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Research Supporting Minerals for Cognitive Health.

The growing population of adults over 55 continues to drive more interest in cognitive health. However, the desire to support brain function isn't exclusive to older patients, as younger people, including Millennials are taking more personal interest in their health. Additionally, more emphasis has been placed on the need for proper nutrition during pregnancy in order to deliver infants with well-developed brain function.

The maintenance of good nutritional status is important for normal cognition. Numerous studies have shown that certain micronutrients are directly or indirectly involved in many aspects of cognitive function. These micronutrients include certain vitamins and minerals. In this article, we focus on minerals that play roles in cognitive function, including magnesium, calcium, iron, zinc, selenium, and iodine.

Magnesium is necessary for the function of many metabolic enzymes involved in brain function. It is a key regulator of calcium channels involved in neurotransmission (eg., NMDA receptors, important to the maintenance of learning and memory). Extracellular Mg+2 is an important regulator of synaptic density and plasticity in the hippocampus and enhances learning abilities, working memory, and both short and long-term memory. Magnesium promotes proper electrical and neurotransmitter functions in the brain. (1) Magnesium induces the production of brain-derived neurotrophicfactor(BDNF), a compound used by the brain to rejuvenate cellular function. Magnesium is required to dissipate the effects of traumatic stress that can occur from intense episodes of fear or anxiety. Magnesium is essential to maintain high brain energy.

Calcium: Intracellular Ca2+ signals play wide ranging functions as a second messenger in many cellular processes, including synaptic transmission and neural plasticity. Neural plasticity is the brain's ability to reorganize itself throughout life. Neural plasticity allows neurons in the brain to compensate for injury and disease and to adjust their activities in response to new situations or changes in the environment. (2) These processes are critical to hippocampal spatial memory formation and storage. Endoplasmic reticulum Ca2+ release channels, the ryanodine receptors (a class of intracellular calcium channels), and the inositol 1, 4, 5-triphosphate receptors contribute to these processes, as well. Calcium ions are important intracellular signals that regulate neuronal gene expression and neuronal secretion of neurotranmitters. Altered Ca 2+ release channel function presumably contributes to the abnormal memory processes that occur during aging and the neuronal death seen in neurodegenerative diseases. (3)

Iron is essential for normal neurological function. It is an important component of hundreds of proteins and enzymes involved in cellular metabolism. Iron deficiency in the very young can lead to permanent learning and memory deficits--impaired cognitive function--as well as emotional problems. Iron is needed for the development oligodendrocytes, which are the brain cells that produce myelin (white matter). The myelin layer or sheath is a protective coating that surrounds fibers called axons. (4) Myelin has a high iron content, and myelin increases the speed at which impulses propagate along the neurons. Iron is an important component of several enzymes that synthesize neurotransmitters. Iron transport proteins are important in particular to the hippocampal neurons, which play a large role in learning and memory. (5)

Zinc has been shown to be essential for neurogenesis, neuronal migration, and synaptogenesis. Its deficiency could interfere with neurotransmission and subsequent neuropsychological behavior. Zinc is present in the brain at high levels. Most of the brain zinc is tightly protein bound, but Zn+2 is present in synaptic vesicles where it plays a role in neurotransmission mediated byglutamate and GABA, which play roles in cortical excitability. (This balance of cortical excitability plays a role in every aspect of human behavior, from abstract thinking to emotional responses.) Deficiency of zinc during critical periods of cognitive development can lead to congenital malformation, deficits in attention, learning, memory, and neuropsychological behavior. (6) New studies have indicated that zinc is critical to communication between neurons in the hippocampus, the brain's learning and memory center.

Selenium in the form of the selenoprotein, selenocysteine, is present at the catalytic site of glutathione peroxidase. Selenium availability regulates glutathione peroxidase enzyme activity, one of the body's master antioxidants. Glutathione peroxidase (GSH-Px) is present throughout the body, but it plays its greatest roles in cognitive function and synaptic plasticity processes. The maintenance of GSH-Px is necessary to fight against reactive oxygen species' potential to cause oxidative damage to neuronal components, which underlies the molecular basis of neurodegeneration and brain aging (See Figure 1). The maintenance of normal glutathione levels is important for acquisition, but not consolidation, of spatial memory. Lack of glutathione induces failures in hippocampal synaptic plasticity mechanisms, possibly related to a spatial memory deficit.

Iodine: This mineral is more important to cognitive function than commonly believed. Iodine is a critical component for thyroid hormone synthesis. The thyroid hormones are involved in the myelination of the central nervous system. A major impact of hypothyroidism due to iodine deficiency is impaired neurodevelopment, particularly at critical periods of fetal development and early in life. In extreme cases, the cognitive effect of developmental iodine deficiency is irreversible mental retardation. Milder cognitive effects include a variety of neurodevelopmental deficits, including intellectual impairment. Correction of mild to moderate iodine deficiency in primary school aged children improves cognition and motor function. (7)

Clinical Study Demonstrating Albion's Zinc Bisglycinate's Impact on Cognition

Objective: The aim of this study was to explore the relationship of zinc nutrition to the severity of attention-deficit/hyperactivity disorder (ADHD) symptoms in a middle-class American sample with well-diagnosed ADHD. Previous reports of zinc in ADHD, including two positive clinical trials of supplementation, have come mainly from countries and cultures with different diets and/or socioeconomic realities.

Method: Children 5-10 years of age with DISC- and clinician-diagnosed ADHD had serum zinc determinations and parent and teacher ratings of ADHD symptoms. Zinc levels were correlated (Pearson's and multiple regression) with ADHD symptom ratings.

Results: Forty-eight children (37 boys, 11 girls; 33 combined type, 15 inattentive) had serum zinc levels with a median/mode at the lowest 30% of the laboratory reference range; 44 children also had parent/teacher ratings. Serum magnesium levels were normal. Nutritional in-take by a parent answered food frequency questionnaire was unremarkable. Serum zinc correlated at r = -0.45 (p = 0.004) with parent-teacher-rated inattention, even after controlling for gender, age, income, and diagnostic subtype, but only at r = -0.20 (p = 0.22) with CPT omission errors. In contrast, correlation with parent-teacher-rated hyperactivity-impulsivity was nonsignificant in the opposite direction.

Conclusion: These findings add to accumulating evidence for a possible role of zinc in ADHD, even for middle-class Americans, and, for the first time, suggest a special relationship to inattentive symptoms. They do not establish either that zinc deficiency causes ADHD nor that ADHD should be treated with zinc. Hypothesis-testing clinical trials are needed. (8)


This study demonstrates that Albion's bisglycinate chelates can cross the blood brain barrier, and, therefore, impact cognitive function. Therefore, the listed minerals (calcium, iron, magnesium, and zinc) as bisglycinate chelates can cross the blood brain barrier and have the impact on cognitive function in the ways that were discussed for each mineral in this newsletter. Albion's Selenium Glycinate Complex is not a chelate; the selenium is separated from the glycine in Gl tract and absorbed as free selenium, which can cross the blood brain barrier. A study by DiSilvestro, et al (9) demonstrated that Albion's Selenium Glycinate Complex significantly raised serum glutathione peroxidase activity, which plays a critical role in protecting the central nervous system and asserting a positive impact on cognitive function.


(1.) Abumaria N, et al. Effects of Elevation of Brain Magnesium on Fear Conditioning, Fear Extinction, and Synaptic Plasticity in the Infralimbic Prefrontal Cortex and Lateral Amygdala. J Neursci. 19 Oct 2011;31(42):14871-14881.

(2.) Neuroplasticlty., 1/29/2016

(3.) Paula-Lima AC, et al. Contribution of Ca2+ release channels to hippocampal synaptic plasticity and spatial memory: potential redox modulation. Antioxid Redox Signal. 2014 Aug20; 21(6) 892-914.

(4.) Williams R. Iron Builds a Better Brain. The Scientist January 9, 2012.

(5.) Fretham SJB, et al. The Role of Iron In Memory and Learning. Adv Nutr. 2011;2:112-121.

(6.) Drake VJ. Micronutrients and Cognitive Function. The Linus Pauling Research Institute Newsletter. Spring/Summer 2011: 12-14.

(7.) Zimmerman MB. The role of Iodine in human growth and development. Seminars in Cell & Developmental Biology. 2011;22:645-652.

(8.) Arnold LE, et al. Serum zinc correlates with parent-and teacher-rated Inattention in children with attention-deficit/hyperactivity disorder. Journal of Child & Adolescent Psychopharmacology. 15.4 (2005): 628-636.

(9.) DiSilvestro RA, et al. Selenium Glycinate Supplementation Effects on Glutathione Peroxidase and PSA in Healthy Middle Aged Men. FASEB J. 2007;21:227.2

by Stephen Ashmead

Stephen Ashmead is Senior Fellow of Chelates for Balchem/Albion Minerals.
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Author:Ashmead, Stephen
Publication:Townsend Letter
Geographic Code:1USA
Date:Nov 1, 2017
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