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.

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.

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.

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.

Food allergies can have fast onset (from seconds to one hour) or slow onset (from hours to several days) depending on mechanism. Symptoms may include: rash, hives, itching of mouth, lips, tongue, throat, eyes, skin, or other areas, swelling of lips, tongue, eyelids, or the whole face, difficulty swallowing, runny or congested nose, hoarse voice, wheezing, shortness of breath, diarrhea, abdominal pain, lightheadedness, fainting, nausea and vomiting. Symptoms of allergies vary from person to person and may vary from incident to incident. Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated by wheezing, a blocked airway and cyanosis, the latter by weak pulse, pale skin, and fainting. When these symptoms occur the allergic reaction is called anaphylaxis. Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show severe symptoms. Untreated, this can proceed to vasodilation, a low blood pressure situation called anaphylactic shock, and death (very rare).

For milk allergy, non-IgE-mediated responses are more common than IgE-mediated. Non-IgE mediated reactions can manifest as dermatitis/eczema and gastrointestinal symptoms, especially in infants and young children. Infants exhibit dermatiis on face, scalp and other parts of the body, while in slightly older children knees and elbows are more commonly afflicted. Children with dermatitis are at greater than expected risk of also exhibiting asthma and allergic rhinitis.

Milk allergy is an adverse immune reaction to one or more of the protein constituents of cow's milk. Symptoms can be rapid or gradual in onset. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. The latter can take hours to days to appear. Presentations may include atopic dermatitis, inflammation of the esophagus, enteropathy involving the small intestine and proctocolitis involving the rectum and colon.

In the United States, 90% of allergic responses to foods are caused by eight foods: cow's milk, eggs, wheat, shellfish, peanuts, tree nuts, fish, and soy beans. Allergy to cow's milk is the most common. The U.S. Food Allergen Labeling and Consumer Protection Act of 2004 requires that the label of a food that contains an ingredient that is or contains protein from these eight major food allergens declare the presence of the allergen on the label. Dairy foods are also on the mandatory labeling list in Japan and the European Union.

Prevention is by avoiding eating foods that contain dairy. Infants should be breastfed for at least four months, preferably six months before introduction of cow's milk. If there is a family history of dairy allergy then an extensively hydrolyzed cow's milk formula is recommended. Soy infant formula can be considered, but about 10 to 15% of babies allergic to cow's milk will also react to soy. In the United States, milk allergy affects between 2% and 3% of babies and young children. The majority of people outgrow milk allergy. Predictors for adult-persistence are anaphylaxis, high milk-specific serum immunoglobulin E (IgE), robust response to the skin prick test and absence of tolerance to milk-containing baked foods. Oral immunotherapy is being researched, but as of 2014 it is of unclear benefit.

The symptoms of short bowel syndrome can include:

- Abdominal pain

- Diarrhea and steatorrhea (oily, bulky stool, which can be malodorous)

- Fluid depletion

- Weight loss and malnutrition

- Fatigue

Persons with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, B (folic acid), and B, calcium, magnesium, iron, and zinc. These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain.

Intestinal failure is decreased intestinal function such that nutrients, water, and electrolytes are not sufficiently absorbed. Short bowel syndrome is when there is less than of working bowel and is the most common cause of intestinal failure.

Chromium deficiency is a proposed disorder that results from an insufficient dietary intake of chromium. Chromium was first proposed as an essential element for normal glucose metabolism in 1959, and was widely accepted as being such by the 1990s. Cases of deficiency have been claimed in hospital patients who were fed defined liquid diets intravenously for long periods of time.

By the turn of the century, these views were being challenged, with subsequent work suggesting that chromium supplements may present a health risk. In spite of this, dietary supplements containing chromium remain widely available.

The symptoms of chromium deficiency caused by long-term total parenteral nutrition are severely impaired glucose tolerance, weight loss, and confusion. However, subsequent studies questioned the validity of these findings.

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.

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.

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.

Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency also contributes (along with iodine deficiency) to Kashin-Beck disease. The primary symptom of Keshan disease is myocardial necrosis, leading to weakening of the heart. Kashin-Beck disease results in atrophy, degeneration and necrosis of cartilage tissue. Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases.

Selenium is also necessary for the conversion of the thyroid hormone thyroxine (T4) into its more active counterpart, triiodothyronine, and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage.

In undiagnosed and untreated children, the accumulation of precursor metabolites due to the deficient activity of galactose 1-phosphate uridylyltransferase (GALT) can lead to feeding problems, failure to thrive, liver damage, bleeding, and infections. The first presenting symptom in an infant is often prolonged jaundice. Without intervention in the form of galactose restriction, infants can develop hyperammonemia and sepsis, possibly leading to shock. The accumulation of galactitol and subsequent osmotic swelling can lead to cataracts which are similar to those seen in galactokinase deficiency. Long-term consequences of continued galactose intake can include developmental delay, developmental verbal dyspraxia, and motor abnormalities. Galactosemic females frequently suffer from ovarian failure, regardless of treatment in the form of galactose restriction.

Selenium deficiency is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported.

Manganese deficiency in humans results in a number of medical problems. Manganese is a vital element of nutrition in very small quantities (adult male daily intake 2.3 milligrams). However, in greater amounts manganese, like most metals, is poisonous when eaten or inhaled.

Vitamin B refers to a group of chemically similar compounds which can be interconverted in biological systems. Vitamin B is part of the vitamin B group of essential nutrients. Its active form, pyridoxal 5′-phosphate, serves as a coenzyme in some 100 enzyme reactions in amino acid, glucose, and lipid metabolism.

Galactose-1-phosphate uridylyltransferase deficiency, also called galactosemia type 1, classic galactosemia or GALT deficiency, is the most common type of galactosemia, an inborn error of galactose metabolism, caused by a deficiency of the enzyme galactose-1-phosphate uridylyltransferase. It is an autosomal recessive metabolic disorder that can cause liver disease and death if untreated. Treatment of galactosemia is most successful if initiated early and includes dietary restriction of lactose intake. Because early intervention is key, galactosemia is included in newborn screening programs in many areas. On initial screening, which often involves measuring the concentration of galactose in blood, classic galactosemia may be indistinguishable from other inborn errors of galactose metabolism, including galactokinase deficiency and galactose epimerase deficiency. Further analysis of metabolites and enzyme activities are needed to identify the specific metabolic error.

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.

Infants are routinely screened for galactosemia in the United States, and the diagnosis is made while the person is still an infant. Infants affected by galactosemia typically present with symptoms of lethargy, vomiting, diarrhea, failure to thrive, and jaundice. None of these symptoms are specific to galactosemia, often leading to diagnostic delays. Luckily, most infants are diagnosed on newborn screening. If the family of the baby has a history of galactosemia, doctors can test prior to birth by taking a sample of fluid from around the fetus (amniocentesis) or from the placenta (chorionic villus sampling or CVS).

A galactosemia test is a blood test (from the heel of the infant) or urine test that checks for three enzymes that are needed to change galactose sugar that is found in milk and milk products into glucose, a sugar that the human body uses for energy. A person with galactosemia doesn't have one of these enzymes. This causes high levels of galactose in the blood or urine.

Galactosemia is normally first detected through newborn screening, or NBS. Affected children can have serious, irreversible effects or even die within days from birth. It is important that newborns be screened for metabolic disorders without delay. Galactosemia can even be detected through NBS before any ingestion of galactose-containing formula or breast milk.

Detection of the disorder through newborn screening (NBS) does not depend on protein or lactose ingestion, and, therefore, it should be identified on the first specimen unless the infant has been transfused. A specimen should be taken prior to transfusion. The enzyme is prone to damage if analysis of the sample is delayed or exposed to high temperatures. The routine NBS is accurate for detection of galactosemia. Two screening tests are used to screen infants affected with galactosemia—the Beutler's test and the Hill test. The Beutler's test screens for galactosemia by detecting the level of enzyme of the infant. Therefore, the ingestion of formula or breast milk does not affect the outcome of this part of the NBS, and the NBS is accurate for detecting galactosemia prior to any ingestion of galactose.

Duarte galactosemia is a milder form of classical galactosemia and usually has no long term side effects.

Cat skin disorders are among the most common health problems in cats.

Skin disorders in cats have many causes, and many of the common skin disorders that afflict people have a counterpart in cats. The condition of a cat's skin and coat can also be an important indicator of its general health. Skin disorders of cats vary from acute, self-limiting problems to chronic or long-lasting problems requiring life-time treatment. Cat skin disorders may be grouped into categories according to the causes.

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.