Obesity Prevention

The Role of Brain and Society on Individual Behavior

Laurette Dube, Antoine Bechara, Alain Dagher, Adam Drewnowski, Jordan LeBel, Philip James, Rickey Y. Yada

• Publisher: Academic Press
• Year: 2010
• ISBN:
  9780080922096
• Topic: Technology & Engineering
• Subtopic: Food Science
• Index: Technology & Engineering

Over the years, approaches to obesity prevention and treatment have gone from focusing on genetic and other biological factors to exploring a diversity of diets and individual behavior modification interventions anchored primarily in the power of the mind, to the recent shift focusing on societal interventions to design "temptation-proof" physical, social, and economic environments. In spite of repeated calls to action, including those of the World Health Organization (WHO), the pandemic continues to progress. WHO recently projected that if the current lifestyle trend in young and adult populations around the world persist, by 2012 in countries like the USA, health care costs may amount to as much as 17.7% of the GDP. Most importantly, in large part due to the problems of obesity, those children may be the first generation ever to have a shorter life expectancy than that of their parents.

Obesity Prevention presents the most current research and proposals for addressing the pandemic. Past studies have focused primarly on either genetic or behavioral causes for obesity, however today's research indicates that a strongly integrated program is the best prospect for success in overcoming obesity. Furthermore, focus on the role of society in establishing an affordable, accessible and sustainable program for implementing these lifestyle changes is vital, particularly for those in economically challenged situations, who are ultimately at the highest risk for obesity.

Using studies from both neuroscience and behavioral science to present a comprehensive overview of the challenges and possible solutions, The brain-to-society approach to obesity prevention focuses on what is needed in order to sustain a healthy, pleasurable and affordable lifestyle.

• Explores the "brain-to-society" approach to obesity prevention, focusing on an integrative approach to addressing the obesity pandemic
• Presents both the nueroscientific and the behavioral factors that impact eating habits
• Identifies the challenges and suggests solutions for altering attitudes toward food on both an individual and a societal level

Chapter 1 The Pleasures and Pains of Brain Regulatory Systems for Eating

Jaak Panksepp,

Department of VCAPP, College of Veterinary Medicine, Washington State University, Pullman, WA, USA

1.1 Introduction

All basic survival needs of the body are represented in genetically ingrained circuits concentrated in subcortical visceral regions of the brain. Energy balance is regulated by a strict equation (Figure 1.1) that has recently been illuminated in great detail. For many decades, abundant evidence has indicated that medial hypothalamic regions, concentrated especially in the arcuate nucleus, contain major detectors for long-term homeostatic energy balance (Panksepp, 1974).

Figure 1.1 A female rat’s approximate yearly energy balance equation.

A great deal is eaten without much change in body weight. With the small increase in body weight, the daily intake error was less than a kilocalorie. The remaining energy was dissipated as heat.

Source: Figure 9.4 of Panksepp (1998: 172), reprinted with permission of Oxford University Press.

Diverse neuropeptidergic details of this circuitry have now been clarified (Horvath and Diano, 2004; Broeberger, 2005; Konturek et al., 2005; Gao and Horvath, 2007; Coll et al., 2008). In brief, there are complex neuropeptide-based neural networks that are able to gauge the energy status of the organism, and to adjust foraging and eating behavior accordingly. This network is constructed of hypothalamic neuropeptides, such as hypocretin/orexin, neuropeptide Y and agouti-related peptide, α-melanocyte-stimulating hormone, and melanin-concentrating hormone; regulatory circuits that are controlled by peripheral signals of lipid status, such as leptin; gastrointestinal hunger hormones, such as ghrelin; as well as more direct metabolic effects on the hypothalamus that are not as well understood. As noted above, this knowledge has been summarized superbly many times.

Often missing from the discussion of energy balance dynamics are the evolved psychological processes that mediate achieved/achieving homeostasis – the nature of the feelings of hunger in the brain, and the large variety of ways the pleasures and displeasures of taste can promote or hinder appetite. This is in addition to the many ways feeding behavior can be disrupted which have no relevance for the normal mechanisms of energy balance regulation. For instance, hunger makes sweetness taste more pleasant, and satiety makes the same sensation feel less pleasant (Cabanac, 1992).

This chapter will briefly focus on the latter factors, since they need to be considered more closely as investigators search for medicinal agents that may help humans better regulate their weight. It should be noted that considerable progress is being made in understanding how the brain codes taste qualities in both animals (Berridge, 2003; Peciña et al., 2006) and humans (Rolls, 2008; Rolls and Grabenhorst, 2009), but little of that work has yet been related to our understanding of appetite control agents.

1.2 Satiety Agents Versus Aversion-Inducing Agents

Presumably, the feeling that accompanies excessive depletion of energy leads to distressing feelings of hunger, while satisfaction of energy needs promotes a mood of contentment. Of course, few investigators of animal models of energy regulation are willing to use such psychological concepts; most restrict their discussions to measurable entities – changes in food intake, body weight, and various body energy distribution parameters. This is understandable, since we have no direct way of monitoring the psychological states of other animals. Yet this is also shortsighted if such states do exist and if they are of first-rate importance for how animals distribute their food-seeking and consummatory behaviors.

We would be wise to reconsider our reluctance to envision the affective controls of animal behavior, using all the indirect methodological approaches at our disposal. Philosophically, to not consider such issues is tantamount to failing to deal with the real complexities of the brain. Practically, the failure to consider such issues may impair our capacity to sift real satiety-producing neural pathways and neurochemical agents from the many other ways that food intake could be disrupted. Since most pre-clinical investigators in the field have been trained in rigorous behavioristic approaches, where any discussion of mental changes in animals is considered to be inappropriate, a full and open discussion of such issues is rare in the literature. However, considering what we now know about brain evolution and the subcortical sources of affective processes in all mammals (Panksepp, 1998, 2005, 2008), wisdom dictates that we begin to evaluate such issues with more intensive methodologies. If adequate empirical approaches for monitoring affective changes did not exist, it would make no sense to suggest that such issues should be considered. Yet adequate comprehensive methodologies are available, albeit rarely used. Among the best measures are positive and negative affective states as can be measured with conditioned place preference (CPP) and conditioned place aversion (CPA) measures (Tzechentke, 2007). As will be noted later, there are also other, more direct behavioral measures, such as the willingness of animals to play. Such affective measures, when used in pre-clinical animal models, would allow us to better ferret out those brain neurochemical pathways that need our most focused attention for the development of optimal appetite-reducing agents.

Why do we need to consider such issues? Any of a large variety of negative affects can reduce feeding in animals, from anger to being “zonked-out” by drugs, with disgust, fearfulness, separation anxiety, and stomach cramps in between. It is important also not to forget the negative feelings arising from a variety of stressors, including fatigue and sickness promoting neurochemical changes in the brain and various painful bodily feelings. If we do not sift such appetite-reducing affects from the normal pathways of satiety at the outset of intensive research programs seeking new satiety-promoting agents, we will be mismanaging our budgets and the efforts of our researchers. Since practically all agents off our pharmaceutical shelves, in high enough doses, can reduce food intake in animals, such affective issues need to be considered at the front end of research programs. Unfortunately, few investigators focus on them as fully as they deserve; usually a conditioned taste-aversion (CTA) paradigm is as far as most are prone to go. This is a good start, but, as will be summarized here, there are many more subtle ways to address such issues.

1.3 Various Methodologies to Evaluate Affective Change in Pre-Clinical Appetite Research

There are many easy ways to reduce feeding pharmacologically, but only a few of these tell us much about the normal mechanisms of energy regulation. As noted, fearful animals eat less than normal. So do angry and sick ones. There are many affective changes beside satiety that can reduce feeding, and investigators interested in seeking satiety agents have not spent enough time sifting those agents that produce the normal, good feeling of satiety after a satisfying meal from all the many other affective changes that can reduce feeding. With the increasing number of neuropeptidergic “satiety agents” that have been discovered in the brain (Table 1.1), we must be increasingly wary that many of them are reducing feeding by changing non-homeostatic affective feelings of animals rather than a feeling of satisfaction that emerges from no longer being hungry.

Table 1.1 Partial list of neuropeptides and other neuromodulators that have been found to reduce feeding and body weight

Various amino acids	Glucagon-like peptide
AgRP	Interleukin-1
Amylin	Interleukin-6
α-MSH	Insulin (central)
Beta-endorphin	Leptin
BDNF	Norepinephrine
Bombesin	Neurotensin
CART	NPY
CCK	Oxytocin
Corticosterone	PrRP
CRH	Peptide YY
Dynorphin	Serotonin
Galanin	Tumor necrosis factor α
Galanin-like peptide	Urocortin

Abbreviations: α-MSH, α-Melanocyte Stimulating Hormone; BDNF, Brain Derived Neutrophic Factor; CART, Cocaine- and Amphetamine-Regulated Transcript Corticotropin-Releasing Hormone; PrRP, Proline-Releasing Peptide.

Sources: Horvath and Diano, 2004; Broeberger, 2005; Konturek et al., 2005; Gao and Horvath, 2007; Coll et al., 2008.

In short, establishing affective criteria whereby one has discovered a “real” satiety agent is critical for future progress in developing medicines that will help people to regulate body weight optimally. When the body is out of homeostatic balance in terms of available energy, one feels hunger pangs and generalized distress that can be easily erased by a restoration of energy homeostasis. When one has eaten a satisfying meal, the stomach is diste...

Table of contents

• Cover
• Title Page
• Copyright
• Table of Contents
• List of Contributors
• Preface
• Acknowledgments
• Introduction: On the Brain-to-Society Model of Motivated Choice and the Whole-of-Society Approach to Obesity Prevention
• Chapter 1: The Pleasures and Pains of Brain Regulatory Systems for Eating
• Chapter 2: The Neurobiology of Appetite: Hunger as Addiction
• Chapter 3: Opioids: Culprits for Overconsumption of Palatable Foods?
• Chapter 4: Taste, Olfactory and Food-texture Processing in the Brain and the Control of Appetite
• Chapter 5: Cortical and Limbic Activation in Response to Low- and High-calorie Food
• Chapter 6: Reward-related Neuroadaptations Induced by Food Restriction: Pathogenic Potential of a Survival Mechanism
• Chapter 7: The Neuroeconomics of Food Selection and Purchase
• Chapter 8: Resisting Temptation: Impulse Control and Trade-offs between Immediate Rewards and Long-term Consequences
• Chapter 9: Hunger, Satiety, and Food Preferences: Effects of the Brain and the Body on the Self-control of Eating
• Chapter 10: Associative Learning and the Control of Food Intake
• Chapter 11: Restrained Eating in a World of Plenty
• Chapter 12: The Genetic Determinants of Ingestive Behavior: Sensory, Energy Homeostasis and Food Reward Aspects of Ingestive Behavior
• Chapter 13: Development of Human Learned Flavor Likes and Dislikes
• Chapter 14: Biopsychological Factors and Body Weight Stability
• Chapter 15: Nutrition, Epigenomics and the Development of Obesity: How the Genome Learns from Experience
• Chapter 16: The Role of Early Life Experiences in Flavor Perception and Delight
• Chapter 17: Implications of the Glycemic Index in Obesity
• Chapter 18: Characterizing the Homeostatic and Hedonic Markers of the Susceptible Phenotype
• Chapter 19: The Carnivore Connection: Cross-population Differences in the Prevalence of Genes Producing Insulin Resistance
• Chapter 20: Neuroanatomical Correlates of Hunger and Satiaty in Lean and Obese Individuals
• Chapter 21: Neuroendocrine Stress Response and Its Impact on Eating Behavior and Body Weight
• Chapter 22: Eating Behavior and Its Determinants: From Gene to Environment
• Chapter 23: The Molecular Regulation of Body Weight: The Role of Leptin, Ghrelin and Hypocretin
• Chapter 24: Energy Balance Regulation: Complex Interplay between the Autonomic and Cognitive/Limbic Brains to Control Food Intake and Thermogenesis
• Chapter 25: Stealth Interventions for Obesity Prevention and Control: Motivating Behavior Change
• Chapter 26: From Diets to Healthy and Pleasurable Everyday Eating
• Chapter 27: Resisting Temptations: How Food-Related Control Abilities can be Strengthened through Implementation Intentions
• Chapter 28: The Dieter’s Dilemma: Identifying When and How to Control Consumption
• Chapter 29: Lifestyle Change and Maintenance in Obesity Treatment and Prevention: A Self-determination Theory Perspective
• Chapter 30: Nutritional Genomics in Obesity Prevention and Treatment
• Chapter 31: Physical Activity for Obese Children and Adults
• Chapter 32: Economic Growth as a Path Toward Poverty Reduction, Better Nutrition and Sustainable Population Growth
• Chapter 33: The Human Agent, Behavioral Changes and Policy Implications
• Chapter 34: The Four Pillars of the Industrial Machine: Can the Wheels be Steered in a Healthier Direction?
• Chapter 35: Libertarian Paternalism: Nudging Individuals toward Obesity Prevention
• Chapter 36: The Current State of the Obesity Pandemic: How We Got Here and Where We Are Going
• Chapter 37: The Underweight/Overweight Paradox in Developing Societies: Causes and Policy Implications
• Chapter 38: The Drivers of Body Weight, Shape and Health: An Indian Perspective of Domestic and International Influences
• Chapter 39: Diets and Activity Levels of Paleolithic versus Modern Humans: Societal Implications for the Modern Overweight Pandemic
• Chapter 40: Agriculture, Food and Health
• Chapter 41: Changing Food Systems in the Developing World
• Chapter 42: Green Revolution 2.5: From Crisis to a New Convergence Between Agriculture, Agri-Food and Health for Healthy Eating Worldwide
• Chapter 43: How High-level Consumer Research Can Create Low-caloric, Pleasurable Food Concepts, Products and Packages
• Chapter 44: Reductions in Dietary Energy Density to Moderate Children’s Energy Intake
• Chapter 45: Nurturing and Preserving the Sensory Qualities of Nature
• Chapter 46: Aligning Pleasures and Profits: Restaurants as Healthier Lifestyle Enablers
• Chapter 47: A Study of Corporate Social Responsibility Activities of 12 Giant Food Companies (1980–2008) in Promoting Healthy Food
• Chapter 48: The Injunctive and Descriptive Norms Governing Eating
• Chapter 49: Family Meal Patterns and Eating in Children and Adolescents
• Chapter 50: Social Influences on Eating in Children and Adults
• Chapter 51: Church and Other Community Interventions to Promote Healthy Lifestyles: Tailoring to Ethnicity and Culture
• Chapter 52: On Gluttony: Religious and Philosophical Responses to the Obesity Epidemic
• Chapter 53: Social Alliances: Moving Beyond Corporate Social Responsibility to Private–Public Partnerships
• Chapter 54: Social Networks, Social Capital and Obesity: A Literature Review
• Chapter 55: From Society to Behavior: Neighborhood Environment Influences
• Chapter 56: Social Determinants of Health and Obesity
• Chapter 57: The Role of the Environment in Socio-Economic Status and Obesity
• Chapter 58: The Economics of Obesity: Why are Poor People Fat?
• Chapter 59: Challenges in Making Broad Healthy Lifestyle Plans: Revisiting the Nature of Health Interventions
• Chapter 60: Social Interactions and Obesity: An Economist’s Perspective
• Chapter 61: A Complex Systems Approach to Understanding and Combating the Obesity Epidemic
• Chapter 62: Conclusion: A Whole-of-Society Approach to Obesity Prevention: New Frontiers in Science, Policy and Action, and the Emerging Models of Capitalism and Society to Make it Possible
• Index