or Food Addicts in Recovery Anonymous and others.

It is quite clear through research, and various studies that overeating causes addictive behaviors.

In some instances, overeating has been linked to the use of medications known as dopamine agonists, such as pramipexole.

Once a child is born prematurely, thought must be given to decreasing the risk for developing NEC. Toward that aim, the methods of providing hyperalimentation and oral feeds are both important. In a 2012 policy statement, the American Academy of Pediatrics recommended feeding preterm infants human milk, finding "significant short- and long-term beneficial effects," including reducing the rate of NEC by a factor of two or more.

A study by researchers in Peoria, IL, published in "Pediatrics" in 2008, demonstrated that using a higher rate of lipid (fats and/or oils) infusion for very low birth weight infants in the first week of life resulted in zero infants developing NEC in the experimental group, compared with 14% with NEC in the control group. (They started the experimental group at 2 g/kg/d of 20% IVFE and increased within two days to 3 g/kg/d; amino acids were started at 3 g/kg/d and increased to 3.5.)

Neonatologists at the University of Iowa reported on the importance of providing small amounts of trophic oral feeds of human milk starting as soon as possible, while the infant is being primarily fed intravenously, in order to prime the immature gut to mature and become ready to receive greater oral intake. Human milk from a milk bank or donor can be used if mother's milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed.

A Cochrane review published in April 2014 has established that supplementation of probiotics enterally "prevents severe NEC as well as all-cause mortality in preterm infants."

Increasing amounts of milk by 30 to 40 ml/kg is safe in infant who are born weighing very little. Not beginning feeding an infant by mouth for more than 4 days does not appear to have protective benefits.

Data from the NICHD Neonatal Research Network's Glutamine Trial showed that the incidence of NEC among extremely low birthweight (ELBW, <1000 g) infants fed with more than 98% human milk from their mothers was 1.3%, compared with 11.1% among infants fed only preterm formula, and 8.2% among infants fed a mixed diet, suggesting that infant deaths could be reduced by efforts to support production of milk by mothers of ELBW newborns.

Research from the University of California, San Diego found that higher levels of one specific human milk oligosaccharide, disialyllacto-N-tetraose, may be protective against the development of NEC.

Typical recovery from NEC if medical, non-surgical treatment succeeds, includes 10–14 days or more without oral intake and then demonstrated ability to resume feedings and gain weight. Recovery from NEC alone may be compromised by co-morbid conditions that frequently accompany prematurity. Long-term complications of medical NEC include bowel obstruction and anemia.

In the United States it caused 355 deaths per 100,000 live births in 2013, down from 484 per 100,000 live births in 2009. Rates of death were almost three times higher for the black populations than for the white populations.

Overall, about 70-80% of infants who develop NEC survive. Medical management of NEC shows an increased chance of survival compared to surgical management. Despite a significant mortality risk, long-term prognosis for infants undergoing NEC surgery is improving, with survival rates of 70–80%. "Surgical NEC" survivors are at risk for complications including short bowel syndrome and neurodevelopmental disability.

In general, the cause of a hyperchloremic metabolic acidosis is a "loss of base", either a gastrointestinal loss or a renal loss.

- Gastrointestinal loss of bicarbonate ()

- Severe diarrhea (vomiting will tend to cause hypochloraemic alkalosis)

- Pancreatic fistula with loss of bicarbonate rich pancreatic fluid

- Nasojejunal tube losses in the context of small bowel obstruction and loss of alkaline proximal small bowel secretions

- Chronic laxative abuse

- Renal causes

- Proximal renal tubular acidosis with failure of resorption

- Distal renal tubular acidosis with failure of secretion

- Long-term use of a carbonic anhydrase inhibitor such as acetazolamide

- Other causes

- Ingestion of ammonium chloride, hydrochloric acid, or other acidifying salts

- The treatment and recovery phases of diabetic ketoacidosis

- Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3-4L can cause acidosis

- Hyperalimentation ("i.e.", total parenteral nutrition)

Hyperchloremic acidosis is a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma bicarbonate concentration, and an increase in plasma chloride concentration (see anion gap for a fuller explanation). Although plasma anion gap is normal, this condition is often associated with an "increased" urine anion gap, due to the kidney's inability to secrete ammonia.

The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of "acidosis"):

- Hyperalimentation

- Acetazolamide and other carbonic anhydrase inhibitors

- Renal tubular acidosis

- Diarrhea: due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na and Cl, results in a decrease in the plasma Na concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringer’s solution are used instead of normal saline to replace GI losses.

- Ureteroenteric fistula - an abnormal connection (fistula) between a ureter and the gastrointestinal tract

- Pancreaticoduodenal fistula - an abnormal connection between the pancreas and duodenum

- Spironolactone

As opposed to high anion gap acidosis (which involves increased organic acid production), normal anion gap acidosis involves either increased production of chloride (hyperchloremic acidosis) or increased excretion of bicarbonate.

In renal physiology, normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is "not" accompanied by an abnormally increased anion gap.

The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second.

Delay in the diagnosis of SMA syndrome can result in fatal catabolysis (advanced malnutrition), dehydration, electrolyte abnormalities, hypokalemia, acute gastric rupture or intestinal perforation (from prolonged mesenteric ischemia), gastric distention, spontaneous upper gastrointestinal bleeding, hypovolemic shock, and aspiration pneumonia.

A 1-in-3 mortality rate for Superior Mesenteric Artery syndrome has been quoted by a small number of sources. However, after extensive research, original data establishing this mortality rate has not been found, indicating that the number is likely to be unreliable. While research establishing an official mortality rate may not exist, two recent studies of SMA syndrome patients, one published in 2006 looking at 22 cases and one in 2012 looking at 80 cases, show mortality rates of 0% and 6.3%, respectively. According to the doctors in one of these studies, the expected outcome for SMA syndrome treatment is generally considered to be excellent.

SMA syndrome is extremely rare, evident in only 0.3% of upper-gastrointestinal-tract barium studies. However, unfamiliarity with this condition in the medical community coupled with its intermittent and nonspecific symptomatology probably results in its underdiagnosis.

As the syndrome involves a lack of essential fat, more than half of those diagnosed are underweight, sometimes to the point of sickliness and emaciation. Females are impacted more often than males, and while the syndrome can occur at any age, it is most frequently diagnosed in early adulthood. The most common co-morbid conditions include mental and behavioral disorders including eating disorders and depression, infectious diseases including tuberculosis and acute gastroenteritis, and nervous system diseases including muscular dystrophy, Parkinson's disease, and cerebral palsy.