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.

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.

Increased consumption of zinc is another cause of copper deficiency. Zinc is often used for the prevention or treatment of common colds and sinusitis (inflammation of sinuses due to an infection), ulcers, sickle cell disease, celiac disease, memory impairment and acne. Zinc is found in many common vitamin supplements and is also found in denture creams. Recently, several cases of copper deficiency myeloneuropathy were found to be caused by prolonged use of denture creams containing high quantities of zinc.

Metallic zinc is the core of all United States currency coins, including copper coated pennies. People who ingest a large number of coins will have elevated zinc levels, leading to zinc-toxicity-induced copper deficiency and the associated neurological symptoms. This was the case for a 57-year-old woman diagnosed with schizophrenia. The woman consumed over 600 coins, and started to show neurological symptoms such as unsteady gait and mild ataxia.

Copper deficiency is a very rare hematological and neurological disorder.

The neurodegenerative syndrome of copper deficiency has been recognized for some time in ruminant animals, in which it is commonly known as "swayback". Copper is ubiquitous, and daily requirement is low, making acquired copper deficiency very rare. Copper deficiency can manifest in parallel with vitamin B12 and other nutritional deficiencies.

The most common cause of copper deficiency is a remote gastrointestinal surgery, such as gastric bypass surgery, due to malabsorption of copper, or zinc toxicity. On the other hand, Menkes disease is a genetic disorder of copper deficiency involving a wide variety of symptoms that is often fatal.

Copper is involved in normalized function of many enzymes, such as cytochrome c oxidase, which is complex IV in mitochondrial electron transport chain, ceruloplasmin, Cu/Zn superoxide dismutase, and in amine oxidases. These enzyme catalyze reactions for oxidative phosphorylation, iron transportation, antioxidant and free radical scavenging and neutralization, and neurotransmitter synthesis, respectively. A regular diet contains a variable amount of copper, but may provide 5 mg/day, of which only 20-50% is absorbed. The diet of the elderly may contain a lower copper content than the recommended daily intake. Dietary copper can be found in whole grain cereals, legumes, oysters, organ meats (particularly liver), cherries, dark chocolate, fruits, leafy green vegetables, nuts, poultry, prunes, and soybeans products like tofu.

The deficiency in copper can cause many hematological manifestations, such as myelodysplasia, anemia, low white blood cell count, and low count of neutrophils(a type of white blood cell that is often called "the first line of defense" for the immune system). Copper deficiency has long been known for as a cause of myelodysplasia (when a blood profile has indicators of possible future leukemia development), but it was not until recently in 2001 that copper deficiency was associated with neurological manifestations. Neurological manifestations seen with copper deficiency may include sensory ataxia (irregular coordination due to proprioceptive loss), spasticity, muscle weakness, and more rarely visual loss due to damage in the peripheral nerves, myelopathy (disease of the spinal cord), and rarely optic neuropathy.

Iron is needed for bacterial growth making its bioavailability an important factor in controlling infection. Blood plasma as a result carries iron tightly bound to transferrin, which is taken up by cells by endocytosing transferrin, thus preventing its access to bacteria. Between 15 and 20 percent of the protein content in human milk consists of lactoferrin that binds iron. As a comparison, in cow's milk, this is only 2 percent. As a result, breast fed babies have fewer infections. Lactoferrin is also concentrated in tears, saliva and at wounds to bind iron to limit bacterial growth. Egg white contains 12% conalbumin to withhold it from bacteria that get through the egg shell (for this reason, prior to antibiotics, egg white was used to treat infections).

To reduce bacterial growth, plasma concentrations of iron are lowered in a variety of systemic inflammatory states due to increased production of hepcidin which is mainly released by the liver in response to increased production of pro-inflammatory cytokines such as Interleukin-6. This functional iron deficiency will resolve once the source of inflammation is rectified; however, if not resolved, it can progress to Anaemia of Chronic Inflammation. The underlying inflammation can be caused by fever, inflammatory bowel disease, infections, Chronic Heart Failure (CHF), carcinomas, or following surgery.

Reflecting this link between iron bioavailability and bacterial growth, the taking of oral iron supplements in excess of 200 mg/day causes a relative overabundance of iron that can alter the types of bacteria that are present within the gut. There have been concerns regarding parenteral iron being administered whilst bacteremia is present, although this has not been borne out in clinical practice. A moderate iron deficiency, in contrast, can provide protection against acute infection, especially against organisms that reside within hepatocytes and macrophages, such as malaria and tuberculosis. This is mainly beneficial in regions with a high prevalence of these diseases and where standard treatment is unavailable.

Though genetic defects causing iron deficiency have been studied in rodents, there are no known genetic disorders of human iron metabolism that directly cause iron deficiency.

Cystathioninuria, also called cystathionase deficiency, is an autosomal recessive metabolic disorder that results in an excess of cystathionine in the urine. It is associated with a congenital dysfunction of the enzyme cystathionase, or acquired deficiency of vitamin B which is essential for the function of this enzyme. The latter is usually related to an overall deficiency of all the B-complex vitamins.

Cystathioninuria is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.

There are many studies about LID and the frequency varies according to country of origin, diet, pregnancy status age, gender, etc. Depending on these previous conditions, the frequency can change from 11% in male athletes (Poland) to 44.7% in children less than 1 year old (China):

Frequency of LID in different countries and populations:

- Poland: 14 of LID (11%) in 131 male athletes and 31 of ID (26%) in 121 female athletes

- India: 27.5% of LID amongst student nurses

- Spain: 14.7% of LID in 211 women of child-bearing age in Barcelona

- China: In 3591 pregnant women and 3721 premenopausal from 15 provinces. It was found: LID 42.6% in pregnant women (urban first-trimester 41.9%) (rural 36.1%) while 34.4% of LID in premenopausal non-pregnant women (urban 35.6%)(rural 32.4%). Pediatric samples: In 9118 children from 31 provinces aged 7 months to 7 years, the global incidence of LID in children was 32.5%. Sub-classifying the cases according to age and origin (global/countryside): less than 1 y (7m to 12m) LID 44.7% (35.8% in countryside), 1 – 3 years LID 35.9% (31% in countryside), 4 to 7 years (LID 26.5%) (30.1% in countryside).

A large British study from 2008 found a median estimated life expectancy of 11.6 years.

Congenital tufting enteropathy is an inherited disorder of the small intestine that presents with intractable diarrhea in young children.

Tricho-hepato-enteric syndrome is estimated to affect 1 in 300,000 to 400,000 live births in Western Europe. This syndrome was first reported in 1982 with a report on 2 siblings, and as of 2008 there were around 25 published cases in medical journals. There seem to be no racial differences in its occurrence. It might be more common, as many genetic diseases, in areas with high levels of consanguinity.

There is no consensus on how to treat LID but one of the options is to treat it as an iron-deficiency anemia with ferrous sulfate (Iron(II) sulfate) at a dose of 100 mg x day in two doses (one at breakfast and the other at dinner) or 3 mg x Kg x day in children (also in two doses) during two or three months. The ideal would be to increase the deposits of body iron, measured as levels of ferritin in serum, trying to achieve a ferritin value between 30 and 100 ng/mL. Another clinical study has shown an increase of ferritin levels in those taking iron compared with others receiving a placebo from persons with LID. With ferritin levels higher than 100 ng/mL an increase in infections, etc. has been reported. Another way to treat LID is with an iron rich diet and in addition ascorbic acid or Vitamin C, contained in many types of fruits as oranges, kiwifruits, etc. that will increase 2 to 5-fold iron absorption.

The GM1 gangliosidoses (or GM1 gangliosidos"i"s) are caused by a deficiency of beta-galactosidase, with resulting abnormal storage of acidic lipid materials in cells of the central and peripheral nervous systems, but particularly in the nerve cells.

GM1 Gangliosidoses are inherited, autosomal recessive sphingolipidoses, resulting from marked deficiency of Acid Beta Galactosidase.

Multiple sulfatase deficiency (also known as "Austin disease", and "mucosulfatidosis") is a very rare autosomal recessive lysosomal storage disease caused by a deficiency in multiple sulfatase enzymes, or in formylglycine-generating enzyme, which activates sulfatases. It is similar to mucopolysaccharidosis.

The prevalence of this disorder has been estimated to be 1/50,000-100,000 per live births in Western Europe. It appears to be higher in areas with high degree of consanguinity and in patients of Arabic origin.

The infants present in the first few days of life with watery diarrhoea. This leads rapidly to dehydration and electrolyte imbalance and metabolic decompensation. Enteral feeding with a protein hydrolysate or amino acid based formulas worsen the diarrhoea and the children rapidly fail to thrive and develop protein energy malnutrition.

In the majority of cases the severity of the malabsorption and diarrhoea make them dependent on daily long term total parentral nutrition.

Hepatic fibrosis and cirrhosis are known complications.

Bowel transplantation may be an option.

Tricho-hepato-enteric syndrome (THE), also known as syndromic or phenotypic diarrhea, is an extremely rare congenital bowel disorder which manifests itself as intractable diarrhea in infants with intrauterine growth retardation, hair and facial abnormalities. Many also have liver disease and abnormalities of the immune system. The associated malabsorption leads to malnutrition and failure to thrive.

It is thought to be a genetic disorder with an autosomal recessive inheritance pattern, although responsible genes have not been found and the exact cause remains unknown. Prognosis is poor; many patients die before the age of 5 (mainly from infections or cirrhosis), although most patients nowadays survive with intravenous feeding (parenteral nutrition).

The amount of iron ingested may give a clue to potential toxicity. The therapeutic dose for iron deficiency anemia is 3–6 mg/kg/day. Toxic effects begin to occur at doses above 10–20 mg/kg of elemental iron. Ingestions of more than 50 mg/kg of elemental iron are associated with severe toxicity.

- A 325-mg tablet of ferrous sulfate heptahydrate has 65 mg (20%) of elemental iron

- A 325-mg tablet of ferrous gluconate has 39 mg (12%) of elemental iron

- A 325-mg tablet of ferrous fumarate has 107.25 mg (33%) of elemental iron

- 200 mg ferrous sulfate, dried, has 65 mg (33%) of elemental iron

In terms of blood values, iron levels above 350–500 µg/dL are considered toxic, and levels over 1000 µg/dL indicate severe iron poisoning.

Manganese deficiency can be easy to spot in plants because, much like magnesium deficiency, the leaves start to turn yellow and undergo interveinal chlorosis. The difference between these two is that the younger leaves near the top of the plant show symptoms first because manganese is not mobile while in magnesium deficiency show symptoms in older leaves near the bottom of the plant.

In nature, iron is usually found in its oxidized form, iron (III) oxide, which is insoluble. Ferrous iron, iron (II), is soluble and its toxicity varies, largely with the integrity of the gastrointestinal lining. Iron supplements are typically used to treat anemia. Modalities include: diet, parasite control, vitamin A, riboflavin (B), vitamin C (for absorption), folate(B), vitamin B and multivitamin-multimineral supplements, with or without iron; potentially avoiding the use of iron only supplements.

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.

X-linked recessive chondrodysplasia punctata is a type of chondrodysplasia punctata that can involve the skin, hair, and cause short stature with skeletal abnormalities, cataracts, and deafness.

This condition is also known as arylsulfatase E deficiency, CDPX1, and X-linked recessive chondrodysplasia punctata 1. The syndrome rarely affects females, but they can be carriers of the recessive allele. Although the exact number of people diagnosed with CDPX1 is unknown, it was estimated that 1 in 500,000 have CDPX1 in varying severity. This condition is not linked to a specific ethnicity. The mutation that leads to a deficiency in arylsulfatase E. (ARSE) occurs in the coding region of the gene.Absence of stippling, deposits of calcium, of bones and cartilage, shown on x-ray, does not rule out chondrodysplasia punctata or a normal chondrodysplasia punctata 1 (CDPX1) gene without mutation. Stippling of the bones and cartilage is rarely seen after childhood. Phalangeal abnormalities are important clinical features to look for once the stippling is no longer visible. Other, more severe, clinical features include respiratory abnormalities, hearing loss, cervical spine abnormalities, delayed cognitive development, ophthalmologic abnormalities, cardiac abnormalities, gastroesophageal reflux, and feeding difficulties. CDPX1 actually has a spectrum of severity; different mutations within the CDPX1 gene have different effects on the catalytic activity of the ARSE protein. The mutations vary between missense, nonsense, insertions, and deletions.

Multiple sulfatase deficiency is thought to be caused by any mutation of the SUMF1 gene which would render its protein product, the formylglycine-generating enzyme (FGE), defective. These mutations result in inactive forms of FGE. This enzyme is required for posttranslational modification of a cysteine residue in the sulfatase enzyme active site into formylglycine, which is required for its proper function.

The only known cause of this condition is a mutation in the X-linked chondrodysplasia punctata 1 (CDPX1) gene. Mutations in this gene result in a deficiency of arylsulfatase E. Only 50-60% of cases have been shown to have mutations in this gene and the cause of the remaining cases is not yet known.The CDPX1 gene is located on the short arm of the X chromosome (Xp22.3) on the Crick (minus) strand. It is 33,614 bases in length.

The mature protein has a molecular weight of 68 kiloDaltons. It is glycosylated and is located in the Golgi apparatus. Its activity may be inhibited by warfarin. It seems likely that warfarin induced embryotoxicity may be due at least in part to this inhibition.

Brachytelephalangic chondrodysplasia punctata (BCDP) is a term used to describe CDPX1 and the non-genetic, or environmentally produced, phenocopies associated with the condition. Causes of BCDP can also come from genetic effects, mainly due to mutations. Keutel syndrome, deficiency of vitamin K epoxide reductase subunit 1 (VKORC1), gamma-glutamyl carboxylase (GGCX), Xp contiguous deletion syndromes, and multiple sulfatase deficiency are all genetic conditions that are associated BCDP.

Secondary hypolactasia or secondary lactase deficiency, also called acquired hypolactasia or acquired lactase deficiency, is caused by an injury to the small intestine. This form of lactose intolerance can occur in both infants and lactase persistent adults and is generally reversible. It may be caused by acute gastroenteritis, coeliac disease, Crohn's disease, ulcerative colitis, chemotherapy, intestinal parasites (such as giardia), or other environmental causes.