The Hunger Games: Mind vs. Physical. Martin Binks, Ph.D. Binks Behavioral Health, PLLC

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The Hunger Games: Mind vs. Physical Martin Binks, Ph.D. Binks Behavioral Health, PLLC Disclosures As previously disclosed, Martin Binks Ph.D. has a financial or other
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The Hunger Games: Mind vs. Physical Martin Binks, Ph.D. Binks Behavioral Health, PLLC Disclosures As previously disclosed, Martin Binks Ph.D. has a financial or other relationship(s) with the following companies relevant to this presentation topic: Binks Behavioral Health, PLLC. Proprietor & CEO 1 Objectives: To discuss the physiology of hunger. To consider environmental, behavioral and emotional contributors to hunger. To discuss intervention strategies (surgical & non-surgical). Physiology of Hunger The gastrointestinal tract is the largest endocrine organ in the body. Produces hormones that have important sensing and signaling roles in regulating body weight and energy expenditure. Dieting and increased energy expenditure can manage excess weight to a degree but it appears to be an uphill struggle. 2 Compensatory changes in gut hormones may contribute to the difficulty with weight-loss through dietary restriction alone. Evidence suggests that alterations in circulating gut hormones may mediate weight-loss and also the metabolic benefits of bariatric surgery. Logically, strategies aimed at modulating circulating gut hormone concentrations or targeting their receptors are being developed as potential pharmacotherapies for obesity. Chandarana, K Endocrine Abstracts (2012) 29 S67.2 Gut hormones: history, physiology and therapeutic opportunities Gut-Brain Axis Hussain SS Bloom SR International Journal of Obesity (2012), 1 9 Dorsoventral Vagal Complex. 3 Leptin Resistance to adiposity signaling hormones (Insulin & Leptin) are features of obesity. Leptin level elevated (but sensitivity reduced) in obesity falls with weight loss. Leptin should signal to decrease food intake with sufficient energy stores. Reduced sensitivity leads to continued consumption even when fat stores are high. Also increased hunger signaling subsequent to weight loss. Ghrelin - The Hunger Hormone Only know orexigenic (hunger producing) gut hormone. Plasma Ghrelin levels elevated before meals, decline post-prandially (after eating) proportionally to calories ingested. Ghrelin rises during weight loss suggesting a role in poor dietary adherence during and regain following weight loss. Strategies to block Ghrelin have been considered in weight loss drug development. 4 Other Gut Hormones Cholecystokinin (CCK) first shown to relate to appetite in gut CCK1 satiety. Peptide YY (PYY) Low during fasting, rises post-prandially (after eating) for several hours in proportion to calories consumed. Slows gastric emptying (perhaps increase satiety) this response is blunted in obesity. Exaggerated PYY responses are noted post RYGB. Peripheral administration has been shown to produce an anorectic response in humans. Glucagon-like peptide-1(glp-1) Secreted post-prandially in the gut in proportion to calories ingested (esp. glucose). Regulates ingestion of glucose and glucose dependant insulin release. Peripheral administration can reduce food intake in humans and has been used in tx of diabetes (Exenatide and Liraglutide). Once daily GLP-1 analogue currently in phase III obesity trials. 5 Summary of gut-brain axis A homeostatic, counter-regulatory system that adapts to energy needs/expenditure & environmental influences on food intake. Modulates our experience & perceptions of hunger/satiety in the context of available energy, energy needs & other (e.g. emotional, reward) needs. The apparent redundancy and counter-regulatory properties of the system prove challenging in developing effective obesity treatments in the context of our current food environment. How might bariatric surgery influence hunger/satiety? 6 Sleep and BMI Linked Internal Clocks (2 genetically determined Chronotypes ) related to morning or evening preference also modulate metabolism: Obese subjects carrying the CLOCK 3111TC/CC polymorphism (evening person). Sleep 20 minutes less. Had a higher intake of transfatty acids and proteins. Ate later in the day but same energy intake of non-carriers. Resistant to weight loss: lost about 2 kg less in 30 wk program. Behavioral factors play a role: Harder to adhere to planning and formal exercise if you are tired. Spontaneous activity like fidgeting, repositioning, gestures etc decreases in sleep deprived people. Systems involved in Sleep-BMI links: Relationships to eating, appetite, obesity and insulin resistance. Lucassen et al. Short sleep and metabolic dysfunction Ann. N.Y. Acad. Sci. 1264; Pharmacotherapy and obesity Prescription Weight Loss Drugs Commonly Target Hunger-Satiety Typical criteria for prescribing: Adults; BMI 30; or BMI 27 with comorbidities such as high blood pressure (hypertension), type 2 diabetes, or high cholesterol (dyslipidemia). Intended as an addition to a reduced calorie diet and exercise for chronic weight management. 8 FDA Approved Anti-Obesity Medications: Longstanding: Orlistat; Lipase inhibitor (Rx: Xenical OTC: Alli ); Blocks a proportion of dietary fat from being absorbed by the gut. No direct impact on hunger/satiety signaling. Phentermine; an appetite suppressant (Adipex- P, Suprenza ); Impacts appetite centers in the brain (via norepinephrine) primarily and may secondarily impact hormones like Leptin (satiety) in periphery. New Phentermine-topiramate extended release (Qsymia ); 1 year weight loss 6.7% (Rec dose). Topiramate may cause weight loss in several ways including increasing feelings of fullness, making foods taste less appealing, and increasing calorie burning. Lorcaserin hydrochloride (Belviq ); 1 year weight loss 3 to 3.7%. Belviq activates the serotonin 2C receptor in the brain. Activation of this receptor may help a person eat less and feel full after eating smaller amounts of food. 9 In the pipeline (Phase II-III clinical trials). Empatic proprietary formulation of zonisamide sustained release (SR) combined with bupropion (SR). Contrave is a fixed dose combination of naltrexone sustained-release (SR) and bupropion (SR). Acts in the brain to regulate appetite and energy balance. Naltrexone was chosen as a complement to bupropion in order to block compensating mechanisms that attempt to prevent long-term, sustained weight loss. Psychological-Behavioral Factors Influencing Hunger & Weight Control: Cravings, Emotions, Stress aka. LIFE 10 Health Commitment Matrix Health Environment Health Knowledge Work & Financial Life Social & Recreational Life Emotional Coping & Stress Management Personal Support System Physical Health Behavioral obesity treatments typically use a combination of Cognitive Behavioral (CBT), Interpersonal Therapy (IPT): CBT Education about the particular behavioral treatment target (e.g. eating, depression, stress management, social support, exercise adherence). Motivational enhancement techniques. Training to help patients identifying antecedents and consequences of behavior, behavioral stimulus control, self-monitoring, self-control strategies, problem-solving, cognitive techniques for identifying and changing maladaptive thoughts and techniques for managing emotional and environmental triggers. 11 Interpersonal Psychotherapy (IPT): Draws links between the experience of interpersonal events and maladaptive behavioral patterns. Provides detailed analysis of the interpersonal context (past and present) of the behavioral treatment target. Formulates a plan to increase the person s effectiveness in interpersonal problem areas. Uses the improvement in interpersonal effectiveness to reduce the need to engage in the problem behaviors. Teaches improved emotion regulation and coping through increased use of social support = reduced reliance on problem coping (eating, exercise avoidance). Food Craving Prevalence & Characteristics Often defined as an intense desire to consume a particular food (or type of food) that is difficult to resist (White et al., 2002). 68% of men and 97% of women report food cravings 2-4 times per week (Weingarten & Elston, 1991; Hill et al., 1991). Food cravings do not result from nutritional deprivation. Difference between cravings and hunger: Cravings are alleviated by eating specific types of foods; hunger is alleviated by eating many types of foods (Pelchat & Schafer, 2000). 12 Associated with BED, NES and BN (Moreno et al., 2009; Jarosz et al., 2007). Cravings are not robust predictors of weight change during dieting (Martin et al., 2006). Cravings for high fat and sweet foods are associated with obesity (White et al., 2002; 2005). Neuroimaging studies have demonstrated that food cues activate brain regions associated with attention, appetitive motivation, and reward (Martin et al., 2010). Cravings appear to develop from conditioning (similar to food aversion): Cravings can develop from pairing food intake with hunger and also emotional states (Gibson & Desmond, 1999; Rogers & Smit, 2000). Cravings Assessment & Treatment Food Craving Inventory (FCI) (White et al., 2002). Sweets, carbs/starches, fast food, fats, high fats, general cravings Analyze how cravings link to eating behavior & weight. Conduct behavioral formulation to identify antecedents and consequences of cravings. Develop strategies for coping with and breaking the craving cycle. CBT - stimulus control; distraction; hunger management; meal structuring. Mindfulness, emotion regulation, stress management. 13 Stress, Appetite and Weight Studies show that increased levels of perceived stress influence eating behavior: More food eaten. Choices higher in fat & sugar (comfort food). May improve mood and decrease stress via opioidergic and dopaminergic neurotransmission. Cortisol and Ghrelin possibly influence eating following a stressful event. Cortisol Chronic stress-induced secretion of cortisol and/or increased hypothalamic, pituitary adrenal axis (HPA) activation may specifically contribute to central/abdominal obesity (linked with poorer health). 14 Ghrelin & Stress Ghrelin may also be affected by psychological stress. Similar to cortisol, stress-induced increases in Ghrelin may influence eating; However less has been published regarding the effects of perceived stress on Ghrelin in humans. Too few studies to conclude anything. Mindfulness Based Stress Reduction (MBSR) Incorporates the practice of mindfulness meditation in a group setting, group dialogue, daily home practice, and providing theoretical material related to stress management and the mind-body connection. Some studies have reported that participating in the MBSR program appears to positively affect the stress response and the hypothalamic, pituitary adrenal axis (HPA) - limited data. 15 Controlling Overeating, Emotional Eating & Binge Eating 1- Identify specific triggers for overeating, binge eating, and emotional eating. 2- Teach the behavior chain analysis technique and alternative coping. Triggers lead to eating off-plan & overeating. Situations People Emotions Time of day Skipping meals Food triggers (sight, smell, thoughts) 16 A Vicious Cycle Triggers (Stress) Overeat again Weight Gain I ll eat something! Dietary Restriction/ Reduced self-care Consequence (guilt) 17 Practical strategies to reduce the likelihood of overeating. Structured nutrition and planning. Exercising. Monitoring, self-awareness and support. Managing stress & emotions. Finding alternatives for pleasure. Coping Without Overeating Ask What do I REALLY need right now. Journal about life, stress, goals etc Do something active. Relax with friends, music, laughter. Talk to a primary support person. Do something creative. Try to see an alternative future. 18 Resources INTRODUCING Presented by: 19 Appendix A: 6 Step Solution: How to take action to improve your health using the Matrix. Health Commitment Matrix Health Environment Health Knowledge Work & Financial Life Social & Recreational Life Emotional Coping & Stress Management Personal Support System Physical Health Binks Behavioral Health PLLC 6 Step Solution: 1. Barriers & Strengths Think about what strengths and barriers exist in each matrix element. Set goals that Reduce Barriers Add strengths. 2. Realistic Planning This simplified approach to goal setting (below) allows you to have a main plan (Plan A) and plan for tough times and setbacks (Plan B) all in one model. 3. Motivators & Milestones - We need to grab all the motivators we can and use them to our best advantage! Upcoming events, reductions on the scale, changes in health indicators - what motivates you? This week, next month, next year combining short - PLUS long- term goals adds to ongoing success. 6 Step Solution: 4. Self-Awareness - We are so busy and so distracted by the way we choose to live our lives these days that being present in the moment appears to have gone. For health we need pause and understand what we truly need emotionally, intellectually and spiritually. Pause and ask what do I really need right now before grabbing the cigarette, the donut, skipping an exercise session rather than the quick fix. 5. Expanded Horizons How do you spend your time? Hobbies, entertainment, sports etc. What ruts are you in? How can we shake things up and make your life more exciting, more interesting. How can you explore new things and think outside the proverbial box. 6- Envisioning My Matrix - In this step you step back a moment and reflect on all the things you have identified through your use of the Health Commitment Matrix exercise. Reflect on what you have learned about yourself, your life, your strengths and barriers. Here is where you bring it all together and decide; Who do I hope to be. You will see how your goals may be fine-tuned and interwoven to create a smooth plan for living your life comfortably, productively and happily as a healthy person. 21 Appendix B: Diagnostic Criteria for Binge Eating (BE) & Night Eating Syndrome (NES) DSM IV Proposed Diagnostic criteria for Binge Eating Disorder; Coded as: Eating Disorder Not Otherwise Specified Source: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition American Psychiatric Association A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: 1) Eating in a discrete period of time (e.g. within any 2-hour period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances. 2) A sense of lack of control over eating during the episode (e.g. a feeling that one cannot stop eating or control what or how much one is eating). B. The binge eating episodes are associated with 3 or more of the following: (1)Eating much more rapidly than normal (2)Eating until feeling uncomfortably full (3)Eating large amounts of food when not feeling physically hungry (4)Eating alone due to being embarrassed by how much one is eating (5)Feeling disgusted with oneself, depressed, or very guilty after overeating 22 DSM IV Proposed Diagnostic criteria for Binge Eating Disorder; Coded as: Eating Disorder Not Otherwise Specified Source: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition American Psychiatric Association C. Marked distress regarding binge eating is present. D. The binge eating occurs, on average, at least 2 days a week for 6 months. E. The binge eating is not associated with the regular use of inappropriate compensatory behaviors (e.g. purging, fasting, excessive exercise) and does not occur exclusively during the course of Anorexia Nervosa or Bulimia Nervosa. Proposed Diagnostic Criteria for NES (Allison et al., 2010) A. The daily pattern of eating demonstrates a greatly increased intake in the evening and/or night-time, as manifested by one or both of the following: 1. At least 25% of daily food intake is consumed after the evening meal. 2. At least 2 eating episodes per week occur upon awakening during the night. B. Awareness and recall of evening and nocturnal eating episodes are present. C. The clinical picture is characterized by at least 3 of the following: 1. Lack of desire to eat in the morning and/or breakfast is omitted on 4 mornings per week. 2. Presence of a strong urge to eat between dinner and bedtime and/or during the night. 3. Sleep onset and/or sleep maintenance insomnia are present 4 nights per week. 4. Presence of a belief that one must eat in order to get to sleep. 5. Mood is frequently depressed and/or mood worsens in the evening. 23 Proposed Diagnostic Criteria for NES D. The disorder is associated with significant distress and/or impairment in functioning. E. The disordered pattern of eating has been maintained for a minimum of 3 months. F. The disorder is not secondary to substance abuse or dependence, a general medical disorder, a medication, or another psychiatric disorder. EDO and Bariatric Surgery: Summary Presurgical EDOs may not be predictive of clinically significant reductions in weight loss nor continued EDO symptoms postsurgically for all patients. Less favorable outcomes are associated with postoperative development or continuation of LOC but weight loss is still significant and likely superior to non-surgical treatments in this population (Devlin et al., 2005; Grilo et al., 2005). Clinicians must monitor patients at risk for EDOs postsurgically to identify those in need of additional treatment (CBT, IPT, DBT). Experience and emerging research suggests that providing treatment for EDO and related psychological issues during both preoperative and postoperative care may be beneficial and ultimately improve outcomes. 24 Appendix C: Pharmacotherapy eating disorders Pharmacotherapy (EDOs) Medication may be appropriate for co-morbid mood or other psychological issues. Meta-analyses on the efficacy of pharmacotherapy for Eating Disorders support moderate effect sizes for short-term symptom improvement. SSRIs most common for EDOs but other medications include SNRIs, SSNRIs, tricyclics, mood stabilizers, topiramate, orlistat, sibutramine (no longer FDA approved). Combined treatment with pharmacotherapy and cognitive behavior therapy has been more effective than either alone (true for most psych issues). 25 Appendix D: A case example of presurgical behavioral intervention Case: Pt is a 58 year old; Caucasian; Female; BMI Disability since 2006: Weight & Psych (Major Depression; Recurrent; Partial Remission) & Generalized Anxiety Disorder (GAD). Taking duloxetine (SSNRI) & Bupropion (NA/DA; RI). Last MD episode 2006 Onset 20yo w weight gain. Same psychiatrist for 20 yrs; LCSW for 1.5 years. Current moderate depression/anxiety managed by therapist; adequate self-care and functionality; Denies binge eating. Sees weight as reason for remaining psychosocial issues. Patient approved with therapist approval and involvement. Worked with therapist to coordinate mood and other therapy efforts with surgical plan. 26 Patient scheduled for surgery; initiated liquid diet; experienced severe distress; anger towards surgical team; unable to comply for even 24 hours. Pt subsequently admits to significant hx of LOC eating and current anxiety over coping without food. Recommended of 4-6 weekly sessions (or more prn). Goal to improve skills relating to identification of emotional and behavioral eating triggers; enhance coping and mood management; improve confidence in non-food based coping; physical activity plan. Identified goal of success in pre-surgical liquid diet. Techniques used: Emotional awareness training: Identification and specific definition of triggers beyond broad categories like Depression. Refined categories e.g. fear of being judged shame over LOC (sig contributor to liquid diet non-adherence). Behavioral distraction techniques: Activities Jar watch TV, read, breathing, walk, visualize (hunger or fear balloon), Internet support, therapist (surgical program) texting. Eating control strategies: Slowed eating with timer (indigestion), delay of cravings, meal frequency, emotional coping before eating. 27 Outcomes: Improved coping and trigger awareness. Regular and largely effective use of strategies. Sig. reduction in interfering thoug
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