Overall, about 65% of people experience some form of lactose intolerance as they age past infancy, but there are significant differences between populations and regions, with rates as low as 5% among Northern Europeans and as high as more than 90% of adults in some communities of Asia.

Some populations, from an evolutionary perspective, have a better genetic makeup for tolerating lactose than others. In Northern European countries, lack of Vitamin D from the sun is balanced by intaking more milk and calcium. These countries have built up tolerance to lactose. Oppositely, regions of the south, Africa for example, rarely experienced Vitamin D deficiency and therefore tolerance from milk consumption did not develop the same way as in Northern European countries. Different populations will present certain gene constructs depending on the evolutionary and cultural pre-settings of the geographical region.

The prognosis of children diagnosed with intolerance to milk is good: patients respond to diet which excludes cow's milk protein and the majority of patients succeed in forming tolerance. Children with non-IgE-mediated cows milk intolerance have a good prognosis, whereas children with IgE-mediated cows milk allergy in early childhood have a significantly increased risk for persistent allergy, development of other food allergies, asthma and rhinoconjunctivitis.

A study has demonstrated that identifying and appropriately addressing food sensitivity in IBS patients not previously responding to standard therapy results in a sustained clinical improvement and increased overall well being and quality of life.

Regular consumption of dairy foods containing lactose can promote a colonic bacteria adaptation, enhancing a favorable microbiome, which allows people with primary lactase deficiency to diminish their intolerance and to consume more dairy foods. The way to induce tolerance is based on progressive exposure, consuming smaller amounts frequently, distributed throughout the day. Lactose intolerance can also be managed by ingesting live yogurt cultures containing lactobacilli that are able to digest the lactose in other dairy products. This may explain why many South Asians, though genetically lactose intolerant, are able to consume large quantities of milk without many symptoms of lactose intolerance, since consuming live yogurt cultures is very common among the South Asian population.

Environmental factors—more specifically, the consumption of lactose—may "play a more important role than genetic factors in the etio-pathogenesis of milk intolerance".

Food intolerance are all other adverse reactions to food. Subgroups include enzymatic (e.g. lactose intolerance due to lactase deficiency), pharmacological (e.g. reactions against biogenic amines, histamine intolerance), and undefined food intolerance (e.g. against some food additives).

Food intolerances can be caused by enzymatic defects in the digestive system, can also result from pharmacological effects of vasoactive amines present in foods (e.g. Histamine), among other metabolic, pharmacological and digestive abnormalities.

Allergies and intolerances to a food group may coexist with separate pathologies; for example, cow's milk allergy (CMA) and lactose intolerance are two distinct pathologies.

Milk allergy typically presents in the first year of life. The majority of children outgrow milk allergy by the age of ten years. One large clinical trial reported resolutions of 19% by age 4 years, 42% by age 8 years, 64% by age 12 years, and 79% by 16 years. Children are be able to tolerate milk as an ingredient in baked goods relative to liquid milk. Resolution was more likely if baseline serum IgE was lower, or if IgE-mediated allergy was absent so that all that was present was cell-mediated, non-IgE allergy.

People with confirmed cow's milk allergy may also demonstrate an allergic response to beef, moreso to rare beef versus well-cooked beef. The offending protein appears to be bovine serum albumin. This is not the same beef allergy that is seen primarily in the southeastern United States, triggered by being bitten by a Lone Star tick.

Milk allergy has consequences. In a U.S. government diet and health surveys conducted in 2007-2010, 6,189 children ages 2-17 years were assessed. For those classified as cow's milk allergic at the time of the survey, mean weight, height and body-mass index were significantly lower than their non-allergic peers. This was not true for children with other food allergies. Diet assessment showed a significant 23% reduction of calcium intake and near-significant trends for lower vitamin D and total calorie intake.

Two reviews on avoiding common allergy-inducing foods during pregnancy or lactation concluded that there is no strong evidence to recommend changes to the diets of pregnant or nursing women as a means of preventing the development of food allergy in their infants. For mothers of infants considered at high risk of developing cow's milk allergy because of a family history, there is some evidence that the nursing mother avoiding allergens may reduce risk of the child developing eczema, but the Cochrane review concluded that more research is needed.

Guidelines from various government and international organizations recommend that for the lowest allergy risk, infants be exclusively breastfed for 4-6 months. There does not appear to be any benefit to extending that period beyond six months. If a nursing mother decides to start feeding with an infant formula prior to four months the recommendation is to use a formula containing cow's milk proteins.

A different consideration occurs when there is a family history - parent or older siblings - of milk allergy. In this situation there are recommendations to avoid formula that contains intact cow's milk proteins. Options are substituting a product containing extensively hydrolyzed protein, or non-dairy protein, or free amino acids. The hydrolyzing process breaks intact proteins into fragments, in theory reducing allergenic potential. In 2006 the U.S. Food and Drug Administration (FDA) rejected a health claim proposed by Nestle that a formula based on partially hydrolyzed whey protein would reduce risk of developing allergy. Ten years later the FDA reconsidered and allowed a health claim, with the caveat that the claim include wording to the effect that the scientific evidence was weak at best. A meta-analysis published the same year disputed this, concluding that based on dozens of clinical trials there was no evidence to support a claim that a partially hydrolyzed formula could reduce the risk of eczema.

Once an infant has demonstrated milk allergy symptoms to a formula containing intact cow's milk proteins, a dairy-based hydrolyzed formula is not appropriate. Soy formula is a common substitution, but infants with milk allergy may have an allergic response to soy formula. Hydrolyzed rice formula is an option, as are the more expensive amino acid-based formulas.

Malabsorption is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to malnutrition and a variety of anaemias.

Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency. A typical Western diet ingested by an adult includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the required sodium, potassium, chloride, calcium, vitamins, and other elements. Salivary, gastric, intestinal, hepatic, and pancreatic secretions add an additional 7–8 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents. This massive load is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1–2 g of nitrogen, and less than 20 mmol each of Na, K, Cl, HCO, Ca, or Mg.

If there is impairment of any of the many steps involved in the complex process of nutrient digestion and absorption, intestinal "malabsorption" may ensue. If the abnormality involves a single step in the absorptive process, as in primary lactase deficiency, or if the disease process is limited to the very proximal small intestine selective malabsorption of only a single nutrient may occur. However, generalized "malabsorption" of multiple dietary nutrients develops when the disease process is extensive, thus disturbing several digestive and absorptive processes, as occurs in coeliac disease with extensive involvement of the small intestine.

The European Food Safety Authority concluded that chromium is not an essential nutrient, making this the only mineral for which the United States and the European Union disagree. The proposed mechanism for cellular uptake of Cr via transferrin has been called into question. There is no proof that chromium supplementation has physiological effects on body mass or composition, and its use as a supplement may be unsafe. A 2014 systematic review concluded that chromium supplementation had no effect on glycemic control, fasting plasma glucose levels, or body weight in people with or without diabetes.

Chromium may be needed as an ingredient in total parenteral nutrition (TPN), since deficiency may occur after months of intravenous feeding with chromium-free TPN. For this reason, chromium is added to normal TPN solutions for people with diabetes, and in nutritional products for preterm infants.

The main purpose of the gastrointestinal tract is to digest and absorb nutrients (fat, carbohydrate, protein, micronutrients (vitamins and trace minerals), water, and electrolytes. Digestion involves both mechanical and enzymatic breakdown of food. Mechanical processes include chewing, gastric churning, and the to-and-fro mixing in the small intestine. Enzymatic hydrolysis is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the intestinal epithelial cells.

Malabsorption constitutes the pathological interference with the normal physiological sequence of digestion (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients.

Intestinal malabsorption can be due to:

- Mucosal damage (enteropathy)

- Congenital or acquired reduction in absorptive surface

- Defects of specific hydrolysis

- Defects of ion transport

- Pancreatic insufficiency

- Impaired enterohepatic circulation

Short bowel syndrome in adults and children is usually caused by surgery. This surgery may be done for:

- Crohn's disease, an inflammatory disorder of the digestive tract

- Volvulus, a spontaneous twisting of the small intestine that cuts off the blood supply and leads to tissue death

- Tumors of the small intestine

- Injury or trauma to the small intestine

- Necrotizing enterocolitis (premature newborn)

- Bypass surgery to treat obesity

- Surgery to remove diseases or damaged portion of the small intestine

Some children are also born with an abnormally short small intestine, known as congenital short bowel.

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.

There is no cure for short bowel syndrome except transplant. In newborn infants, the 4-year survival rate on parenteral nutrition is approximately 70%. In newborn infants with less than 10% of expected intestinal length, 5 year survival is approximately 20%. Some studies suggest that much of the mortality is due to a complication of the total parenteral nutrition (TPN), especially chronic liver disease. Much hope is vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower.

Although promising, small intestine transplant has a mixed success rate, with postoperative mortality rate of up to 30%. One-year and 4-year survival rate are 90% and 60%, respectively.

A deficiency of vitamin B alone is relatively uncommon and often occurs in association with other vitamins of the B complex. The elderly and alcoholics have an increased risk of vitamin B deficiency, as well as other micronutrient deficiencies. Evidence exists for decreased levels of vitamin B in women with type 1 diabetes and in patients with systemic inflammation, liver disease, rheumatoid arthritis, and those infected with HIV. Use of oral contraceptives and treatment with certain anticonvulsants, isoniazid, cycloserine, penicillamine, and hydrocortisone negatively impact vitamin B status. Hemodialysis reduces vitamin B plasma levels.

In the US, the Dietary Reference Intake for adults is 55 µg/day. In the UK it is 75 µg/day for adult males and 60 µg/day for adult females. 55 µg/day recommendation is based on full expression of plasma glutathione peroxidase. Selenoprotein P is a better indicator of selenium nutritional status, and full expression of it would require more than 66 µg/day.

Adverse effects have been documented from vitamin B supplements, but never from food sources. Damage to the dorsal root ganglia is documented in human cases of overdose of pyridoxine. Although it is a water-soluble vitamin and is excreted in the urine, doses of pyridoxine in excess of the dietary upper limit (UL) over long periods cause painful and ultimately irreversible neurological problems. The primary symptoms are pain and numbness of the extremities. In severe cases, motor neuropathy may occur with "slowing of motor conduction velocities, prolonged F wave latencies, and prolonged sensory latencies in both lower extremities", causing difficulty in walking. Sensory neuropathy typically develops at doses of pyridoxine in excess of 1,000 mg per day, but adverse effects can occur with much less, so doses over 200 mg are not considered safe. Symptoms among women taking lower doses have been reported.

Existing authorizations and valuations vary considerably worldwide. As noted, the U.S. Institute of Medicine set an adult UL at 100 mg/day. The European Community Scientific Committee on Food defined intakes of 50 mg of vitamin B per day as harmful and established a UL of 25 mg/day. The nutrient reference values in Australia and New Zealand recommend an upper limit of 50 mg/day in adults. "The same figure was set for pregnancy and lactation as there is no evidence of teratogenicity at this level. The UL was set based on metabolic body size and growth considerations for all other ages and life stages except infancy. It was not possible to set a UL for infants, so intake is recommended in the form of food, milk or formula." The ULs were set using results of studies involving long-term oral administration of pyridoxine at doses of less than 1 g/day. "A no-observed-adverse-effect level (NOAEL) of 200 mg/day was identified from the studies of Bernstein & Lobitz (1988) and Del Tredici "et al" (1985). These studies involved subjects who had generally been on the supplements for five to six months or less. The study of Dalton and Dalton (1987), however, suggested the symptoms might take substantially longer than this to appear. In this latter retrospective survey, subjects who reported symptoms had been on supplements for 2.9 years, on average. Those reporting no symptoms had taken supplements for 1.9 years."

Because of the ease of therapy (dietary exclusion of fructose), HFI can be effectively managed if properly diagnosed. In HFI, the diagnosis of homozygotes is difficult, requiring a genomic DNA screening with allele specific probes or an enzyme assay from a liver biopsy. Once identified, parents of infants who carry mutant aldolase B alleles leading to HFI, or older individuals who have clinical histories compatible with HFI can be identified and counselled with regard to preventive therapy: dietary exclusion of foods containing fructose, sucrose, or sorbitol. If possible, individuals who suspect they might have HFI, should avoid testing via fructose challenge as the results are non-conclusive for individuals with HFI and even if the diagnostic administration fructose is properly controlled, profound hypoglycemia and its sequelae can threaten the patient's well-being.

Treatment of HFI depends on the stage of the disease, and the severity of the symptoms. Stable patients without acute intoxication events are treated by careful dietary planning that avoids fructose and its metabolic precursors. Fructose is replaced in the diet by glucose, maltose or other sugars. Management of patients with HFI often involves dietitians who have a thorough knowledge of what foods are acceptable.

In some regions (e.g. much of the northeastern and northwestern US and adjacent Canada, and the southeastern US), selenium deficiency in some animal species is common unless supplementation is carried out. Selenium deficiency is responsible (either alone or together with vitamin E deficiency) for many of the cases of WMD ("white muscle disease"), evidenced at slaughter or during necropsy by whitish appearance of striated muscle tissue due to bleaching by peroxides and hydroperoxides. Although this degenerative disease can occur in foals, pigs and other animal species, ruminants are particularly susceptible. In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain. Sheep are more susceptible than cattle to WMD, and goats are more susceptible than sheep. Because of selenium's role in certain peroxidases (converting hydroperoxides to alcohols) and because of the antioxidant role of vitamin E (preventing hydroperoxide formation), a low level of Se can be somewhat (but not wholly) compensated by a high level of vitamin E. (In the animal, localization of peroxidases and vitamin E differs, partly because of the fat-solubility of vitamin E.) Some studies have indicated that about 0.12 or 0.23 mg Se per kg of dry matter intake may be sufficient for avoiding Se deficiency in sheep in some circumstances. However, somewhat higher Se intake may be required for avoidance of WMD where certain legumes are consumed. The cyanogenic glycosides in some white clover ("Trifolium repens") varieties may influence the Se requirement, presumably because of cyanide from the aglycone released by glucosidase activity in the rumen and inactivation of glutathione peroxidases by the effect of absorbed cyanide on the glutathione moiety.

In areas where selenium deficiency in livestock is a concern, selenium (as selenite) may be supplemented in feed. In some countries, e.g. the US and Canada, such supplementation is regulated. Neonate ruminants at risk of WMD may be administered both Se and vitamin E by injection; some of the WMD myopathies respond only to Se, some only to vitamin E, and some to either.

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.

Galactose is converted into glucose by the action of three enzymes, known as the Leloir pathway. There are diseases associated with deficiencies of each of these three enzymes:

Cats cannot synthesize vitamin A from plant beta-carotene, and therefore must be supplemented with retinol from meat. A deficiency in vitamin A will result in a poor coat, with hair loss, with scaly and thickened skin. However an excess of vitamin A, called hypervitaminosis A, can result from over feeding cod liver oil, and large amounts of liver. Signs of hypervitaminosis A are overly sensitive skin, and neck pain causing the cat to be unwilling to groom its self, resulting in a poor coat. Supplementing vitamin A with retinol to a deficient cat, and feeding a balanced diet to a cat with hypervitaminosis A will treat the underlying nutritional disorder.

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.

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.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.

Manganese is a component of some enzymes and stimulates the development and activity of other enzymes. Manganese superoxide dismutase (MnSOD) is the principal antioxidant in mitochondria. Several enzymes activated by manganese contribute to the metabolism of carbohydrates, amino acids, and cholesterol.

A deficiency of manganese causes skeletal deformation in animals and inhibits the production of collagen in wound healing.

Manganese is found in leafy green vegetables, fruits, nuts, cinnamon and whole grains. The nutritious kernel, called wheat germ, which contains the most minerals and vitamins of the grain, has been removed from most processed grains (such as white bread). The wheat germ is often sold as livestock feed. Many common vitamin and mineral supplement products fail to include manganese in their compositions. Relatively high dietary intake of other minerals such as iron, magnesium, and calcium may inhibit the proper intake of manganese.