Once again, I make testament to the sheer awe and wonder of the human being and pay homage to all its incredible machinations. Far too much attention is given to big macronutrients and vitamins that we are all too familiar with and not enough attention gets given to a small but essential group of elements that arguably influence every single biochemical process in the human body. We all know what protein and carbohydrates are and we all know what to associate vitamin D and C with but despite these being major components of the food we eat; we should familiarise ourselves with the trace elements. Despite the periodic table of elements being so vast and complex, only a small percentage of the elements have been identified to play pivotal roles in physiology. Armed with the knowledge of how these elements impact health, empowers one to enhance their pantry and refrigerator whenever they suspect they may be lacking or deficient in one of these elements. 

It is estimated that 98% of the body mass of man is made up of nine non-metallic elements. The four main electrolytes (sodium, calcium, potassium, magnesium) only constitute about 1.89% of that mass, while 0.02% or 8.6 grams is comprised of 11 trace elements. As I mentioned above, despite these elements comprising such a minute portion of a human’s mass, their physiological and biochemical implications are tremendous (Prashanth et al, 2015). Trace elements have several primary functions, including acting as a co-factor for enzymes that catalyse a myriad of reactions, donating or accepting electrons in redox reactions for the generation and use of metabolic energy, and supporting the structure and stability of certain molecules (Al-Fartusie & Mohssan, 2017).  Below is a list of the major trace elements, their dietary sources and dietary intake recommendations and I’ve written about them in order from the well-known elements to the least known. 

Trace element	Recommended daily intake (RDI)	Recommended dietary allowance (RDA)	Tolerable upper intake level (UL)	Dietary sources
Copper	2000 mcg (micrograms)	Children 1 to 3 years old: 340 mcg/day; 4 to 8 years old: 440 mcg/day; 9 to 13 years old: 700 mcg/day; 14 to 18 years old: 890 mcg/day Men and women aged 19 years and older: 900 mcg/day Pregnancy: 1000 mcg/day Lactation: 1300 mcg/day	Children 1 to 3 years old: 1 mg/day; 4 to 8 years old: 3 mg/day; 9 to 13 years old: 5 mg/day; 14 to 18 years old: 8 mg/day Adults 19 years old and above (including lactation): 10 mg/day Pregnancy: 8 mg/day	Oysters, other shell fish, whole grains, beans, nuts, potatoes, organ meats (kidney, liver), dark leafy greens, dried fruits, and yeast
Iron	18 mg	Children 1 to 3 years old: 7 mg/day; 4 to 8 years old: 10 mg/day; 9 to 13 years old: 8 mg/day Boys 14 to 18 years old: 11 mg/day Girls 14 to 18 years old: 15 mg/day Adults: 8 mg/day for men aged 19 and older and women aged 51 and older Women 19 to 50 years old: 18 mg/day Pregnant women: 27 mg/day Lactating mothers: 10 mg/day	Infants and children from birth to the age of 13: 40 mg/day Children aged 14 and adults (including pregnancy and lactation): 45 mg/day	Haem iron: liver, meat, poultry, and fish Nonheme iron: cereals, green leafy vegetables, legumes, nuts, oilseeds, jaggery, and dried fruits
Zinc	15 mg	Infants and children 7 months old to 3 years old: 3 mg/day; 4 to 8 years old: 5 mg/day; 9 to 13 years old: 8 mg/day Girls 14 to 18 years old: 9 mg/day Boys and men aged 14 and older: 11 mg/day Women 19 years old and above: 8 mg/day Pregnant women: 11 mg/day Lactating women: 12 mg/day	Infants: 4-5 mg/day Children 1 to 3 years old: 7 mg/day; 4 to 8 years old: 12 mg/day; 9 to 13 years old: 23 mg/day;14 to 18 years old: 34 mg/day Adults 19 years old and above (including pregnancy and lactation): 40 mg/day	Animal food: meat, milk, and fish Bioavailability of zinc in vegetable food is low
Cobalt	6 mcg	Infants: 0.5 mcg Children 1–3 years old: 0.9 mcg; 4–8 years old: 1.2 mcg; 9–13 years old: 1.8 mcg Older children and adults: 2.4 mcg Pregnant women: 2.6 mcg Lactating mothers: 2.8 mcg	Not known	Fish, nuts, green leafy vegetables (broccoli, spinach), cereals, and oats
Chromium	120 mcg	Children 1 to 3 years old: 11 mcg; 4 to 8 years old: 15 mcg Boys 9 to 13 years old: 25 mcg Men 14 to 50 years old: 35 mcg Men 51 years old and above: 30 mcg Girls 9 to 13 years old: 21 mcg; 14 to 18 years old: 24 mcg Women 19 to 50 years old: 25 mcg; 51 years old and above: 20 mcg Pregnant women: 30 mcg Lactating women: 45 mcg	Doses larger than 200 mcg are toxic	Best sources: processed meats, whole grains, and spices
Molybdenum	75 mcg	Children 1 to 3 years old: 17 mcg/day; 4 to 8 years old: 22 mcg/day; 9 to 13 years old: 34 mcg/day; 14 to 18 years old: 43 mcg/day Men and women aged 19 years and above: 45 mcg/day Pregnancy and lactation: 50 mcg/day	Children: 300–600 mcg/day Adults (including pregnancy and lactation): 1100–2000 mcg/day	Animal food: liver; vegetables: lentils, dried peas, kidney beans, soybeans, oats, and barley
Selenium	70 mcg	Children 1–3 years old: 20 micrograms/day Children 4–8 years old: 30 micrograms/day Children 9–13 years old: 40 micrograms/day Adults and children 14 years old and above: 55 micrograms/day Pregnant women: 60 micrograms/day Breastfeeding women: 70 micrograms/day	The safe upper limit for selenium is 400 micrograms a day in adults	Liver, kidney, seafood, muscle meat, cereal, cereal products, dairy products, fruits, and vegetables, brazil nuts
Iodine	150 mcg	Children 1 to 8 years old: 90 mcg/day; 9 to 13 years old: 120 mcg/day Children aged 14 and adults: 150 mcg/day Pregnant women: 209 mcg/day Lactating mothers: 290 mcg/day	Children 1 to 3 years old: 200 mcg/day; 4 to 8 years old: 300 mcg/day; 9 to 13 years old: 600 mcg/day; 14 to 18 years old: 900 mcg/day Adults above the age of 19 including pregnant and breastfeeding women: 1100 mcg/day	Best sources: seafoods (sea fish and sea salt) and cod liver oil Small amounts: milk, vegetables, and cereals (Bhattacharya et al, 2016)

Iodine

Anyone who has a remote idea of what iodine is will likely tell you that it has something to do with the thyroid gland and this is true because iodine is a central component of both thyroid hormones, T3 (triiodothyronine, the more active form) and T4 (thyroxine). When iodine is deficient, thyroid-stimulating hormone (TSH) is secreted from the pituitary gland, which increases the expression of the sodium-iodide symporter (membrane protein that transports molecules) to maximise the uptake of iodine into thyroid cells. A sudden rise in iodine intake when the person was deficient can result in hyperthyroidism because thyrocytes in the nodules (formed as a result of iodine deficiency) of the thyroid can be insensitive to TSH control and thus overproduce thyroid hormone (Zimmerman & Boelaert, 2015). The implication here is that as a trace element, either too much or too little intake can lead to dysfunction and disease.   

To highlight the importance of iodine for thyroid function, 70-80% of all the iodine in a healthy adult (~20mg) is stored in the thyroid gland. However, iodine also has critical implications in other areas, such as the brain, because thyroid hormone receptors in the central nervous system mediate most of the activities of T3. In the developing brain, iodine is involved in the acceleration of myelination, and improving cell migration, differentiation and maturation. Thyroid hormones also modulate the expression of genes associated with synaptic plasticity and memory. Therefore, iodine deficiency in utero can lead to poorer cognitive outcomes in children and cause neurodevelopmental disorders, such as cretinism (Zimmerman, 2011). 

Zinc

Zinc is the 24^th most abundant element in the earth’s crust and plays integral roles in cellular respiration, immune function, protein synthesis, wound healing, DNA synthesis and cell division. Zinc has a high turnover rate so adequate dietary intake is essential to meet the body’s demands and given that there are estimated to be 3000 proteins in the zinc proteome (potential proteins in a genome), it pays to say that zinc is a critical trace element. In terms of functions, zinc is a structural component of different proteins involved in the transcriptional machinery (transcription factors and ribosomes) and is also a master growth and proliferation factor, involved in regulating cell division. As the immune system is highly proliferative, zinc is crucial for maintain optimal immune responses. Zinc’s immune-related functions are;

• Acting as a chemo-attractant for polymorphonuclear cells of the innate system (neutrophils, eosinophils, basophils, and mast cells)
• Increases phagocytosis and NADPH (nicotinamide adenine dinucleotide phosphate) production, which regulates superoxide anion production that destroys pathogens after phagocytosis
• Modulates natural killer (NK) cell response and increases their cytotoxicity and differentiation of CD34+ cells towards natural killer cells
• Increases production of B cells and T cells and differentiation of pre-T cells into mature T cells
• Balancing of T-cell subsets between cytotoxic T cells and total T cells (zinc deficiency can lead to a dysfunction of the immune system and trigger autoimmune reactions) (Bonaventura et al, 2015) 

Furthermore, zinc is required for the catalytic activity of more than 200 enzymes and approximately 10% of all human proteins may potentially bind to zinc. Carbonic anhydrase and carboxypeptidase are examples of zinc-containing enzymes that are vital to the processes of carbon dioxide regulation and protein digestion, as carbonic anhydrase converts carbon dioxide into bicarbonate and vice versa for exhalation via the lungs and carboxypeptidase breaks down peptide bonds in proteins.  

It is important to note that as zinc is a trace element, excessive consumption of zinc can impair copper absorption because both metals require metallothionein proteins for absorption (Osredkar & Sustar, 2011). 

 Copper

Inorganic elements, such as copper and iron are neither created nor destroyed, once they have been solubilized from the earth’s crust, and therefore exist under strict homeostatic regulation. After the inception of photosynthetic organisms, such as cyanobacteria, the solubility of iron decreased, and the biological roles of copper expanded. Copper exists in either a reduced state (Cu+) or an oxidized state (Cu2+). Reduced copper has an affinity for thiol and thioether groups (cysteine or methionine) and oxidized copper coordinates with oxygen or imidazole nitrogen groups (aspartic/glutamic acid or histidine, therefore copper interacts with a wide array of protein to catalyse a myriad of biochemical reactions. The brain and the heart are major storage sites of copper in the human body because they have a high demand for mitochondrial oxidative phosphorylation, which is an essential process for energy production and is partly dependent on copper (Festa & Thiele, 2011).

Most of the copper in humans (~150 mg) is bound to ceruloplasmin (a copper-containing protein) and in red blood cells, it is bound to the copper-zinc metalloenzyme, superoxide dismutase, a very powerful antioxidant. Copper is also a component of other enzymes, such as cytochrome oxidase, monoamine oxidase, catalase, peroxidase, ascorbic acid oxidase, lactase and tyrosinase. This elucidates that copper is necessary for many metabolic reactions, including energy production (as mentioned above), antioxidant production, metabolism of neurotransmitters, vitamin C, protein and carbohydrates, and production of structural components of tissues (Al-Fartusie & Mohssan, 2017) & (Prashanth et al, 2015). Additionally, copper is vital in the metabolism of iron as both ferroxidases, ceruloplasmin and hephaestin catalyse the oxidation of iron released from enterocytes (intestinal cells) and convert ferrous iron (Fe2+) to ferric iron (Fe3+). Without adequate production of these copper proteins, iron will accumulate in tissues and cause oxidative stress (Coffey & Ganz, 2017).  

Silicon

Silicon is the second most abundant element in the earth’s crust and the third most abundant trace element in humans, existing primarily as oxygen-containing silica and silicates. Silica is present at 1-10 parts-per-million in hair, nails, and the epidermis, indicating that it is an integral component of integumentary structures. Additionally, silica is involved in bone mineralization, collagen synthesis, and prevention of skin aging. Orthosilicic acid-releasing zeolites (crystalline earth metals containing silica) can induce osteoblastogenesis, formation of extracellular matrix, induced synthesis of osteocalcin and activity of alkaline phosphatase, both produced by osteoblasts and reflect bone formation activity (Sigel et al, 2013, p. 452-463).

In relation to bone and integumentary health, the reason silica is involved in their structural formation is because it is necessary for the synthesis of collagen and glycosaminoglycan, which are required for bone matrix formation and are also integral components of connective tissues. Diets that are low in silica have been associated with skull and bone disabilities. Another benefit of silica is its role in mineral balance, as silica has been shown to increase the absorption and utilization of magnesium and cooper (Farooq & Dietz, 2015).  

Selenium

Selenium as a trace element, exerts its effects through the action of at least 25 different selenoproteins. Enzymes, such as glutathione peroxidases (GPxs) and thioredoxin reductases (TrxRs) require selenium to function and protect against oxidative stress, so selenium is involved in the prevention and management of a wide variety of conditions that involve inflammation. For example, GPxs, TrxRs, and selenoprotein P can maintain redox homeostasis and error-free protein folding, which prevents DNA oxidative mutagenic stress that drives cancer. Selenoproteins also inhibit cell proliferation, stimulate apoptosis and reduce metastasis arresting the cell cycle in the G1 phase. Additionally, selenium metabolites, such as methylselenol, selenodiglutathione, selenomethionine, and hydrogen selenide also exert anticarcinogenic effects by enhancing apoptosis, inhibiting activator protein 1 transcription factor (inflammatory gene expression regulator) and cell proliferation (Barchielli et al, 2022). 

Paradoxically, selenolates may exert anticarcinogenic effects by catalysing the opposite of their anti-inflammatory actions by reacting with molecular oxygen to produce superoxide. The superoxide, being a strong oxidant, may push a cancer cell over an oxidative cliff, causing it to die via apoptosis.  Selenium supplementation at a dose of 200 micrograms per day in the form of selenized yeast led to significant reductions in colon, prostate, and lung cancers. Additionally, total cancer mortality over a ten-year period was also significantly reduced because of selenium supplementation. Deficiency in selenium is linked to two conditions in humans, Keshan disease, a type of cardiomyopathy that may have a viral aetiology, and Kashin-Back disease, an osteoarticular disorder that resembles rheumatoid arthritis but is more severe. It’s thought that selenium deficiency causes decreased expression of glutathione reductase, and in turn, result in oxidative stress that drives myocardial injury. The discovery of Keshan disease and selenium-contain proteins is what established selenium as an essential trace element for humans (Reich & Hondal, 2016).  

Manganese

The average human contains about 12 milligrams of manganese and over 40% of it is stored in the skeletal system and the rest is stored in the liver, pancreas, brain, kidneys, and central nervous system (Al-Fartusie & Mohssan, 2017). Manganese supports biochemical functions pertaining to bone formation, fat and carbohydrate metabolism, blood sugar regulation, and calcium absorption. Despite copper and magnesium being able to substitute for manganese as a cofactor for some enzymes, manganese is essential for a series of enzymes (manganoproteins) that influence brain function, including glutamine synthetase (GS), superoxide dismutase 2 (SOD2), arginase, pyruvate decarboxylase, and serine/threonine phosphatase.

• Glutamine synthetase, the most abundant manganoprotein, converts glutamate to glutamine
  • It is expressed in astrocytes and decreased expression of GS from manganese deficiency can lead to excitotoxicity due to increased glutamate trafficking 
• Superoxide dismutase 2 is a mitochondrial enzyme that detoxifies superoxide anions through the formation of hydrogen peroxide
  • Low SOD2 activity can increase the susceptibility to mitochondrial inhibitor-induced toxicity and oxidative stress 
• Arginase regulates the elimination of ammonia from the body by converting L-arginine, from ammonia, to L-ornithine and urea, as part of the urea cycle
  • L-arginine is also converted to nitric oxide by nitric oxide synthetase in neurons, supporting blood flow in the brain
• Pyruvate carboxylase is essential for glucose metabolism and interacts with manganese to synthesize oxaloacetate, a precursor of the energy-generating TCA (tricarboxylic acid) cycle  
• Threonine/serine phosphatase (protein phosphatase 1) is involved in glycogen metabolism
  • Neurotrophin synthesis, which promotes neuronal survival and synaptic membrane receptors and channels (synaptic structure) (Bowman et al, 2011)       

Chromium

The role of chromium as a trace element became apparent after a small group of patients who were on parenteral (intravenous) nutrition, developed symptoms of adult-onset diabetes, which were reversed when chromium was added to their diet. Additionally, low chromium diets have been associated with the development of insulin resistance and increases in serum glucose tend to be accompanied to by increases in urinary chromium excretion. Chromodulin, the active binding site of chromium, activates tyrosine kinase activity of insulin-activated insulin receptors and phosphotyrosine phosphatase in adipocyte membranes. These processes are necessary for insulin signalling, implying that chromium plays an important role in carbohydrate metabolism (Vincent, 2004). Aside from carbohydrate metabolism, chromium has also been implicated in stimulating fatty acid and cholesterol synthesis from acetate in the liver. (Al-Fartusie & Mohssan, 2017)

Boron

In biochemistry, boron, or boric acid, forms ester complexes with hydroxyl groups of organic compounds, which results in the formation of complexes with several biologically important sugars. These sugars include ribose, a component of adenosine. The beneficial attributes of boron are thought to occur through its effect on the action of biomolecules containing adenosine or formed from adenosine precursors. For example, S-adenosylmethionine (SAMe), which I wrote an article about, and diadenosine phosphates have very high affinity for boron than other boron ligands recognized in animal tissues. Diadenosine phosphates function as signalling proteins in neuronal responses and SAMe is a widely used enzyme substrate that functions primarily in methylation reactions, which influence genetic activity (DNA/RNA), proteins, phospholipids, hormones and neurotransmitters.

These effects may explain why boron supplementation has been shown markers of inflammation in arthritis cases, improve markers of bone formation and structure, and improve electroencephalogram (EEG) readings (less activity in lower frequencies and increased activity in higher, dominant frequencies), translating to improved psychomotor skills of motor speed and dexterity and attention and short-term memory (Nielsen, 2014) & (Khaliq et al, 2018).    

Cobalt

The average human contains about 1.1 grams of cobalt with the daily requirement sitting at around 0.0001 mg/day and it is found in the environment combined with elements such as oxygen, sulphur, and arsenic. It is widely spread in nature, being found in rocks, soil, plants, and animals, and humans can acquire cobalt through skin contact, inhalation, and oral routes but most of the cobalt that humans consume comes from the diet. Cobalt plays a role in methionine metabolism by influencing the transfer of enzymes like homocysteine methyltransferase (Bhattacharya et al, 2016). Cobalt is a core constituent of cobalamin, or vitamin B12, which is produced as hydroxocobalamin within bacteria and converts to methylcobalamin and 5’-deoxyadenosylcobalamon, the enzymatically active cofactor forms of B12. Vitamin B12-containing cobalt salts, stimulate the production of erythropoietin, the hormone that triggers red blood cell formation (Prashanth et al, 2015). Additionally, cobalt is involved in the formation of amino acids (for myelin sheath generation) and neurotransmitters and deficiency in this element can cause anaemia and hypothyroidism or symptoms that are associated with disruption of vitamin B12 synthesis (Al-Fartusie & Mohssan, 2017). 

Molybdenum

Molybdenum is an integral component five key enzymes, referred to as molybdoenzymes, which metabolize a wide range of endogenous and exogenous compounds, including 

• sulphur-containing amino acids by sulfite oxidase, 
• purines by xanthine oxidoreductase, 
• aldehydes by aldehyde oxidase
• amidoximes by mitochondrial amidoxime reducing components.

These are all examples of molybdoenzymes and a lack sulfite oxidase, from molybdenum deficiency could be lethal, due to the accumulation of sulfite. In humans, molybdate anion, the naturally occurring form of molybdenum, is transported into cells and encompassed within the molybdenum cofactor (Moco), which is integrated into molybdoenzymes for their functionality and the synthesis of Moco is dependent on iron, copper, ATP, and six proteins. The basis of molybdoenzymes in humans lies in their integral role in the metabolism of amino acids and the catabolism (breakdown) of toxic substrates and pharmaceuticals. For example, retardation, seizures and neonatal death ca be the consequence in the mutation of sulfite oxidase genes, as sulfite oxidase degrades cysteine and methionine (sulfur amino acids) and oxidises toxic sulfite into sulfate. Additionally, accumulation of xanthine, from a lack of xanthine oxidoreductase can lead to kidney damage due to obstruction of renal tracts from xanthine stone formation (Foteva et al, 2023).

References

Al-Fartusie, F.S. & Mohssan, S.N. (2017). Essential trace elements and their vital roles in human body. Indian journal of advances in chemical science, 5(3), 127-136.  http://www.ijacskros.com/5%20Volume%203%20Issue/10.22607IJACS.2017.503003.pdf

Barchielli, G., Capperucci, A., & Tanini, D. (2022). The role of selenium in pathologies: an updated review. Antioxidants, 11(2), 251. https://doi.org/10.3390/antiox11020251

Bhattacharya, P.T., Misra, S.R., & Hussain, M. (2016). Nutritional aspects of essential trace elements in oral health and disease: an extensive review. Scientifica, 2016. https://doi.org/10.1155/2016/5464373

Bonaventura, P., Benedetti, G., Albarède, F., & Miossec, P. (2015). Zinc and its role in immunity and inflammation. Autoimmunity reviews, 14(4), 277-285. https://cdn.doctorcarnivoor.nl/wp-content/uploads/2020/10/13191105/Zinc-and-its-role-in-immunity-and-inflammation_2015.pdf

Bowman, A.B., Kwakye, G.F., Hernanxez, E.H., & Aschner, M. (2011). Role of manganese in neurodegenerative diseases. Journal of trace elements in medicine and biology, 25(4), 191-203.  http://www.peirsoncenter.com/uploads/6/0/5/5/6055321/nihms320402.pdf

Coffey, R., & Ganz, T. (2017). Iron homeostasis: an anthropocentric perspective. Journal of biological chemistry, 292(31), 12727-12734. https://doi.org/10.1074/jbc.R117.781823

Farooq, M.A., & Dietz, K.J. (2015). Silicon as versatile player in plant and human biology: overlooked and poorly understood. Frontiers in plant science, 6, 994.  https://doi.org/10.3389%2Ffpls.2015.00994

Festa, R.A., & Thiele, D.J. (2011). Copper: an essential metal in biology. Current biology, 21(21), 877-883. https://doi.org/10.1016/j.cub.2011.09.040

Foteva, V., Fisher, J.J., Qiao, Y., & Smith, R. (2023). Does the micronutrient molybdenum have a role in gestational complications and placental health? Nutrients, 15(15), 3348.  https://doi.org/10.3390/nu15153348

Khaliq. H., Juming, Z., & Ke-Mei, P. (2018). The physiological role of boron on health. Biological trace element research, 186(1), 31-51.  https://www.researchgate.net/profile/Haseeb-Khaliq/publication/323792821_The_Physiological_Role_of_Boron_on_Health/links/5b708af7299bf14c6d9ad27d/The-Physiological-Role-of-Boron-on-Health.pdf

Nielsen, F.H. (2014). Update on human health effects of boron. Journal of trace elements in medicine and biology, 28(4), 383-387. https://doi.org/10.1016/j.jtemb.2014.06.023

Osredkar, J., & Sustar, N. (2011). Copper and zinc, biological role and significance of copper/zinc imbalance. The journal of clinical toxicology. https://www.researchgate.net/profile/Josko-Osredkar/publication/276948688_Copper_and_Zinc_Biological_Role_and_Significance_of_CopperZinc_Imbalance/links/56d551da08aefd177b10a2f6/Copper-and-Zinc-Biological-Role-and-Significance-of-Copper-Zinc-Imbalance.pdf

Prashanth, L., Kattapagari, K.K., Chitturi, R.T., Baddam, V.R.R., et al. (2015). A review on role of essential trace elements in health and disease. Journal of Dr. NTR University of Health Sciences, 4(2), 75-85.  https://journals.lww.com/jntr/Fulltext/2015/04020/A_review_on_role_of_essential_trace_elements_in.2.aspx

Reich, H.J., & Hondal, R.J. (2016). Why nature chose selenium. ACS chemical biology, 11(4), 821-841. https://www2.chem.wisc.edu/areas/reich/papers/Reich-2016-Why-Selenium-ACS-Chem-Biol.pdf

Sigel, A., Sigel, H., & Sigel, R.K.O. (Eds.) (2013). Interrelations between essential metal ions and human diseases. Springer. https://books.google.com.au/books?hl=en&lr=&id=6OIlBAAAQBAJ&oi=fnd&pg=PA451&ots=nNMwOjcZXQ&sig=o8SLFNOAwYdb5NX58se4ZGduY_w&redir_esc=y#v=onepage&q&f=false

Vincent, J.B. (2004). Recent advances in the nutritional biochemistry of trivalent chromium. Proceedings of the nutrition society, 63(1), 41-47. https://doi.org/10.1079/PNS2003315

Zimmermann, M.B., & Boelaert, K. (2015). Iodine deficiency and thyroid disorders. The Lancet diabetes & endocrinology, 3(4), 286-295. https://www.uni-potsdam.de/fileadmin/projects/international-nutrition/images/Workshop_2015_Thailand/Iodine_deficiency_and_Thyroid_disorder.pdf

Zimmerman, M.B. (2011). The role of iodine in human growth and development. Seminars in cell & developmental biology, 22(6), 645-652. https://doi.org/10.1016/j.semcdb.2011.07.009