Syndromes associated with nutritional deficiency and excess

Department of Dermatology, University of Connecticut School of Medicine, Farmington, CT, USA.
Clinics in dermatology (Impact Factor: 2.47). 11/2010; 28(6):669-85. DOI: 10.1016/j.clindermatol.2010.03.029
Source: PubMed


Normal functioning of the human body requires a balance between nutritional intake and metabolism, and imbalances manifest as nutritional deficiencies or excess. Nutritional deficiency states are associated with social factors (war, poverty, famine, and food fads), medical illnesses with malabsorption (such as Crohn disease, cystic fibrosis, and after bariatric surgery), psychiatric illnesses (eating disorders, autism, alcoholism), and medications. Nutritional excess states result from inadvertent or intentional excessive intake. Cutaneous manifestations of nutritional imbalance can herald other systemic manifestations. This contribution discusses nutritional deficiency and excess syndromes with cutaneous manifestations of particular interest to clinical dermatologists.

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    • "Previous studies have revealed a significantly increased incidence of Zn 21 deficiency in autistic patients compared to controls (Walsh et al., 2001, 2002; Jen and Yan, 2010; Yasuda et al., 2011) as well as an elevation of Cu 21 in samples of subjects with autism (Lakshmi Priya and Geetha, 2011). Moreover, further studies underlined that the Cu 21 / Zn 21 ratio is increased in subjects with autism (Faber et al., 2009). "
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    ABSTRACT: The establishment and maintenance of synaptic contacts as well as synaptic plasticity are crucial factors for normal brain function. The functional properties of a synapse are largely dependent on the molecular setup of synaptic proteins. Multidomain proteins of the ProSAP/Shank family act as major organizing scaffolding elements of the postsynaptic density (PSD). Interestingly, ProSAP/Shank proteins at glutamatergic synapses have been linked to a variety of Autism Spectrum Disorders (ASDs) including Phelan McDermid Syndrome, and deregulation of ProSAP/Shank has been reported in Alzheimer's disease. Although the precise molecular mechanism of the dysfunction of these proteins remains unclear, an emerging model is that mutations or deletions impair neuronal circuitry by disrupting the formation, plasticity and maturation of glutamatergic synapses. Several PSD proteins associated with ASDs are part of a complex centered around ProSAP/Shank proteins and many ProSAP/Shank interaction partners play a role in signaling within dendritic spines. Interfering with any one of the members of this signaling complex might change the output and drive the system towards synaptic dysfunction. Based on recent data, it is possible that the concerted action of ProSAP/Shank and Zn(2+) is essential for the structural integrity of the PSD. This interplay might regulate postsynaptic receptor composition, but also transsynaptic signaling. It might be possible that environmental factors like nutritional Zn(2+) status or metal ion homeostasis in general intersect with this distinct pathway centered around ProSAP/Shank proteins and the deregulation of any of these two factors may lead to ASDs. © 2013 Wiley Periodicals, Inc. Develop Neurobiol, 2013.
    Full-text · Article · Feb 2014 · Developmental Neurobiology
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    • "It is phosphorylated again in the liver and released into the blood circulation in its active forms. The recommended daily intake ranges from 0.1 to 2mg, depending on age and gender [1] [55]. "
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    ABSTRACT: Vitamins represent fundamental substrates for various physiologic functions occurring in human body. This review seeks to highlight their relevance in skin biology and to describe the cutaneous manifestations correlated with their deficiency.
    Full-text · Article · Jan 2013
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    • "However, Zn 2+ deficiency might not only be a biomarker for autism, but indeed a risk factor. Many autistic children have Zn 2+ -deficiency (Walsh et al., 2001, 2002; Jen and Yan, 2010; Yasuda et al., 2011). In a recent study, hair Zn 2+ concentrations from 1,967 children with autism were investigated and an incidence rate of Zn 2+ -deficiency in the infant-group aged 0–3- year-old was estimated 43.5% in male and 52.5% in female. "
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    ABSTRACT: Autism is a neurodevelopmental disorders characterized by impairments in communication and social behavior, and by repetitive behaviors. Although genetic factors might be largely responsible for the occurrence of autism they cannot fully account for all cases and it is likely that in addition to a certain combination of autism-related genes, specific environmental factors might act as risk factors triggering the development of autism. Thus, the role of environmental factors in autism is an important area of research and recent data will be discussed in this review. Interestingly, the results show that many environmental risk factors are interrelated and their identification and comparison might unveil a common scheme of alterations on a contextual as well as molecular level. For example, both, disruption in the immune system and in zinc homeostasis may affect synaptic transmission in autism. Thus, here, a model is proposed that interconnects the most important and scientifically recognized environmental factors. Moreover, similarities in how these risk factors impact synapse function are discussed and a possible influence on an already well described genetic pathway leading to the development of autism via zinc homeostasis is proposed.
    Full-text · Article · Nov 2012 · Frontiers in Psychiatry
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