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science nutrition blog

science nutrition <strong>blog</strong>

By Michael J. Rudolph, Ph.D.

 

New research says that too much iron, copper and manganese boosts oxidative damage, inflammation and chronic disease.1-6

Iron is an essential trace element typically found in enzymes and proteins that participate in numerous biological processes such as enzymatic reactions and the transport of oxygen throughout the body. Iron deficiency is one of the most common deficiencies in the USA, according to the CDC, creating a large demand for iron-containing supplements. However, the use of iron-containing supplements doesn’t seem to be such a good idea as the daily requirement for iron ranges from 8 milligrams for men to 18 milligrams for premenopausal women, which is normally the amount of iron found in most multivitamin and mineral products. So, you may be asking, are multivitamins good for your health, and why shouldn’t you take these iron-containing supplements, especially if they’re providing the daily requirement? Because you’re also getting generous amounts of iron from your diet, as many common foods are heavily fortified with iron such as cereals, bread and pasta. So, supplementing a diet with iron-fortified foods will conceivably lead to the consumption of too much iron, which may not sound so terrifying. That is, until you realize that several recent studies have shown that too much iron in the diet can increase oxidative stress and boost inflammation7, which is a hallmark for many life-threatening diseases.

Iron is found in the body in two forms: one form is bound to the prosthetic heme group, while the other is in a free form unbound to heme. The free form of iron can be harmful because it reacts with other compounds in the body, producing free radicals causing irreparable oxidative damage to key components of the cell, including proteins, lipids and DNA. Consequently, when inside the cell, the free form of iron is stored inside a protein called ferritin, which prevents the unwanted release of iron to avoid oxidative damage. In fact, studies have shown that increased dietary iron intake increases cellular levels of ferritin to provide greater storage capacity for the additionally ingested iron. Yet, unexpectedly, greater ferritin levels induced by iron intake actually triggers inflammation7, increasing the risk for obesity8 and diabetes.7,9 This is likely because higher ferritin levels function as a signal to the body that a lot of iron is around. The body responds to this signal by activating the immune system, which can prevent the release of iron from the primary iron-storage site, the liver. So, essentially, the body is doing its best to lower serum iron levels despite the fact that it could cause chronic inflammation and disease. In addition, this unexpected inflammation from too much iron intake may also be due to iron intake exceeding the storage capacity of ferritin, resulting in the release of free iron into the cell, causing additional oxidative damage and inflammation. Iron has been suggested as a risk factor for cardiovascular disease and different types of cancer.

Comparable to iron, the element copper also generates oxidative damage, particularly in neurons, making too much copper intake in the diet unhealthy, as evidence shows that ingestion of copper from supplement pills, along with a high fat diet, contributes to the onset of Alzheimer’s disease.10 More specifically, it was shown that serum copper levels were elevated in patients with Alzheimer’s disease and this higher copper level correlated with loss of cognition. In addition, copper accumulation in certain tissues has also been associated with certain pathologies including cancer, as copper can contribute to the growth of certain cancers while improving cancer metastasis in other forms.11,12

Excessive consumption of the element manganese has also been identified as a health risk, as accumulation of manganese in the central nervous system promotes neurotoxicity, resulting in the neurological brain disorder manganism. In addition, elevated serum levels of manganese have been found in different neurodegenerative diseases, including Parkinson’s disease13,14,15 where manganese has been shown to promote the production of the abnormal protein aggregates called Lewy bodies that apparently contribute to Parkinson’s disease.

 

Manganese’s deleterious influence on health is likely due, in part, from oxidative damage within the body, as manganese can generate free radicals in a similar fashion to iron and copper. Manganese also tends to accumulate in specific cells in the brain called the astrocytes, causing them to malfunction. Since the astrocyte normally provides essential nutrients to neurons, malfunction of the astrocyte prevents the required nutrition for the neuron, thus depleting neuronal function and promoting neurodegeneration.16 Because of the inherent medical risks associated with superfluous iron, copper and manganese intake, Thermo Heat Multi does not contain any form of these elements.

TOO MUCH CALCIUM INCREASES CARDIOVASCULAR DISEASE RISK

Calcium intake has been promoted for quite some time because of its apparent ability to improve bone health. Calcium is also required for many other essential bodily functions, including nerve function, muscular contraction and the regulation of certain hormones.12 ,17 As a result, most multivitamins contain a considerable amount of the daily recommended allowance for calcium.

However, a few recent studies indicate that calcium supplementation may not be as beneficial to bone health as once thought and may actually be detrimental to cardiovascular health. The first report states that while calcium may slow bone loss to some degree, there is no significant reduction in fracture prevention.13,18 In a second report by the National Institutes of Health, it was shown that calcium supplements, not dietary calcium, increased the risk of death from cardiovascular disease.14,19 Because of the apparent adverse effects associated with calcium supplementation along with an inability to enhance bone health, Thermo Heat Multi does not contain any form of calcium.

 

©Published by Advanced Research Media, Inc. 2022

©Reprinted with permission from Advanced Research Media, Inc.

 

For most of Michael Rudolph’s career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a research scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biological effects of exercise as a fellow at Harvard Medical School and Columbia University. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK – leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a Senior Scientist working at the New York Structural Biology Center where he investigates the molecular nature of human illness and disease.

 

References:

 

  1. Cheng R, Dhorajia VV, Kim J, Kim Y. Mitochondrial iron metabolism and neurodegenerative diseases. Neurotoxicology. 2022 Jan;88:88-101. doi: 10.1016/j.neuro.2021.11.003. Epub 2021 Nov 5. PMID: 34748789; PMCID: PMC8748425.

 

  1. Yuan J, Liu T, Zhang Y. An Iron Metabolism-Related Gene Signature for the Prognosis of Colon Cancer. Front Cell Dev Biol. 2022 Jan 18;9:786684. doi: 10.3389/fcell.2021.786684. PMID: 35118074; PMCID: PMC8804292.

 

  1. Iglesias-Vázquez L, Arija V, Aranda N, Aglago EK, Cross AJ, Schulze MB, Quintana Pacheco D, Kühn T, Weiderpass E, Tumino R, Redondo-Sánchez D, de Magistris MS, Palli D, Ardanaz E, Laouali N, Sonestedt E, Drake I, Rizzolo L, Santiuste C, Sacerdote C, Quirós R, Amiano P, Agudo A, Jakszyn P. Factors associated with serum ferritin levels and iron excess: results from the EPIC-EurGast study. Eur J Nutr. 2022 Feb;61(1):101-114. doi: 10.1007/s00394-021-02625-w. Epub 2021 Jul 2. PMID: 34213605.

 

  1. Armstrong A, Mandala A, Malhotra M, Gnana-Prakasam JP. Canonical Wnt Signaling in the Pathology of Iron Overload-Induced Oxidative Stress and Age-Related Diseases. Oxid Med Cell Longev. 2022 Jan 25;2022:7163326. doi: 10.1155/2022/7163326. PMID: 35116092; PMCID: PMC8807048.

 

  1. Meng H, Wang Y, Ruan J, et al. Decreased Iron Ion Concentrations in the Peripheral Blood Correlate with Coronary Atherosclerosis. Nutrients. 2022;14(2):319. Published 2022 Jan 13. doi:10.3390/nu14020319

 

  1. Tsvetkov P, Coy S, Petrova B, Dreishpoon M, Verma A, Abdusamad M, Rossen J, Joesch-Cohen L, Humeidi R, Spangler RD, Eaton JK, Frenkel E, Kocak M, Corsello SM, Lutsenko S, Kanarek N, Santagata S, Golub TR. Copper induces cell death by targeting lipoylated TCA cycle proteins. Science. 2022 Mar 18;375(6586):1254-1261. doi: 10.1126/science.abf0529. Epub 2022 Mar 17. PMID: 35298263.

 

  1. Andrews M, Soto N and Arredondo-Olguin M. Association between ferritin and hepcidin levels and inflammatory status in patients with type 2 diabetes mellitus and obesity. Nutrition 2015;31, 51-57.

 

  1. Iwasaki T, Nakajima A, et al. Serum ferritin is associated with visceral fat area and subcutaneous fat area. Diabetes Care 2005;28, 2486-2491.

 

  1. Jiang R, Manson JE, et al. Body iron stores in relation to risk of type 2 diabetes in apparently healthy women. Jama 2004;291, 711-717.

 

  1. Brewer GJ. Alzheimer's disease causation by copper toxicity and treatment with zinc. Front Aging Neurosci 2014;6, 92.

 

  1. MacDonald G, Nalvarte I, et al. Memo is a copper-dependent redox protein with an essential role in migration and metastasis. Sci Signal 2014;7, ra56.

 

  1. Jimenez-Jimenez FJ, Molina JA, et al. Cerebrospinal fluid levels of transition metals in patients with Parkinson's disease. J Neural Transm 1998;105, 497-505.

 

  1. Takagi Y, Okada A, et al. Evaluation of indexes of in vivo manganese status and the optimal intravenous dose for adult patients undergoing home parenteral nutrition. Am J Clin Nutr 2002;75, 112-118.

 

  1. Hozumi I, Hasegawa T, et al. Patterns of levels of biological metals in CSF differ among neurodegenerative diseases. J Neurol Sci 2011;303, 95-99.

 

  1. Sidoryk-Wegrzynowicz M and Aschner M. Manganese toxicity in the central nervous system: the glutamine/glutamate-gamma-aminobutyric acid cycle. J Intern Med 2013;273, 466-477.

 

  1. Brady DC, Crowe MS, et al. Copper is required for oncogenic BRAF signalling and tumorigenesis. Nature 2014;509, 492-496.

 

  1. Larsson SC. Are calcium supplements harmful to cardiovascular disease? JAMA Intern Med 2013;173, 647-648.

 

  1. Reid IR. Should we prescribe calcium supplements for osteoporosis prevention? J Bone Metab 2014;21, 21-28.

 

  1. Bolland MJ, Avenell A, et al. Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. Bmj 2010;341, c3691.