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Why Do Children Lose Their Brains?
Why Do Children Lose Their Brains?
Why Do Children Lose Their Brains?
Ebook47 pages31 minutes

Why Do Children Lose Their Brains?

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Children are exposed to unacceptable and high risk. The prevalence of Autism Spectrum Disorders (ASD) does not stop growing and the genetic alterations associated with ASD are not enough to explain this alarming increase. The book Why do children lose their brains? details the villains of their main contribution.

LanguageEnglish
Release dateApr 16, 2020
Why Do Children Lose Their Brains?
Author

Carlos Herrero Carcedo

Autor de dos Libros con tapa: Manual Básico de Farmacología y 200 Ideas para Mejorar la Rentabilidad de tu Farmacia, una publicación en la revista Alimentación, Equipos y Tecnología: La histamina en las distintas etapas de fabricación de conservas de atún y seis Ebooks: Disruptores Endocrinos, La Salud no es un Negocio, Obesidad Infantil. Rista. Respuesta Insuficientemente Adecuada, Vivir sin Cáncer, Ser Mayor sin Edad y Predisposición a Ser Homosexual.Posee tres licenciaturas (Farmacia, Ciencias Químicas, Ciencia y Tecnología de los Alimentos) y experiencia en los departamentos de Calidad, Producción y Ventas.

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    Book preview

    Why Do Children Lose Their Brains? - Carlos Herrero Carcedo

    WHY DO CHILDREN

    LOSE THEIR BRAINS?

    Carlos Herrero Carcedo

    www.carlosherrerocarcedo.com

    WHY DO CHILDREN

    LOSE THEIR BRAINS?

    Carlos Herrero Carcedo

    www.carlosherrerocarcedo.com

    Copyright© 2020 by Carlos Herrero Carcedo

    All rights reserved

    LEGAL WARNING

    It is strictly prohibited without the written permission of the copyright holder, the reproduction of this work by any means or process including reprography and computer processing.

    TABLE OF CONTENTS

    1. The Triad: Thyroid Hormones, Epigenetics and Endocrine Disruptors with DNT/NT effects

    2. Thyroid Hormones

    3. Epigenetics

    4. Endocrine Disruptors with DNT/NT Effects

    5. Mechanisms of Action DNT/NT

    6. Autism Spectrum Disorders (ASD)

    7. Abbreviations

    1. The Triad: Thyroid Hormones, Epigenetics and Endocrine Disruptors with DNT/NT Effects

    Thyroid hormones are essential for the proper functioning of the brain throughout the entire life of a person. However, the structural and functional alterations of the central nervous system caused by the deficiency or the excess of these thyroid hormones are very different in the adult, the adolescent and the fetus.

    During the development of the person, the thyroid hormones exert their action in almost all the tissues of the organism but it is in the brain where a deep and critical dependence is produced with respect to the perfect synchronized activity of the thyroid hormonal system. The fetal brain generates 250.000 neurons per minute and changes in shape and size during the first years of life, reaching 75% and 90% of its definitive size at 2 and 6 years of age, respectively. The brain of an adult individual has 86.000 millions of neurons, which grow, develop and interconnect throughout their existence. Thyroid hormones act at the genomic level, regulating the expression of genes through binding to their nuclear receptors, and through extragenomic mechanisms of action in cellular organelles located outside the nucleus.

    Similarly, in the development, function and neuronal plasticity, epigenetics are also actively involved. The anomalous variations of the normal epigenetic patterns, generated by the direct impact of the environment, can cause neurological disorders of diverse nature. Epigenetic changes are the chemical modifications established on DNA and histones that do not alter the DNA sequence but regulate gene expression for the formation of proteins, that is, the activation or deactivation of the genes. The epigenome of each person is modified, naturally, when the cells specialize and in the course of the different stages of life. These chemical marks on DNA and histones, established as adaptation to inappropriate external factors of the environment, can induce undesirable epigenetic patterns that adversely modify gene expression and cellular metabolic activities. The different epigenetic chemical labels found among the monozygotic

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