Since biotin is in many foods at low concentrations, deficiency is rare except in locations where malnourishment is very common. Pregnancy, however, alters biotin catabolism and despite a regular biotin intake, half of the pregnant women in the U.S. are marginally biotin deficient.

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.

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.

Based on the results of worldwide screening of biotinidase deficiency in 1991, the incidence of the disorder is:

5 in 137,401 for profound biotinidase deficiency

- One in 109,921 for partial biotinidase deficiency

- One in 61,067 for the combined incidence of profound and partial biotinidase deficiency

- Carrier frequency in the general population is approximately one in 120.

In the United States, biotin supplements are readily available without a prescription in amounts ranging from 1,000 to 10,000 micrograms (30 micrograms is identified as Adequate Intake).

The term fatty acid oxidation disorder (FAOD) is sometimes used, especially when there is an emphasis on the oxidation of the fatty acid.

In addition to the fetal complications, they can also cause complications for the mother during pregnancy.

Examples include:

- trifunctional protein deficiency

- MCADD, LCHADD, and VLCADD

Incomplete list of various fatty-acid metabolism disorders.

- Carnitine Transport Defect

- Carnitine-Acylcarnitine Translocase (CACT) Deficiency

- Carnitine Palmitoyl Transferase I & II (CPT I & II) Deficiency

- 2,4 Dienoyl-CoA Reductase Deficiency

- Electron Transfer Flavoprotein (ETF) Dehydrogenase Deficiency (GAII & MADD)

- 3-Hydroxy-3 Methylglutaryl-CoA Lyase (HMG) Deficiency

- Very long-chain acyl-coenzyme A dehydrogenase deficiency (VLCAD deficiency)

- Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency (LCHAD deficiency)

- Medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency)

- Short-chain acyl-coenzyme A dehydrogenase deficiency (SCAD deficiency)

- 3-hydroxyacyl-coenzyme A dehydrogenase deficiency (M/SCHAD deficiency)

Raw eggs should be avoided in those with biotin deficiency, because egg whites contain high levels of the anti-nutrient avidin. The name avidin literally means that this protein has an "avidity" (Latin: "to eagerly long for") for biotin. Avidin binds irreversibly to biotin and this compound is then excreted in the urine.

Mitochondrial trifunctional protein deficiency is an autosomal recessive fatty acid oxidation disorder that prevents the body from converting certain fats to energy, particularly during periods without food. People with this disorder have inadequate levels of an enzyme that breaks down a certain group of fats called long-chain fatty acids.

This condition is very rare; approximately 600 cases have been reported worldwide. In most parts of the world, only 1% to 2% of all infants with high phenylalanine levels have this disorder. In Taiwan, about 30% of newborns with elevated levels of phenylalanine have a deficiency of THB.

Pregnancy also poses as another high risk factor for vitamin D deficiency. The status levels of vitamin D during the last stages of pregnancy directly impact the new borns first initial months of life. Babies who are exclusively breastfed with minimal exposure to sunlight or supplementation can be at greater risk of vitamin D deficiency,as human milk has minimal vitamin D present. Recommendations for infants of the age 0–12 months are set at 5 ug/day, to assist in preventing rickets in young babies. 80% of dark skinned and or veiled women in Melbourne were found to have serum levels lower than 22.5 nmol/L considering them to be within moderate ranges of vitamin D deficiency.

Although rickets and osteomalacia are now rare in Britain, osteomalacia outbreaks in some immigrant communities included women with seemingly adequate daylight outdoor exposure wearing typical Western clothing. Having darker skin and reduced exposure to sunshine did not produce rickets unless the diet deviated from a Western omnivore pattern characterized by high intakes of meat, fish, and eggs, and low intakes of high-extraction cereals. In sunny countries where rickets occurs among older toddlers and children, vitamin D deficiency has been attributed to low dietary calcium intakes. This is characteristic of cereal-based diets with limited access to dairy products. Rickets was formerly a major public health problem among the US population; in Denver, where ultraviolet rays are about 20% stronger than at sea level on the same latitude, almost two-thirds of 500 children had mild rickets in the late 1920s. An increase in the proportion of animal protein in the 20th-century American diet coupled with increased consumption of milk fortified with relatively small quantities of vitamin D coincided with a dramatic decline in the number of rickets cases. One study of children in a hospital in Uganda however showed no significant difference in vitamin D levels of malnourished children compared to non-malnourished children. Because both groups were at risk due to darker skin pigmentation, both groups had vitamin D deficiency. Nutritional status did not appear to play a role in this study.

Severe zinc deficiency is rare, and is mainly seen in persons with acrodermatitis enteropathica, a severe defect in zinc absorption due to a congenital deficiency in the zinc carrier protein ZIP4 in the enterocyte. Mild zinc deficiency due to reduced dietary intake is common. Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency. Zinc deficiency is thought to be a leading cause of infant mortality.

Providing micronutrients, including zinc, to humans is one of the four solutions to major global problems identified in the Copenhagen Consensus from an international panel of economists.

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.

Australia's vitamin D deficiency levels in recent years have been on the increase, due to factors such as the long-term success of SunSmart government campaigns like Slip, Slop, Slap as well as Cancer Council Australia that have increased the general public's awareness of the risks associated with excessive sun exposure and skin cancers. The 'sun smart' campaign created in 1988 had a significant impact on the public approach and behaviours towards sun exposure. The success of this campaign reduced the sunburn rate by 50%, which researchers believe to have contributed to the rise in vitamin D deficiencies across Australia.

In addition to the reduced sun exposure amongst the Australia populations, there have been decreases in the form of dietary intake as many people are no longer taking fatty fish oil tablets as a method of regulating vitamin D.

Other factors previously mentioned are sun exposure, geographical longitude as well as season change. Greater latitudes receive sunlight that is of lesser ultra radiation strength in contrast to regions close to the equator, who receive lower variation to hours of daylight during the summer periods.

There is an increased risk of vitamin D deficiency in people who are considered overweight or obese based on their body mass index (BMI) measurement. The relationship between these conditions is not well understood. There are different factors that could contribute to this relationship, particularly diet and sunlight exposure. Alternatively, vitamin D is fat-soluble therefore excess amounts can be stored in fat tissue and used during winter, when sun exposure is limited.

A 1999 retrospective study of 74 cases of neonatal onset found that 32 (43%) patients died during their first hyperammonemic episode. Of those who survived, less than 20% survived to age 14. Few of these patients received liver transplants.

Some situations that increase the need for folate include the following:

- hemorrhage

- kidney dialysis

- liver disease

- malabsorption, including celiac disease and fructose malabsorption

- pregnancy and lactation (breastfeeding)

- tobacco smoking

- alcohol consumption

Management for mitochondrial trifunctional protein deficiency entails the following:

- Avoiding factors that might precipitate condition

- Glucose

- Low fat/high carbohydrate nutrition

Folate is found in leafy green vegetables. Multi-vitamins also tend to include Folate as well as many other B vitamins. B vitamins, such as Folate, are water-soluble and excess is excreted in the urine.

When cooking, use of steaming, a food steamer, or a microwave oven can help keep more folate content in the cooked foods, thus helping to prevent folate deficiency.

Folate deficiency during human pregnancy has been associated with an increased risk of infant neural tube defects. Such deficiency during the first four weeks of gestation can result in structural and developmental problems. NIH guidelines recommend oral B vitamin supplements to decrease these risks near the time of conception and during the first month of pregnancy.

The life expectancy of patients with homocystinuria is reduced only if untreated. It is known that before the age of 30, almost one quarter of patients die as a result of thrombotic complications (e.g., heart attack).

Zinc deficiency in children can cause delayed growth and has been claimed to be the cause of stunted growth in one third of the world's population.

Vitamin E deficiency is rare and is almost never caused by a poor diet. Instead, there are three specific situations when a vitamin E deficiency is likely to occur:

- Premature, very low birth weight infants - birth weights less than 1500 grams, or 3.5 pounds. A neonatologist, a pediatrician specializing in the care of newborns, typically evaluates the nutritional needs of premature infants.

- Rare disorders of fat metabolism - There is a rare genetic condition termed isolated vitamin E deficiency or 'ataxia with isolated with vitamin E deficiency', caused by mutations in the gene for the tocopherol transfer protein. These individuals have an extremely poor capacity to absorb vitamin E and develop neurological complications that are reversed by high doses of vitamin E.

- Fat malabsorption - Some dietary fat is needed for the absorption of vitamin E from the gastrointestinal tract. Anyone diagnosed with cystic fibrosis, individuals who have had part or all of their stomach removed or who have had a gastric bypass, and individuals with malabsorptive problems such as Crohn's disease, liver disease or exocrine pancreatic insufficiency may not absorb fat (people who cannot absorb fat often pass greasy stools or have chronic diarrhea and bloating). Abetalipoproteinemia is a rare inherited disorder of fat metabolism that results in poor absorption of dietary fat and vitamin E. The vitamin E deficiency associated with this disease causes problems such as poor transmission of nerve impulses, muscle weakness, and degeneration of the retina that can cause blindness.

It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age (i.e., over 90).

People dependent on food grown from selenium-deficient soil may be at risk for deficiency. Increased risk for developing various diseases has also been noted, even when certain individuals lack optimal amounts of selenium, but not enough to be classified as deficient.

For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with cholesterol-lowering drugs (e.g., statins) may resemble the pathology of selenium deficiency.

This disorder, epidemiologically speaking, is thought to affect approximately 1 in 50,000 newborns according to Jethva, et al. While in the U.S. state of California there seems to be a ratio of 1 in 35,000.