Personalized Nutrition as Medical Therapy for High-Risk Diseases

★★★★★ 4.2 116 reviews

US$18.02
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Management number 233459898 Release Date 2026/06/27 List Price US$18.02 Model Number 233459898
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Personalized nutrition involves the formulation of individualized nutritional recommendations to promote and maintain health based on an individual's genetic makeup and other unique intrinsic and extrinsic factors. Implementing personalized nutrition plans for individuals with certain diseases or who are in danger of developing health conditions could help control the onset and severity of symptoms. Personalized Nutrition as Medical Therapy for High-Risk Diseases offers a practical guide for physicians seeking to provide tailored dietary recommendations to their patients with disease treatment, modulation and prevention in mind.The book focuses on the biological mechanisms of specific diseases and provides evidence for how personalized nutrition positively impacts them. It explores conditions including cardiovascular diseases, hypertension, hypercholesteromia, diabetes, obesity, Crohn's disease, as well as multiple pediatric, renal and psychological disorders.Features:· Includes case studies that document how people respond differently towards food depending on their genetic structure and other factors.· Discusses genome wide association studies (GWIMS) to understand the interplay between genetic susceptibility and dietary interactions.· Provides users information to effectively implement personalized nutrition into practice.· Identifies possible challenges to the implementation of personalized nutritional interventions in a clinical setting.This book is for medical practitioners and will also appeal to researchers and students. Read more

ASIN B087CB9SSF
XRay Not Enabled
Format Print Replica
ISBN13 978-1351621847
Edition 1st
Language English
File size 24.2 MB
Page Flip Not Enabled
Publisher CRC Press
Word Wise Not Enabled
Print length 364 pages
Accessibility Learn more
Publication date April 18, 2020
Enhanced typesetting Not Enabled

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