Lactose intolerance is a condition in which people have symptoms due to the decreased ability to digest lactose, a sugar found in milk products. Those affected vary in the amount of lactose they can tolerate before symptoms develop. Symptoms may include abdominal pain, bloating, diarrhea, gas, and nausea. These symptoms typically start between half and two hours after drinking milk or eating milk products. Severity depends on the amount a person eats or drinks. It does not cause damage to the gastrointestinal tract.

Lactose intolerance is due to the lack of enzyme lactase in the small intestines to break lactose down into glucose and galactose. There are four types: primary, secondary, developmental, and congenital. Primary lactose intolerance is when the amount of lactase declines as people age. Secondary lactose intolerance is due to injury to the small intestine such as from infection, celiac disease, inflammatory bowel disease, or other diseases. Developmental lactose intolerance may occur in premature babies and usually improves over a short period of time. Congenital lactose intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth.

Diagnosis may be confirmed if symptoms resolve following eliminating lactose from the diet. Other supporting tests include a hydrogen breath test and a stool acidity test. Other conditions that may produce similar symptoms include irritable bowel syndrome, celiac disease, and inflammatory bowel disease. Lactose intolerance is different from a milk allergy. Management is typically by decreasing the amount of lactose in the diet, taking lactase supplements, or treating the underlying disease. People are usually able to drink at least one cup of milk per sitting without developing significant symptoms, with greater amounts tolerated if drunk with a meal or throughout the day.

The exact number of adults with lactose intolerance is unknown. One estimate puts the average at 65% of the global population. Rates of lactose intolerance vary between regions, from less than 10% in Northern Europe to as high as 95% in parts of Asia and Africa. Onset is typically in late childhood or early adulthood. The ability to digest lactose into adulthood evolved in several human populations independently probably as an adaptation to domestication of dairy animals 10,000 years ago.

Lactose intolerance primarily refers to a syndrome having one or more symptoms upon the consumption of food substances containing lactose. Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms. "Lactose malabsorption" refers to the physiological concomitant of lactase deficiency (i.e., the body does not have sufficient lactase capacity to digest the amount of lactose ingested). Hypolactasia (lactase deficiency) is distinguished from alactasia (total lack of lactase), a rare congenital defect.

Lactose intolerance is not an allergy, because it is not an immune response, but rather a sensitivity to dairy caused by lactase deficiency. Milk allergy, occurring in only 4% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction.

Food intolerance is more chronic, less acute, less obvious in its presentation, and often more difficult to diagnose than a food allergy.

Symptoms of food intolerance vary greatly, and can be mistaken for the symptoms of a food allergy. While true allergies are associated with fast-acting immunoglobulin IgE responses, it can be difficult to determine the offending food causing a food intolerance because the response generally takes place over a prolonged period of time. Thus, the causative agent and the response are separated in time, and may not be obviously related. Food intolerance symptoms usually begin about half an hour after eating or drinking the food in question, but sometimes symptoms may be delayed by up to 48 hours.

Food intolerance can present with symptoms affecting the skin, respiratory tract, gastrointestinal tract (GIT) either individually or in combination. On the skin may include skin rashes, urticaria (hives), angioedema, dermatitis, and eczema. Respiratory tract symptoms can include nasal congestion, sinusitis, pharyngeal irritations, asthma and an unproductive cough. GIT symptoms include mouth ulcers, abdominal cramp, nausea, gas, intermittent diarrhea, constipation, irritable bowel syndrome (IBS),

and may include anaphylaxis.

Food intolerance has been found associated with irritable bowel syndrome and inflammatory bowel disease, chronic constipation, chronic hepatitis C infection, eczema, NSAID intolerance, respiratory complaints, including asthma, rhinitis and headache, functional dyspepsia, eosinophilic esophagitis

and ENT illnesses.

Sucrose intolerance, also called sucrase-isomaltase deficiency, congenital sucrase-isomaltase deficiency (CSID), or genetic sucrase-isomaltase deficiency (GSID), is the condition in which sucrase-isomaltase, an enzyme needed for proper metabolism of sucrose (sugar) and starch (i.e., grains and rice), is not produced or the enzyme produced is either partially functional or non-functional in the small intestine. All GSID patients lack fully functional sucrase, while the isomaltase activity can vary from minimal functionality to almost normal activity. The presence of residual isomaltase activity may explain why some GSID patients are better able to tolerate starch in their diet than others with GSID.

The highest prevalence rates are seen in the Inuit populations of Greenland (5–10%), Alaska (3–7%) and Canada (about 3%). European descent prevalence ranges from 0.2% to 0.05%. There is a lower prevalence reported in African Americans and Hispanics compared to Caucasians.

Sucrose intolerance can be caused by genetic mutations in which both parents must contain this gene for the child to carry the disease (so-called primary sucrose intolerance). Sucrose intolerance can also be caused by irritable bowel syndrome, aging, or small intestine disease (secondary sucrose intolerance). There are specific tests used to help determine if a person has sucrose intolerance. The most accurate test is the enzyme activity determination, which is done by biopsying the small intestine. This test is a diagnostic for GSID. Other tests which can aid in the diagnosis of GSID but which are not truly diagnostic for the disease are the sucrose breath test, and a genetic test which tests for the absence of certain genes which are thought to be responsible for GSID.

Sucrose (also termed "saccharose") is a disaccharide and is a two-sugar chain composed of glucose and fructose which are bonded together. A more familiar name is table, beet, or cane sugar. It was believed that most cases of sucrose intolerance were to do an autosomal recessive, genetic, metabolic disease. Based on new data patients with heterozygous and compound heterozygous genotypes can have symptom presentation as well. GSID involves deficiency in the enzyme sucrase-isomaltase, which breaks apart the glucose and fructose molecules. When disaccharides are consumed, they must be broken down into monosaccharides by enzymes in the intestines before they can be absorbed. Monosaccharides, or single sugar units, are absorbed directly into the blood.

A deficiency of sucrase may result in malabsorption of sugar, which can lead to potentially serious symptoms. Since sucrose-isomaltase is involved in the digestion of starches, some GSID patients may not be able to absorb starches as well. It is important for those with sucrose intolerance to minimize sucrose consumption as much as possible. Dietary supplements or medications may be taken as a substitute for the enzyme missing or to introduce healthy bacteria into the immune system.

The key identifying feature of HFI is the appearance of symptoms with the introduction of fructose to the diet. Affected individuals are asymptomatic and healthy, provided they do not ingest foods containing fructose or any of its common precursors, sucrose and sorbitol. In the past, infants often became symptomatic when they were introduced to formulas that were sweetened with fructose or sucrose. These sweeteners are not common in formulas used today. Symptoms such as vomiting, nausea, restlessness, pallor, sweating, trembling and lethargy can also first present in infants when they are introduced to fruits and vegetables. These can progress to apathy, coma and convulsions if the source is not recognized early.

When patients are diagnosed with HFI, a dietary history will often reveal an aversion to fruit and other foods that contain large amounts of fructose. Most adult patients do not have any dental caries.

Inborn errors of carbohydrate metabolism are inborn error of metabolism that affect the catabolism and anabolism of carbohydrates.

An example is lactose intolerance.

Carbohydrates account for a major portion of the human diet. These carbohydrates are composed of three principal monosaccharides: glucose, fructose and galactose; in addition glycogen is the storage form of carbohydrates in humans. The failure to effectively use these molecules accounts for the majority of the inborn errors of human carbohydrates metabolism.

Food hypersensitivity is used to refer broadly to both food intolerances and food allergies. There are a variety of earlier terms which are no longer in use such as "pseudo-allergy".

Food intolerance reactions can include pharmacologic, metabolic, and gastro-intestinal responses to foods or food compounds. Food intolerance does not include either psychological responses or foodborne illness.

A non-allergic food hypersensitivity is an abnormal physiological response. It can be difficult to determine the poorly tolerated substance as reactions can be delayed, dose-dependent, and a particular reaction-causing compound may be found in many foods.

- Metabolic food reactions are due to inborn or acquired errors of metabolism of nutrients, such as in diabetes mellitus, lactase deficiency, phenylketonuria and favism.

- Pharmacological reactions are generally due to low-molecular-weight chemicals which occur either as natural compounds, such as salicylates and amines, or to food additives, such as preservatives, colouring, emulsifiers and taste enhancers. These chemicals are capable of causing drug-like (biochemical) side effects in susceptible individuals.

- Gastro-intestinal reactions can be due to malabsorption or other GI Tract abnormalities.

- Immunological responses are mediated by non-IgE immunoglobulins, where the immune system recognises a particular food as a foreign body.

- Toxins may either be present naturally in food, be released by bacteria, or be due to contamination of food products. Toxic food reactions are caused by the direct action of a food or substance without immune involvement.

- Psychological reactions involve manifestation of clinical symptoms caused not by food but by emotions associated with food. These symptoms do not occur when the food is given in an unrecognisable form.

Elimination diets are useful to assist in the diagnosis of food intolerance. There are specific diagnostic tests for certain food intolerances.

Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration.

A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:

- double vision or blurry vision

- unclear thinking

- insomnia

- heart palpitation or fibrillation

- fatigue

- dizziness

- light-headedness

- sweating

- headaches

- depression

- nervousness

- muscle twitches

- irritability

- tremors

- flushing

- craving sweets

- increased appetite

- rhinitis

- nausea, vomiting

- panic attack

- numbness/coldness in the extremities

- confusion

- irrationality

- bad temper

- paleness

- cold hands

- disorientation

- the need to sleep or 'crash'

- coma can be a result in severe untreated episodes

The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body’s response to low blood sugar levels following periods of glucose deficiency.

Gastrointestinal symptoms may include any of the following: abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation), nausea, aerophagia, gastroesophageal reflux disease, and aphthous stomatitis.

Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent. Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with steatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with primary or secondary disaccharidase deficiency. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohn disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption.

Hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism caused by a deficiency of the enzyme aldolase B. Individuals affected with HFI are asymptomatic until they ingest fructose, sucrose, or sorbitol. If fructose is ingested, the enzymatic block at aldolase B causes an accumulation of fructose-1-phosphate. This accumulation has downstream effects on gluconeogenesis and regeneration of adenosine triphosphate (ATP). Symptoms of HFI include vomiting, hypoglycemia, jaundice, hemorrhage, hepatomegaly, hyperuricemia and potentially kidney failure. While HFI is not clinically a devastating condition, there are reported deaths in infants and children as a result of the metabolic consequences of HFI. Death in HFI is always associated with problems in diagnosis.

HFI is an autosomal recessive condition caused by mutations in the "ALDOB" gene, located at 9q22.3. HFI is typically suspected based on dietary history, especially in infants who become symptomatic after breast feeding. This suspicion is typically confirmed by molecular analysis. Treatment of HFI involves strict avoidance of fructose in the diet. Older patients with HFI typically self-select a diet low in fructose, even before being diagnosed.

Some prefer to classify malabsorption clinically into three basic categories:

1. selective, as seen in lactose malabsorption.

2. partial, as observed in abetalipoproteinaemia.

3. total, as in exceptional cases of coeliac disease.

Reported symptoms of NCGS are similar to those of celiac disease, with most patients reporting both gastrointestinal and non-gastrointestinal symptoms. In the "classical" presentation of NCGS, gastrointestinal symptoms are similar to those of irritable bowel syndrome, and are also not distinguishable from those of wheat allergy, but there is a different interval between exposure to wheat and onset of symptoms. Wheat allergy has a fast onset (from minutes to hours) after the consumption of food containing wheat and can be anaphylaxic.

Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within 4 hours after a high carbohydrate meal in people who do not have diabetes.

The condition is related to homeostatic systems utilised by the body to control blood sugar levels. It is variously described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be less if one has undertaken a lot of physical activity within the next few hours after consumption.

The alleged mechanism for the feeling of a crash is correlated with an abnormally rapid rise in blood glucose after eating. This normally leads to insulin secretion (known as an "insulin spike"), which in turn initiates rapid glucose uptake by tissues either accumulating it as glycogen or utilizing it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash".. A deeper cause might be hysteresis effect of insulin action, i.e., the effect of insulin is still prominent even if both plasma glucose and insulin levels were already low, causing a plasma glucose level eventually much lower than the baseline level.

Sugar crashes are not to be confused with the after-effects of consuming large amounts of "protein", which produces fatigue akin to a sugar crash, but are instead the result of the body prioritising the digestion of ingested food.

The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.

To assist diagnosis, a doctor can order an HbA1c test, which measures the blood sugar average over the two or three months before the test. The more specific 6-hour glucose tolerance test can be used to chart changes in the patient's blood sugar levels before ingestion of a special glucose drink and at regular intervals during the six hours following to see if an unusual rise or drop in blood glucose levels occurs.

According to the U.S. National Institute of Health (NIH), a blood glucose level below 70 mg/dL (3.9 mmol/L) at the time of symptoms followed by relief after eating confirms a diagnosis for reactive hypoglycemia.

The most common clinical history in patients with glycogen-storage disease type 0 (GSD-0) is that of an infant or child with symptomatic hypoglycemia or seizures that occur before breakfast or after an inadvertent fast. In affected infants, this event typically begins after they outgrow their nighttime feeds. In children, this event may occur during acute GI illness or periods of poor enteral intake.

Mild hypoglycemic episodes may be clinically unrecognized, or they may cause symptoms such as drowsiness, sweating, lack of attention, or pallor. Uncoordinated eye movements, disorientation, seizures, and coma may accompany severe episodes.

Glycogen-storage disease type 0 affects only the liver. Growth delay may be evident with height and weight percentiles below average. Abdominal examination findings may be normal or reveal only mild hepatomegaly.Signs of acute hypoglycemia may be present, including the following:

There are often no visible symptoms of hyperinsulinemia unless hypoglycaemia (low blood sugar) is present.

Some patients may experience a variety of symptoms when hypoglycaemia is present, including:

- Temporary muscle weakness

- Brain fog

- Fatigue

- Temporary thought disorder, or inability to concentrate

- Visual problems such as blurred vision or double vision

- Headaches

- Shaking/Trembling

- Thirst

If a person experiences any of these symptoms, a visit to a qualified medical practitioner is advised, and diagnostic blood testing may be required.

Galactosemia (British galactosaemia) is a rare genetic metabolic disorder that affects an individual's ability to metabolize the sugar galactose properly. Galactosemia follows an autosomal recessive mode of inheritance that confers a deficiency in an enzyme responsible for adequate galactose degradation.

Friedrich Goppert (1870–1927), a German physician, first described the disease in 1917, with its cause as a defect in galactose metabolism being identified by a group led by Herman Kalckar in 1956.

Its incidence is about 1 per 60,000 births for people of European ancestry. In other populations the incidence rate differs. Galactosaemia is about one hundred times more common (1:480 births) within the Irish Traveller population.

Intestinal involvement can cause mild malabsorption with steatorrhea, greasy stools, but usually requires no treatment.

The classic symptoms of coeliac disease include pale, loose, and greasy stool (steatorrhoea) and weight loss or failure to gain weight. More common symptoms are subtle or primarily occur in organs other than the bowel itself. It is also possible to have coeliac disease without any classic symptoms whatsoever. This represents at least 43% of the cases in children. Many adults with subtle disease only have fatigue or anaemia.

Lactose is a disaccharide sugar composed of galactose and glucose that is found in milk. Lactose can not be absorbed by the intestine and needs to be split in the small intestine into galactose and glucose by the enzyme called lactase; unabsorbed lactose can cause abdominal pain, bloating, diarrhea, gas, and nausea.

In most mammals, production of lactase diminishes after infants are weaned from maternal milk. However, 5% to 90% of the human population possess an advantageous autosomal mutation in which lactase production persists after infancy. The geographic distribution of lactase persistence is concordant with areas of high milk intake. Lactase non-persistence is common in tropical and subtropical countries. Individuals with lactase non-persistency may experience nausea, bloating and diarrhea after ingesting dairy.

Hypoglycemia is the central clinical problem, the one that is most damaging, and the one that most often prompts the initial diagnosis.

Maternal glucose transferred across the placenta prevents hypoglycemia in a fetus with GSD I, but the liver is enlarged with glycogen at birth. The inability to generate and release glucose soon results in hypoglycemia, and occasionally in lactic acidosis fulminant enough to appear as a primary respiratory problem in the newborn period. Neurological manifestations are less severe than if the hypoglycemia were more acute. The brain's habituation to mild hypoglycemia is at least partly explained by use of alternative fuels, primarily lactate.

More commonly, infants with GSD I tolerate without obvious symptoms a chronic, mild hypoglycemia, and compensated lactic acidosis between feedings. Blood glucose levels are typically 25 to 50 mg/dl (1.4–2.8 mM). These infants continue to need oral carbohydrates every few hours. Many never sleep through the night even in the second year of life. They may be pale, clammy, and irritable a few hours after a meal. Developmental delay is not an intrinsic or inevitable effect of glucose-6-phosphatase deficiency but is common if the diagnosis is not made in early infancy.

Although mild hypoglycemia for much of the day may go unsuspected, the metabolic adaptations described above make severe hypoglycemic episodes, with unconsciousness or seizure, uncommon before treatment. Episodes which occur are likely to happen in the morning before breakfast. GSD I is therefore a potential cause of ketotic hypoglycemia in young children.

Once the diagnosis has been made, the principal goal of treatment is to maintain an adequate glucose level and prevent hypoglycemia.

Hypoglycemia in early infancy can cause jitteriness, lethargy, unresponsiveness, or seizures. The most severe forms may cause macrosomia in utero, producing a large birth weight, often accompanied by abnormality of the pancreas. Milder hypoglycemia in infancy causes hunger every few hours, with increasing jitteriness or lethargy. Milder forms have occasionally been detected by investigation of family members of infants with severe forms, adults with the mildest degrees of congenital hyperinsulinism have a decreased tolerance for prolonged fasting. Other presentations are:

The variable ages of presentations and courses suggest that some forms of congenital hyperinsulinism, especially those involving abnormalities of K channel function, can worsen or improve with time the potential harm from hyperinsulinemic hypoglycemia depends on the severity, and duration. Children who have recurrent hyperinsulinemic hypoglycemia in infancy can suffer harm to the brain

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

Corn/Maize allergy is a type of food allergy. It can be a difficult allergy to manage, particularly in the United States, due to the various food products which contain various forms of corn, such as corn starch, modified food starch, vinegar, and vanilla extract, among many others. However, it is an allergy that often goes unrecognized.