A positive diagnosis test for thiamine deficiency can be ascertained by measuring the activity of the enzyme transketolase in erythrocytes (Erythrocyte Transketolase Activation Assay). Thiamine, as well as its phosphate derivatives, can also be detected directly in whole blood, tissues, foods, animal feed, and pharmaceutical preparations following the conversion of thiamine to fluorescent thiochrome derivatives (Thiochrome Assay) and separation by high-performance liquid chromatography (HPLC). In recent reports, a number of Capillary Electrophoresis (CE) techniques and in-capillary enzyme reaction methods have emerged as potential alternative techniques for the determination and monitoring of thiamine in samples.

The normal thiamine concentration in EDTA-blood is about 20-100 µg/l.

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.

Many people with beriberi can be treated with thiamine alone. Given thiamine intravenously (and later orally), rapid and dramatic recovery can occur within hours. In situations where concentrated thiamine supplements are unavailable, feeding the person with a thiamine-rich diet (e.g. whole grain brown bread) will lead to recovery, though at a much slower rate.

Following thiamine treatment, rapid improvement occurs, in general, within 24 hours. Improvements of peripheral neuropathy may require several months of thiamine treatment.

Common investigations include blood urea nitrogen (BUN) and electrolytes, liver function tests, urinalysis, and thyroid function tests. Hematological investigations include hematocrit levels, which are usually raised in HG. An ultrasound scan may be needed to know gestational status and to exclude molar or partial molar pregnancy.

Hyperemesis gravidarum is considered a diagnosis of exclusion. HG can be associated with serious problems in the mother or baby, such as Wernicke's encephalopathy, coagulopathy, peripheral neuropathy.

Women experiencing hyperemesis gravidarum often are dehydrated and lose weight despite efforts to eat. The onset of the nausea and vomiting in hyperemesis gravidarum is typically before the twenty-second week of pregnancy.

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.

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.

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.

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).

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.

Diagnosis is very difficult, and usually one of exclusion. SMA syndrome is thus considered only after patients have undergone an extensive evaluation of their gastrointestinal tract including upper endoscopy, and evaluation for various malabsorptive, ulcerative and inflammatory instestinal conditions with a higher diagnostic frequency. Diagnosis may follow x-ray examination revealing duodenal dilation followed by abrupt constriction proximal to the overlying SMA, as well as a delay in transit of four to six hours through the gastroduodenal region. Standard diagnostic exams include abdominal and pelvic computed tomography (CT) scan with oral and IV contrast, upper gastrointestinal series (UGI), and, for equivocal cases, hypotonic duodenography. In addition, vascular imaging studies such as ultrasound and contrast angiography may be used to indicate increased bloodflow velocity through the SMA or a narrowed SMA angle.

Despite multiple case reports, there has been controversy surrounding the diagnosis and even the existence of SMA syndrome since symptoms do not always correlate well with radiologic findings, and may not always improve following surgical correction. However, the reason for the persistence of gastrointestinal symptoms even after surgical correction in some cases has been traced to the remaining prominence of reversed peristalsis in contrast to direct peristalsis.

Since females between the ages of 10 and 30 are most frequently afflicted, it is not uncommon for physicians to initially and incorrectly assume that emaciation is a choice of the patient instead of a consequence of SMA syndrome. Patients in the earlier stages of SMA syndrome often remain unaware that they are ill until substantial damage to their health is done, since they may attempt to adapt to the condition by gradually decreasing their food intake or naturally gravitating toward a lighter and more digestible diet.

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.

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.