Iron deficiency: Differential effects on monoamine transporters

Burhans, Maggie S.; Dailey, Catherine; Beard, Zachary; Wiesinger, Jason A.; Murray‐Kolb, Laura E.; Jones, Byron C.; Beard, John L.

doi:10.1080/10284150500047070

Cited by 123 publications

(98 citation statements)

References 30 publications

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“…For instance, the basal ganglia become high in iron concentration and are more highly interconnected with REM-regulatory structures in the mesopontine tegmentum than with any other brain region (35,36). Some changes induced by early iron deficiency in the basal ganglia are not corrected with iron supplementation (2,8,9,37).…”

Section: Discussionmentioning

confidence: 99%

Iron Deficiency Anemia in Infancy Is Associated with Altered Temporal Organization of Sleep States in Childhood

et al. 2007

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ABSTRACT:The highest prevalence of iron deficiency anemia (IDA) in infancy coincides with a time of rapid changes in sleep organization. Since IDA in infancy is associated with long-lasting neurofunctional effects despite iron treatment, the normal development of sleep patterns might be affected. Night polysomnographic recordings were performed in 55 healthy 4-y-old children (former IDA ϭ 27, nonanemic controls ϭ 28). Both groups were followed from infancy and were similar in background characteristics. The duration of each waking episode was measured, as was the duration of each episode of nonrapid eye movement (NREM) sleep stages 1 (NREM1), 2 (NREM2), and 3-4 (SWS), and rapid eye movement (REM) sleep. The data were analyzed according to the successive thirds of the total sleep time (TST). Relative to controls, former IDA children showed: a) longer duration of REM sleep episodes in the first third and shorter in the last third; b) more REM sleep episodes in the first third and fewer in the second third; and c) shorter latency to the first REM sleep episode and shorter NREM stage 2 and SWS episodes within the first sleep cycle. The results show that early IDA is associated with long-lasting alterations in the temporal organization of sleep patterns. T his study considered the long-lasting impact of iron deficiency anemia (IDA) in infancy on the organization of sleep states. Iron deficiency-the most common preventable nutritional deficiency in the world and a major cause of anemia-is associated with alterations in development and behavior, particularly during infancy and toddlerhood when there is rapid growth and high need for iron (1,2). We previously reported that infants with IDA showed alterations in sensory pathway functioning and motor activity patterns, with some differences persisting despite timely correction of anemia with carefully supervised iron therapy (3-6). Other studies find poorer mental, motor, and social-emotional functioning in IDA infants, again with differences observed years after iron treatment (2,7). Additionally, animal studies show that rodents that experience early iron deficiency also have persisting behavioral differences related to motor function, learning and memory, and emotional responses (2,8,9).The quality and quantity of sleep are increasingly recognized as important factors in human development, with concomitant effects on affective behavior and cognitive performance (10,11). The organization of sleep depends on various mechanisms involving both neural and humoral processes, several of which are affected by iron deficiency. In rodent models, early iron deficiency impairs several neurotransmitter systems, myelin formation and maintenance, and metabolic neuronal activity (8,12). When iron deficiency occurs during central nervous system (CNS) development in infancy, changes in several functions are not completely reversed with iron therapy at weaning (2,8,9,12).Because iron deficiency in human infants is most prevalent during the latter part of the brain growth spurt, the norma...

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Section: Discussionmentioning

confidence: 99%

Iron Deficiency Anemia in Infancy Is Associated with Altered Temporal Organization of Sleep States in Childhood

et al. 2007

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“…Other nutrients which are altered in patients with major depression and that can influence neurotransmitter production include tryptophan (and other large neutral amino acids: valine, leucine, isoleucine, phenylalanine and tyrosine) (Maes et al, 2011c, Markus, 2008, Toker et al, 2010, folic acid (Miller, 2008, Stahl, 2008, zinc , Szewczyk et al, 2011, vitamin B12 (Bottiglieri, 1996, Deana et al, 1977), vitamin B6 (Calderon-Guzman et al, 2004, Demisch and Kaczmarczyk, 1991, Hartvig et al, 1995 and iron (Baumgartner et al, 2012, Burhans et al, 2005, Coe et al, 2009). Omega-3 EFAs are also able to modify monoaminergic neurotransmission (Chalon, 2006, Su, 2009).…”

Section: Diet and Its Effect On Neurotransmittersmentioning

confidence: 99%

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

Lopresti

Hood

Drummond

2013

Journal of Affective Disorders

532

412

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Research on major depression has confirmed that it is caused by an array of biopsychosocial and lifestyle factors. Diet, exercise and sleep are three such influences that play a significant mediating role in the development, progression and treatment of this condition. This review summarises animal and human-based studies on the relationship between these three lifestyle factors and major depressive disorder, and their influence on dysregulated pathways associated with depression, namely neurotransmitter processes, immuno-inflammatory pathways, hypothalamic-pituitary-adrenal (HPA) axis disturbances, oxidative stress and antioxidant defence systems, neuroprogression, and mitochondrial disturbances. Increased attention in future clinical studies on the influence of diet, sleep and exercise on major depressive disorder and investigations of their effect on physiological processes will help to expand our understanding and treatment of major depressive disorder. Mental health interventions, taking into account the bidirectional relationship between these lifestyle factors and major depression are also likely to enhance the efficacy of interventions associated with this disorder.

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“…Studies in rodents have shown that iron deficiency disrupts dopaminergic signaling (Beard et al 1994;Nelson et al 1997;Erikson et al 2000Erikson et al , 2001Burhans et al 2005). This is associated with cognitive impairment potentially alleviated by psychostimulants (Mohamed et al 2011).…”

Section: Discussionmentioning

confidence: 99%

“…In rats, iron deficiency reduces the density of the dopamine transporter and the dopamine D 1 and D 2 receptors in the basal ganglia (Beard et al 1994;Nelson et al 1997;Erikson et al 2000Erikson et al , 2001Burhans et al 2005). In children, iron deficiency has been associated with motor, attentional, and memory dysfunction as well as internalizing symptoms (Lozoff et al 2000;GranthamMcGregor and Ani 2001;McCann and Ames 2007).…”

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confidence: 99%

Serum Ferritin, Weight Gain, Disruptive Behavior, and Extrapyramidal Symptoms in Risperidone-Treated Youth

Calarge

Murry

Ziegler

et al. 2016

Journal of Child and Adolescent Psychopharmacology

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Background: Iron deficiency disrupts dopaminergic signaling in rodents, resulting in cognitive deficits that may be reversed with psychostimulants. In humans, iron deficiency with or without anemia has similarly been found to cause neuropsychological and behavioral impairments. However, the clinical effects of low body iron stores in antipsychotic-treated children have not been examined. Methods: Medically healthy, 5-to 17-year-old boys treated with risperidone for at least 1 year were enrolled between February 2009 and November 2013 in a multiphase study, examining the skeletal effects of calcium and vitamin D supplementation in risperidone-induced hyperprolactinemia. Anthropometric measures were collected and medical and pharmacy records were reviewed to obtain treatment history. Psychiatric diagnoses were based on clinical interviews, structured interviews, rating scales, and a review of their medical records. Extrapyramidal symptoms were assessed, and a food frequency questionnaire was completed in a subsample. Laboratory tests, including ferritin concentration (a marker of body iron status), were obtained upon study entry. Results: A total of 114 participants (mean age: 11.0 -2.6 years) were included, the vast majority (>90%) having attentiondeficit/hyperactivity disorder and/or disruptive behavior disorder. They had taken risperidone for an average 3.1 -2.0 years. Their serum ferritin concentration was 37.3 -25.6 lg/L with 21% of the sample having a level <20 lg/L, despite appropriate daily dietary iron intake. Ferritin concentration was inversely associated with weight gain following risperidone treatment onset but was not significantly associated with prolactin. After adjusting for the weight-adjusted dose of psychostimulants and risperidone and the daily dose of selective serotonin reuptake inhibitors, ferritin was inversely associated with the severity of disruptive behavior and positively associated (albeit marginally) with prosocial behavior. No association was found between ferritin concentration and extrapyramidal symptoms. Conclusions: Body iron stores are inversely related to risperidone-induced weight gain, even after extended treatment and despite adequate iron intake. Low iron stores are associated with poorer treatment response. Future research should examine iron absorption during antipsychotic treatment and whether repleting iron stores would facilitate clinical response.

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Iron deficiency: Differential effects on monoamine transporters

Cited by 123 publications

References 30 publications

Iron Deficiency Anemia in Infancy Is Associated with Altered Temporal Organization of Sleep States in Childhood

Iron Deficiency Anemia in Infancy Is Associated with Altered Temporal Organization of Sleep States in Childhood

A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise

Serum Ferritin, Weight Gain, Disruptive Behavior, and Extrapyramidal Symptoms in Risperidone-Treated Youth

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