Lifestyle Medicine for Prediabetes, Type 2 Diabetes, and Cardiometabolic Disease

Cover
Half Title
Series Page
Title Page
Copyright Page
Table of Contents
Foreword
Preface
Editors
Contributors
Chapter 1 Epidemiology, Drivers, and Public Health Challenges of Prediabetes, Type 2 Diabetes, and Cardiometabolic-Based Chronic Disease
1.1 Introduction
1.2 The Dysglycemia-Based Chronic Disease Model
1.3 Definition of DBCD Stages
1.3.1 DBCD Stage 1: Insulin Resistance
1.3.2 DBCD Stage 2: Prediabetes
1.3.3 DBCD Stage 3: Type 2 Diabetes
1.3.4 DBCD Stage 4: Type 2 Diabetes with Complications
1.4 DBCD Prevalence
1.5 Atherosclerotic Risk Factors
1.5.1 Tobacco Use
1.5.2 Excessive Alcohol Consumption
1.5.3 Hyperlipidemia
1.5.4 Hypertension
1.5.5 Adiposity-Based Chronic Disease
1.6 Drivers of Insulin Resistance and Cardiometabolic-Based Chronic Disease
1.6.1 Primary Drivers
1.6.2 Genetics and Epigenetics
1.6.3 Environmental and Behavioral Factors
1.6.4 Secondary/Metabolic Drivers
1.6.5 Costs of Type 2 Diabetes
1.6.6 Costs of Prediabetes
1.6.7 Worldwide Costs
1.7 Conclusion
References
Chapter 2 The Evolutionary Biology and Human History of Cardiometabolic Disease
2.1 Introduction
2.2 Natural History
2.3 Informational Physiology–Genetics,Epigenetics, and Microflora
2.3.1 The Thrifty Gene Hypothesis
2.3.1.1 The Drifty Phenotype
2.3.2 Epigenetic Change
2.3.2.1 GI Microbiota
2.4 Environment and Behavior
2.4.1 Hunter-Gatherers
2.4.1.1 Milk and Dairy
2.5 A History of Type 2 Diabetes and Atherosclerotic Disease
2.5.1 Type 2 Diabetes
2.5.2 Atherosclerosis
2.6 Conclusion
References
Chapter 3 The Role of Cardiac Energetics in Cardiometabolic-Based Chronic Disease
3.1 Background
3.2 Cardiac Energy Metabolism
3.2.1 Cardiac Energy Metabolism in Normal Hearts
3.2.2 Cardiac Energy Metabolism in Obesity
3.2.3 Cardiac Energy Metabolism in Type 2 Diabetes
3.2.4 The Impact of High Cardiac Fatty Acid β-Oxidation on Cardiac Function
3.3 Molecular Mechanisms that Contribute to the Altered Cardiac Energetics
3.3.1 Epigenetics-Mediated Dysregulation of Gene Expression
3.3.2 Post-Translational Modification
3.3.3 Cardiac Insulin Resistance
3.3.4 Lipotoxicity
3.3.5 Glucotoxicity
3.3.6 Cardiac Inflammation
3.4 Lifestyle Interventions and Surgical Procedures for Treating Obesity and T2D
3.4.1 Caloric Restriction
3.4.2 Physical Activity
3.5 Pharmacological Approaches for Treating Obesity and T2D
3.5.1 Antihyperglycemic Drugs
3.5.1.1 Metformin
3.5.1.2 Sodium-Glucose Cotransporter 2 Inhibitors
3.5.1.3 Glucagon-LikePeptide-1 Receptor Agonists
3.5.1.4 Dipeptidyl Peptidase 4 Inhibitors
3.5.1.5 Thiazolidinediones
3.5.1.6 Glitazars
3.5.2 Lipid-LoweringDrugs
3.5.2.1 Statins
3.5.2.2 Fibrates
3.5.2.3 Nicotinic Acid
3.5.3 Drugs that Inhibit Fatty Acid β-Oxidation
3.5.3.1 CPT1 Inhibitors
3.5.3.2 Fatty Acid ß-Oxidation Inhibitors
3.5.4 Drugs that Stimulate Glucose Oxidation
3.5.5 Potential Future Therapeutic Approaches
3.5.5.1 Inhibition of Myocardial Fatty Acid Uptake
3.5.5.2 Reversible CPT1 Inhibition
3.5.5.3 Potent Stimulators of Glucose Oxidation
3.5.5.4 Stimulation of Ketone Oxidation
3.5.5.5 Stimulation of BCAA Oxidation
3.6 Bariatric Procedures
3.7 Concluding Remarks
References
Chapter 4 Endocrine-Disrupting Chemicals
Abbreviations
4.1 Introduction
4.2 Common Endocrine-Disrupting Chemicals
4.2.1 Bisphenol A
4.2.2 Phthalates
4.2.3 Atrazine
4.2.4 Polychlorinated Biphenyls and Polybrominated Diphenyl Ethers
4.2.5 Dichlorodiphenyltrichloroethane and Dichlorodiphenyldichloroethylene
4.3 Body Burden and Lipophilicity of EDC
4.4 Outcomes of Exposure
4.5 Mechanism of Action
4.6 Effect of EDC on Cardiometabolic Drivers
4.7 The Association between EDC and Obesogenesis
4.7.1 Bisphenol A
4.7.2 Phthalates
4.7.3 Persistent Organic Pollutants
4.7.4 Polychlorinated Biphenyls
4.8 Mechanisms of EDC Action in Obesogenesis
4.8.1 Receptor-Mediated Increase in Adipogenesis
4.8.2 Effect on Transport Proteins
4.8.3 Effect on Hormone Axes
4.8.4 Effect on Enzymes
4.8.5 Effect on Adipokines and Neuropeptides
4.8.6 Effect on Epigenetics
4.9 Physiological Models of Increased Adipogenesis
4.9.1 Increase in Caloric Intake
4.9.2 Decrease in Locomotor Activity
4.9.3 Alterations in Gut Microbiota
4.10 Factors Affecting Metabolic Responses to EDC
4.10.1 Sex
4.10.2 Dose of EDC
4.10.3 Time of Exposure
4.11 The Association between EDC and Diabetes Mellitus
4.11.1 Individual Compounds and the Risk of Diabetes
4.11.1.1 Persistent Organic Pollutants
4.11.1.2 Bisphenol A
4.11.1.3 Phthalates
4.11.1.4 Perfluoroalkyl Substances
4.11.1.5 Metals
4.12 Mechanisms Implicated in Diabetes
4.12.1 Insulin Resistance and Prediabetes
4.12.1.1 Altered Insulin and Glucagon Secretion
4.12.2 β-Cell Depletion and Type 1 Diabetes
4.13 The Association between EDC and Atherosclerosis
4.13.1 Pathogenesis of Atherosclerosis
4.13.2 Data on EDC and Atherosclerosis
4.13.3 Mechanisms of EDC-Mediated Atherosclerosis
4.13.3.1 Hyperlipidemia
4.13.3.2 Chronic Inflammation
4.13.3.3 Mitochondrial Dysfunction
4.13.3.4 Epigenetic Changes
4.14 Methods for EDC Detection and Exposure Mitigation
4.14.1 Screening for EDC Exposure
4.14.2 Organized Efforts to Decrease EDC Exposure
4.14.3 Individual Efforts to Decrease EDC Exposure
4.15 Conclusion
References
Chapter 5 Primordial Prevention of Cardiometabolic Risk Factors Using Lifestyle Medicine – Implementing Early Childhood Health Promotion
5.1 Introduction: What is Primordial Prevention, Its Biological Basis, and the Obstacles to Effective Implementation?
5.1.1 Definition
5.1.2 Biological Basis: Link between Cardiovascular Risk Factors in Children and Disease in Adulthood
5.1.2.1 Unhealthy Weight
5.1.2.2 Unhealthy Diet
5.1.2.3 Insufficient Physical Activity
5.1.2.4 Smoking/Smoking Exposure
5.1.2.5 Blood Pressure, Blood Cholesterol, and Blood Glucose
5.1.3 Schools as the Main Focus for Primordial Prevention Strategies
5.2 Evidence: Design of Studies, Clinical Evidence, and Conclusions from Large-Scale Studies on Preschool-Based Interventions on Cardiovascular Health Promotion
5.2.1 School-Based Interventions for Primordial Prevention
5.2.2 Scientific Evaluation of School-Based Interventions on Health Promotion
5.2.3 Assessment Tools within RCTs
5.2.4 Implementation of RCTs on Health Promotion in Early Childhood
5.3 Synthesis: Core Elements (Theory,Data, Challenges, Updated Strategies, and Implementation Tactics)
5.3.1 Building a Team and Stakeholder Relationships
5.3.2 Need for Intervention Adaptability
5.3.3 Role of Teachers on School-Based Intervention Success
5.3.4 Role of Families in Intervention Success
5.3.5 Sustained Efficacy of School-Based Interventions
5.4 Conclusions
References
Chapter 6 Primary Prevention of Type 2 Diabetes and Cardiometabolic-Based Chronic Disease Using Lifestyle Medicine
6.1 Introduction
6.2 Progression of Impaired Glucose Tolerance and Impaired Fasting Glucose to T2D
6.3 Dietary Modification and Primary Prevention of T2D
6.3.1 Macronutrients–Fat
6.3.2 Macronutrients–Carbohydrates
6.3.3 Vitamins and Minerals
6.3.4 Individual Foods
6.3.5 Dietary Patterns
6.4 Role of Physical Activity in the Prevention of T2D
6.4.1 Acute Effects of Exercise
6.4.2 Postexercise Effects
6.4.3 Resistance Exercise Effects
6.4.4 Effects of Chronic Training
6.5 Physical Activity and Effect on Oxidative Stress and Inflammation
6.6 Overview of Key Lifestyle Medicine Clinical Trials
6.7 Conclusion
References
Chapter 7 Secondary Prevention Example: Using Lifestyle Medicine in Patients with Type 2 Diabetes
7.1 Introduction
7.2 Early Observations
7.3 The Look AHEAD Trial
7.3.1 Look AHEAD: Primary Outcome
7.3.2 Look AHEAD: Secondary Outcomes
7.4 The EUROASPIRE Trials
7.5 Nutritional Approaches for Secondary Prevention
7.6 Conclusion
References
Chapter 8 Tertiary Prevention Using Lifestyle Medicine for Cardiometabolic-Based Chronic Disease
8.1 Introduction
8.2 Complication 1: Cardiovascular Disease
8.2.1 Atherosclerosis
8.2.1.1 Context
8.2.1.2 Lifestyle Interventions
8.2.2 Heart Failure
8.2.2.1 Context
8.2.2.2 Lifestyle Interventions
8.2.3 Atrial Fibrillation
8.2.3.1 Context
8.2.3.2 Lifestyle Interventions
8.3 Complication 2: Diabetic Nephropathy
8.3.1 Context
8.3.2 Lifestyle Interventions
8.3.2.1 Nutrition
8.3.2.2 Physical Activity
8.3.2.3 Behavior
8.4 Complication 3: Diabetic Neuropathy
8.4.1 Context
8.4.2 Lifestyle Interventions
8.4.2.1 Nutrition
8.4.2.2 Physical Activity
8.4.2.3 Behavior
8.5 Complication 4: Diabetic Retinopathy
8.5.1 Context
8.5.2 Lifestyle Interventions
8.5.2.1 Nutrition
8.5.2.2 Physical Activity
8.5.2.3 Behavior
8.6 Conclusion
References
Chapter 9 The Mediterranean Diet
9.1 Historical Context
9.2 Components
9.3 Molecular Mechanisms
9.3.1 Lipid Lowering
9.3.2 Oxidative Stress and Inflammation
9.3.3 Cancer
9.3.4 Nutrient Sensing
9.3.5 Gut Microbiota
9.4 Clinical Studies
9.4.1 Cardiovascular Disease
9.4.2 Obesity
9.4.3 Type 2 Diabetes
9.4.4 Cancer
9.4.5 Longevity
References
Chapter 10 Vegan Diets for Diabetes Prevention and Management of Cardiometabolic Risk
10.1 Observational Studies on Dietary Patterns and Diabetes Prevalence
10.2 Clinical Trials of Plant-Based Dietary Interventions for Type 2 Diabetes Management
10.3 Nutritional Interventions for Neuropathy
10.4 Diet and Type 1 Diabetes
10.5 Nutrition and Gestational Diabetes
10.6 Influence on Cardiovascular Risk Factors
10.7 Body Weight
10.8 Plasma Lipids
10.9 Blood Pressure
10.10 Nutritional Adequacy
10.11 Acceptability
10.12 How to Begin
10.13 Medications
10.14 Plant-Based Diets in the COVID-19 Era
10.15 Resources
References
Chapter 11 Physical Activity
11.1 Introduction
11.2 Recommended Physical Activity
11.3 Physical Inactivity
11.4 Physiological Mechanisms
11.4.1 Glucose Metabolism
11.4.2 Lipid Metabolism
11.4.3 Skeletal Muscle
11.4.4 Adipose Tissue
11.4.5 Cardiovascular System
11.4.5.1 Cardiac Effects
11.4.5.2 Vascular Endothelium
11.4.6 Hepatic Metabolism
11.4.7 Central Nervous System Effects
11.4.7.1 Hypothalamus
11.4.7.2 Psychological Effects
11.4.7.3 Sleep
11.4.8 Stem Cell Regeneration
11.5 Prescription of Activity
11.5.1 Prolonged Healthspan
References
Chapter 12 Psychological Stress, Behavioral Modification, and Cardiometabolic Health
12.1 Introduction
12.2 The Psychological Stress Response
12.2.1 Insulin Resistance
12.2.2 Cortisol
12.2.3 Autonomic Dysfunction
12.3 The Role of Mood Disorders and Emotional Stress on Developing Cardiometabolic Disease
12.3.1 Depression
12.3.2 Anxiety
12.3.3 Personality Traits
12.3.4 Environmental Distress
12.4 The Stress Response and Microvascular and Macrovascular Complications
12.5 Lifestyle Intervention
12.5.1 Physical Activity
12.5.2 Sleep Hygiene
12.5.3 Dietary Patterns
12.5.4 Stress Reduction
12.6 Connecting the Psychological Stress Response with Cardiovascular Disease
12.7 Connecting the Psychological Stress Response with Adiposity-Based Chronic Disease
12.8 Evidence-Based Methods of Behavioral Modification
References
Chapter 13 Sleep Hygiene
13.1 Sleep and Glucose Homeostasis
13.2 Mechanism of Sleep Deprivation and Disturbance Leading to Increased Insulin Resistance
13.2.1 Hormonal Dysregulation
13.2.2 Inflammation
13.2.3 Sympathetic Nervous System Activity
13.2.4 Hyperactivity of Orexin System
13.2.5 Reduced Energy Expenditure
13.2.6 Reduction in Melatonin Production
13.3 Sleep Architecture and Insulin Resistance in Adolescents
13.4 Sleep Architecture and Insulin Resistance in Night Shift Workers
13.5 Possible Mechanism of Insulin Resistance in Shift Workers
13.5.1 Clock Control of Insulin Sensitivity
13.5.2 Problems in Glucose Homeostasis Arising from Misalignment/Shift Work
13.5.3 Desynchronization between Organs
13.6 Relationship of Nocturnal Light Exposure and Insulin Resistance
13.7 Screen time and Metabolic Health
13.8 Obstructive Sleep Apnea and T2D
13.9 What Should Clinicians Tell Patients?
References
Chapter 14 Transculturalizing Lifestyle Medicine for Managing Cardiometabolic-Based Chronic Disease
Abbreviations
14.1 Cultural Influence of Lifestyle on Cardiometabolic Disease
14.2 Prevalence and Burden of Cardiometabolic Disease by Ethnocultural Populations
14.3 Response to the Stressor Environment by Ethnocultural Groups
14.4 Transcultural Lifestyle Medicine
14.5 Transcultural Adaptation of Evidence
14.6 Implementation of a Transculturalized Cardiometabolic Model Using Lifestyle Medicine
14.6.1 Contextualization
14.6.2 Complication-Based Approach
14.6.3 Implementation: Case Study
14.6.3.1 Scenario
14.6.3.2 Patient Presentation
14.6.3.3 Cultural Factors
14.6.3.4 Analysis
14.7 Conclusion
References
Chapter 15 Socioeconomics and Infrastructure
15.1 Introduction
15.2 Socioeconomic Challenges
15.2.1 Social Determinants of Cardiometabolic Health
15.2.2 Transcultural Factors
15.2.3 Healthcare System Economics
15.3 Infrastructural Challenges
15.4 Implementation Science
15.4.1 Gaps
15.4.1.1 Research
15.4.1.2 Knowledge
15.4.1.3 Practice
15.4.2 Logistics
15.4.2.1 Inception
15.4.2.2 Champions
15.4.2.3 Teams
15.4.2.4 Resources
15.4.2.5 Community
15.4.2.6 Financial
15.4.3 Technology
15.4.4 Sustainability
15.4.4.1 Exemplars
15.5 Conclusions
References
Chapter 16 Synthesis and Core Recommendations for Using Lifestyle Medicine to Reduce Dysglycemia and Cardiometabolic Risk
16.1 Part 1: Problem–Whyis Structured Lifestyle Medicine needed in the Dysglycemia and Cardiometabolic Spaces?
16.1.1 Aspect 1: Epidemiology–Linking Dysglycemia and Other Determinants with Cardiometabolic Risk
16.1.2 Aspect 2: Mechanisms–Mapping Lifestyle Interventions to Cardiometabolic Risk Reduction
16.1.3 Aspect 3: Wanting Preventative Care versus Doing Preventive Care
16.2 Part 2: Premise–Correct Modeling of Chronic Disease Leads to Tactical Advantages
16.2.1 Aspect 1: The 3-Dimensional Cardiometabolic-Based Chronic Disease Model
16.2.2 Aspect 2: The Patient as an Agent of Change
16.2.3 Aspect 3: The Specialized Field of Lifestyle Medicine
16.3 Part 3: Evidence–Lifestyle Medicine as an Evolving Science
16.4 Synthesis and Core Recommendations
References
Index