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.

Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous. Wet beriberi is characterized by:

- Increased heart rate

- Vasodilation leading to decreased systemic vascular resistance, and high output cardiac failure

- Elevated jugular venous pressure

- Dyspnea (shortness of breath) on exertion

- Paroxysmal nocturnal dyspnea

- Peripheral edema (swelling of lower legs)

Gastrointestinal beriberi causes abdominal pain. Gastrointestinal beriberi is characterized by:

- Abdominal pain

- Nausea

- Vomiting

- Lactic acidosis

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.

When vomiting is severe it may result in the following:

- Loss of 5% or more of pre-pregnancy body weight

- Dehydration, causing ketosis, and constipation

- Nutritional disorders such as vitamin B1 (thiamine) deficiency, vitamin B6 deficiency or vitamin B12 deficiency

- Metabolic imbalances such as metabolic ketoacidosis or thyrotoxicosis

- Physical and emotional stress of pregnancy on the body

- Difficulty with activities of daily living

Symptoms can be aggravated by hunger, fatigue, prenatal vitamins (especially those containing iron), and diet. Many people with HG are extremely sensitive to odors in their environment; certain smells may exacerbate symptoms. Excessive salivation, also known as sialorrhea gravidarum, is another symptom experienced by some women.

Hyperemesis gravidarum tends to occur in the first trimester of pregnancy and lasts significantly longer than morning sickness. While most women will experience near-complete relief of morning sickness symptoms near the beginning of their second trimester, some sufferers of HG will experience severe symptoms until they give birth to their baby, and sometimes even after giving birth.

A small percentage rarely vomit, but the nausea still causes most (if not all) of the same issues that hyperemesis with vomiting does.

Hyperemesis gravidarum (HG) is a pregnancy complication that is characterized by severe nausea, vomiting, weight loss, and possibly dehydration. Signs and symptoms may also include vomiting several times a day and feeling faint. Hyperemesis gravidarum is considered more severe than morning sickness. Often symptoms get better after the 20th week of pregnancy but may last the entire pregnancy duration.

The exact causes of hyperemesis gravidarum are unknown. Risk factors include the first pregnancy, multiple pregnancy, obesity, prior or family history of HG, trophoblastic disorder, and a history of eating disorders. Diagnosis is usually made based on the observed signs and symptoms. HG has been technically defined as more than three episodes of vomiting per day such that weight loss of 5% or three kilograms has occurred and ketones are present in the urine. Other potential causes of the symptoms should be excluded including urinary tract infection and high thyroid levels.

Treatment includes drinking fluids and a bland diet. Recommendations may include electrolyte-replacement drinks, thiamine, and a higher protein diet. Some women require intravenous fluids. With respect to medications pyridoxine or metoclopramide are preferred. Prochlorperazine, dimenhydrinate, or ondansetron may be used if these are not effective. Hospitalization may be required. Psychotherapy may improve outcomes. Evidence for acupressure is poor.

While vomiting in pregnancy has been described as early as 2,000 BC, the first clear medical description of hyperemesis gravidarum was in 1852 by Antoine Dubois. Hyperemesis gravidarum is estimated to affect 0.3–2.0% of pregnant women. While previously known as a common cause of death in pregnancy, with proper treatment this is now very rare. Those affected have a low risk of miscarriage but a higher risk of premature birth. Some pregnant women choose to have an abortion due to HG's symptoms.

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.

The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth (i.e. the earlier a baby is born, the later signs of NEC are typically seen). Initial symptoms include feeding intolerance, increased gastric residuals, abdominal distension and bloody stools. Symptoms may progress rapidly to abdominal discoloration with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support.

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)

The diagnosis is usually suspected clinically but often requires the aid of diagnostic imaging modalities, most commonly radiography. Specific radiographic signs of NEC are associated with specific Bell's stages of the disease:

Bell's stage 1/Suspected disease:

- Mild systemic disease (apnea, lethargy, bradycardia, temperature instability)

- Mild intestinal signs (abdominal distention, increased gastric residuals, bloody stools)

- Non-specific or normal radiological signs

Bell's stage 2/Definite disease:

- Mild to moderate systemic signs

- Additional intestinal signs (absent bowel sounds, abdominal tenderness)

- Specific radiologic signs (pneumatosis intestinalis or portal venous air)

- Laboratory changes (metabolic acidosis, thrombocytopaenia)

Bell's stage 3/Advanced disease:

- Severe systemic illness (hypotension)

- Additional intestinal signs (striking abdominal distention, peritonitis)

- Severe radiologic signs (pneumoperitoneum)

- Additional laboratory changes (metabolic and respiratory acidosis, disseminated intravascular coagulation)

More recently ultrasonography has proven to be useful as it may detect signs and complications of NEC before they are evident on radiographs, specifically in cases that involve a paucity of bowel gas, a gasless abdomen, or a sentinel loop. Diagnosis is ultimately made in 5–10% of very low-birth-weight infants (<1,500g).

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.

Signs and symptoms include early satiety, nausea, vomiting, extreme "stabbing" postprandial abdominal pain (due to both the duodenal compression and the compensatory reversed peristalsis), abdominal distention/distortion, burping (eructation), external hypersensitivity or tenderness of the abdominal area, reflux, and heartburn. In infants, feeding difficulties and poor weight gain are also frequent symptoms.

In some cases of SMA syndrome, severe malnutrition accompanying spontaneous wasting may occur. This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms.

"Food fear" is a common development among patients with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver (pressure applied below the umbilicus in cephalad and dorsal direction) elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a supine (face up) position.

Superior mesenteric artery (SMA) syndrome is a gastro-vascular disorder in which the third and final portion of the duodenum is compressed between the abdominal aorta (AA) and the overlying superior mesenteric artery. This rare, potentially life-threatening syndrome is typically caused by an angle of 6°–25° between the AA and the SMA, in comparison to the normal range of 38°–56°, due to a lack of retroperitoneal and visceral fat (mesenteric fat). In addition, the aortomesenteric distance is 2–8 millimeters, as opposed to the typical 10–20. However, a narrow SMA angle alone is not enough to make a diagnosis, because patients with a low BMI, most notably children, have been known to have a narrow SMA angle with no symptoms of SMA syndrome.

SMA syndrome was first described in 1861 by Carl Freiherr von Rokitansky in victims at autopsy, but remained pathologically undefined until 1927 when Wilkie published the first comprehensive series of 75 patients. According to a 1956 study, only 0.3% of patients referred for an upper-gastrointestinal-tract barium studies fit this diagnosis, making it one of the rarest gastrointestinal disorders known to medical science. Recognition of SMA syndrome as a distinct clinical entity is controversial, due in part to its possible confusion with a number of other conditions, though it is now widely acknowledged.

SMA syndrome is also known as Wilkie's syndrome, cast syndrome, mesenteric root syndrome, chronic duodenal ileus and intermittent arterio-mesenteric occlusion.

It is distinct from Nutcracker syndrome, which is the entrapment of the left renal vein between the AA and the SMA, although it is possible to be diagnosed with both conditions.