Minerals are critical in supporting several key functions related to mood disorders, including neuro transmitter synthesis, cellular metabolism, and immunocompetence. While micronutrient deficiencies were presumably thought to occur in lower-income countries, micronutrient depletion has emerged as a form of “type B” malnutrition in industrialized countries despite food surpluses. Modern-day malnutrition has been attributed to poor dietary patterns, marked by excess intake of refined sugars and the absence of nutrient-dense foods.
The significance of various nutrients for mental health status has been established, but whether poor nutritional status is a causative agent or an effect of poor mental health continues to be debated. However, the prevalence of poor nutrition among depressed persons is indisputable—nutritional deficiencies have frequently been associated with the incidence and increased risk of depressive symptoms.
In a population study that included 13,486 children and adolescents, excess consumption of low nutritional content foods was correlated with increased aggression, violent behaviors, and psychiatric distress.1 Earlier clinical studies also indicated a positive correlation between rates of depression and poor nutrition. In a study that comprised 184 elderly participants, researchers found that up to 50% had identified nutritional inadequacies and comorbid depression.2
The role of micronutrients in the pathophysiology of depression
Current research illustrates the vast array of mental health complications that may arise because of micronutrient deficiencies, including impairments in cognitive function and neuromotor performance, effects on brain morphology, and disruption of neurochemical pathways. Micronutrients are vital in enzymatic reactions responsible for neurotransmitter synthesis and preservation, and mineral deficits have been identified in the pathophysiology of depressive symptoms.3
Minerals are essential in the enzymatic activation of brain-derived neurotrophic factor (BDNF), a protein that regulates neuronal plasticity and promotes the maturation and differentiation of new neurons within the CNS and the peripheral nervous system. Animal studies have shown that stress can reduce BDNF expression and activity in the hippocampus, and clinical studies have echoed similar findings in which serum BDNF levels are reported to be lower in depressed patients than in controls.4,5 Augmentation strategies that can facilitate BDNF expression have been emerging as an area of interest among researchers.
Augmentation strategies with zinc
As one of the most abundant trace minerals in the brain, zinc supports several physiological functions and possesses immuno-modulation properties. Zinc also activates hippocampal neurogenesis through the upregulation of BDNF, while inhibiting glutamate and N-methyl-D-aspartate (NMDA) activity.
The bioavailability of zinc can influence CNS function through a variety of mechanisms, and diets scarce in zinc have been known to result in behavioral disturbances and diminished brain function. In a meta-analysis that evaluated 17 studies with 1643 depressed and 804 control participants, peripheral serum zinc concentrations were approximately -1.85 µmol/L lower in depressed participants.6 Moreover, low serum plasma zinc levels have been associated with impairments in information processing and impulsivity in humans.7
Dr. Greenblatt is Chief Medical Officer and Vice President of Medical Services, Walden Behavioral Care, Waltham, MA; Assistant Clinical Professor, Tufts University School of Medicine, Boston, MA; and Assistant Clinical Professor, Dartmouth College Geisel School of Medicine, Hanover, NH. Ms. To is a research assistant for Psychiatry Redefined, Manchester, NH, and a BSN/MSN candidate at Regis College, Weston, MA. Ms. Dimino is a research assistant at Psychiatry Redefined. The authors report no conflicts of interest concerning the subject matter of this article.
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