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Nutrition Therapy for the Addicted Brain (June 2016) by David Wiss MS RDN

  1. Nutrition Therapy for the Addicted Brain *June 2016*
  2. ASAM Disclosure of Relevant Financial Relationships Content of Activity: “Nutrition Therapy for the Addicted Brain” Date of Activity: June 4, 2016 Name Commercial Interests Relevant Financial Relationships: What Was Received Relevant Financial Relationships: For What Role No Relevant Financial Relationships with Any Commercial Interests David Wiss MS RDN Nutrition in Recovery, Founder and Owner
  3. LECTURE OBJECTIVES 1. Discuss the impact of addictive substances on nutritional status 2. Explore disordered and dysfunctional eating patterns in addicted populations 3. Propose nutrition therapy guidelines for specific substances and for poly-substance abuse
  4. SECTIONS 1. Background 2. Food and Mood 3. Substance Use Disorders 4. Food Addiction 5. Disordered Eating 6. Hormones 7. Gut Microbiome 8. Nutrition Therapy 9. Conclusions
  5. 1. Background
  6. BACKGROUND • Substance Use Disorders (SUDs) assoc. w/ vitamin & mineral deficiencies1-6 • What about altered neuro- circuitry? • Nutrition-related hormones? • Leptin, ghrelin, insulin • Gut microbiome? • We need to know more! 1. Estevez, J. F. D., Estevez, F. D., Calzadilla, C. H., Rodriquez, E. M. R., Romero, C. D., & Serra-Majem, L. (2004). Application of linear discriminant analysis to the biochemical and haematological differentiation of opiate addicts from healthy subjects: A case-control study. European Journal of Clinical Nutrition, 58, 449-455 2. Heathcote, J., & Taylor, K. B. (1981). Immunity and nutrition in heroin addicts. Drug and alcohol dependence, 8, 245-255. 3. Hossain, K. J., Kamal, M. M., Ahsan, M, & Islam, S. N. (2007). Serum antioxidant micromineral (Cu, Zn, Fe) status of drug dependent subjects: Influence of illicit drugs and lifestyle. Substance Abuse Treatment, Prevention, and Policy, 2(12). Retrieved from 4. Islam, S. K. N., Hoassain, K. J., & Ahsan, M. (2001). Serum vitamin E, C, and A status of the drug addicts undergoing detoxification: influence of drug habit, sexual practice and lifestyle factors. European Journal of Clinical Nutrition, 55, 1022-1027. 5. Ross, L. J., Wilson, M., Banks, M., Rezannah, F., & Daglish, M. (2012). Prevalence of malnutrition and nutritional risk factors in patients undergoing alcohol and drug treatment. Nutrition, 28, 738-743. 6. Saeland, M., Haugen, M., Eriksen, F. L., Wandel, M., Smehaugen, A., Bohmer, T., & Oshaug, A. (2011). High sugar consumption and poor nutrient intake among drug addicts in Oslo, Norway. British Journal of Nutrition, 105, 618-624.
  7. NUTRITION AND DRUG ADDICTION • Primary Malnutrition • Displaced, reduced, compromised food intake • Secondary Malnutrition • Alterations in: • Absorption • Metabolism • Utilization • Excretion • Due to compromised health: • Oral • Gastrointestinal • Circulatory • Metabolic • Neurological Immune system Inadequate response to disease
  8. DRUG ADDICTION VS. ALCOHOL • Negative effect of alcohol on nutritional status well-described • Protocols in place (i.e. thiamine) • Illicit drug-induced malnourishment largely unknown • Primary or secondary? • Poly-drug abuse • Ethical/legal challenges with controlled trial research • Poor patient follow-up Most data speculative, underpowered, retrospective
  9. CURRENT CLIMATE …Little progress incorporating dietitians into drug rehabilitation programs despite continued explosion of drug abuse • Lack of interest from RDs??? • Associated stigmas of drug abuse • Difficulties conducting research on this population • Non-collaboration between public and private sector • Limited funding for new initiatives
  10. SYSTEMS INFLUENCING FOOD INTAKE • Homeostatic System • Post-consummatory • Post-absorptive • Hedonic/Pleasure-Reward System • Consummatory • Interaction between homeostatic and hedonic mechanisms
  11. HOMEOSTATIC SYSTEM • Key Components: • Hypothalamus • Adiposity Signals • Leptin • Insulin • Appetite-regulating gastrointestinal (GI) hormones • Orexigenic (appetite enhancing) • Anorexigenic (suppressing) • Nutrient-related signals • Vagus nerve
  12. HEDONIC/PLEASURE-REWARD SYSTEM • Brains response to rewarding events essential for survival: • Eating behavior • Sexual behavior • Associated pleasure influences future behavior • Ensures survival as a species • Hedonic system • Drawn toward pleasurable activities • “Reward” (dopamine) • Cognitive and emotional factors
  13. INTERACTION BETWEEN HOMEOSTATIC AND HEDONIC MECHANISMS • Homeostatic • Availability of fuel • Hedonic • Desire for and pursuit of food • “Wanting” Homeostatic signals SHOULD provide feedback to mesolimbic circuitry so that one’s metabolic state will ultimately influence the hedonic value of food…
  14. OVERFEEDING? • Sufficient energy stores SHOULD reduce brain’s response to highly palatable food • Higher fat stores SHOULD decrease food intake and rev up metabolism • SHOULD suppress the drive to overconsume food • Modulate sensory properties • Taste, odor
  15. HEDONIC OVERRIDES HOMEOSTATIC • Pleasurable effect of highly palatable food very MOTIVATING • “Food Motivation” • Contemporary food is supercharging our reward systems! • Hedonic drive (once provided evolutionary advantage) has now transformed into a burden
  16. 2. Food and Mood
  17. FOOD & MOOD – Carbohydrates • Carbohydrate ingestion: • Insulin promotes the cellular uptake of glucose & amino acids (AA) (except for tryptophan) • Tryptophan brain Leyse-Wallace, R. (2008). Linking nutrition to mental health. Lincoln, NE: iUniverse.
  18. FOOD & MOOD – Protein • AAs are the building blocks of neurotransmitters including: • Serotonin • Dopamine & Norepinephrine • Acetylcholine (inhibitory/excitatory) • Histamine (inflammatory response) • Glycine (inhibitory) Dekker, T. (2000). Nutrition & recovery. Canada: Centre for Addiction and Mental Health.
  19. DOPAMINE • Catecholamine neurotransmitter • Dopamine is the major brain chemical involved in addiction • Important in: • Movement (muscle control) • Motivation and attention • Reward • Well-being
  20. FOOD & MOOD – Protein • Tyrosine
  21. FOOD & MOOD – Protein • Dopamine and norepinephrine are often associated with alcohol / drug abuse Low dopamine associated with drug abuse…(receptor dysfunction) What can mimic the reward one gets from drug use?
  22. FOOD & MOOD – Fat • Prevalence of depression lower as fish consumption increases (omega-3)1 • Deficiencies alter fluidity in membranes affecting neurotransmission • Protective effect on bipolar, depression Omega-3 & depression is controversial2 1. Leyse-Wallace, R. (2008). Linking nutrition to mental health. Lincoln, NE: iUniverse. 2. Bloch, M. H., & Hannestad, J. (2012). Omega-3 fatty acids and the treatment of depression: Systematic review and meta- analysis. Molecular Psychiatry, 17(12), 1272-1282. doi:10.1038/mp.2011.100
  23. 3. Substance Use Disorders (SUDs)
  24. POLY-SUBSTANCE ABUSE • 24-hr recalls of 20 F IV drug users revealed > ½ of foods consumed not classifiable into “food groups”1 • Preference for easily ingested/digested foods (i.e. cereal) • Difficulty w/ raw vegetables & meat Digestive issues & preference for hedonistic foods rich in sugar/salt/fat 1. Baptiste, F., & Hamelin, A. (2009). Drugs and diet among women street sex workers and injection drug users in Quebec city. Canadian Journal of Urban Research, 18(2), 78-95.
  25. POLY-SUBSTANCE ABUSE • Added sugar 30% intake of drug addicts in Norway (n=220)1 • Sugar & sugar-sweetened foods preferred > 60% of respondents • 70% vit. D deficiency • Low levels of vit. C • Elevated serum Cu 1. Saeland, M., Haugen, M., Eriksen, F. L., Wandel, M., Smehaugen, A., Bohmer, T., & Oshaug, A. (2011). High sugar consumption and poor nutrient intake among drug addicts in Oslo, Norway. British Journal of Nutrition, 105, 618- 624. doi:10.1017/S0007114510003971
  26. OPIATES • Infrequent eating, little interest in food (appetite suppression) • Reduced gastric motility1 • Delayed gastric emptying • Impaired gastrin release • Constipation while using • Diarrhea while detoxing • GI discomfort for several months • Compromised gut health Impaired absorption of AA, vit/min 1. White, R. (2012). Drugs and nutrition: How side effects can influence nutritional intake. Proceedings of the Nutrition Society, 69, 558- 564. doi:10.1017/S0029665110001989
  27. OPIATES • Quick, convenient, cheap, sweet foods1 • Low fiber • Easily digestible • Calorically dense Ice cream • Fruit/vegetable consumption generally low 1. Neale, J., Nettleton, S., Pickering, L., & Fischer, J. (2012). Eating patterns among heroin users: a qualitative study with implications for nutritional interventions. Addiction, 107, 635- 641. doi:10.1111/j.1360-0443.2011.03660.x
  28. COCAINE • Reduced appetite, nausea • Affinity for high-sugar food/drink1 • Addicts in detox prefer highest conc. of sucrose solution offered • Brain reward (dopamine) • In large national sample, cocaine users more likely to have BP than heroin or meth2 CKD or CVD 1. Janowsky, D. S., Pucilowski, O., & Buyinza, M. (2003). Preference for higher sucrose concentrations in cocaine abusing-dependent patients. Journal of Psychiatric Research, 37, 35-41. 2. Akkina, S. K., Ricardo, A. C., Patel, A., Das, A., Bazzano, L. A., Brecklin, C. ...Lash, J. P. (2012). Illicit drug use, hypertension, and chronic kidney disease in the US adult population. Translational Research, 160(6), 391-398.
  29. COCAINE • Low levels of omega-3 and omega-6 linked to relapse1 • May stem from increased anxiety associated w/ low PUFA2 • Addiction stripping brain EFAs3 • Impaired utilization of AAs for NT synthesis (serotonin, dopamine) • Amino acid therapy??? 1. Buydens-Branchey, L., Branchey, M., McMakin, D. L., & Hibbeln, J. R. (2003). Polyunsaturated fatty acid status and relapse vulnerability in cocaine addicts. Psychiatry Research, 120, 29-35. doi:10.1016/S0165-1781(03)00168-9 2. Buydens-Branchey, L., & Branchey, M. (2006). N-3 polyunsaturated fatty acids decrease anxiety feelings in a population of substance abusers. Journal of Clinical Psychopharmacology, 26(6). doi:10.1097/ 3. 1. Grotzkyj-Giorgi, M. (2009). Nutrition and addiction – can dietary changes assist with recovery?. Drugs and Alcohol Today, 9(2), 24-28.
  30. COCAINE – AMINO ACID THERAPY? • N-acetylcysteine (NAC) • Proposed pharmacological treatment for relapse prevention1 (animal models) • Evidence suggesting long-term efficacy of therapeutic AA programs is lacking • Need more controlled trials • Increasing overall protein can promote NT synthesis is less urgent manner • Assuming addict is safe and food is available Long-term sustainable behavior change 1. LaRowe, S. D., Myrick, H., Hedden, S., Mardikian, P., Saladin, M., McRae, A., ...Malcolm, R. (2007). Is cocaine desire reduced by n-acetylcysteine? American Journal of Psychiatry, 164(7), 1115-1117.
  31. METHAMPHETAMINE • Disrupts energy metabolism1 • Changes in gene expression and proteins associated with muscular homeostasis/contraction • Maintenance of oxidative status • Oxidative phosphorylation • Fe and Ca homeostasis • Ferritin down regulation free iron • Harmful free radicals via Fenton rxn • Pyruvate pathways diverted towards fermentation to lactic acid 1. Sun, L., Li, H., Seufferheld, M .J., Walters Jr., K. R., Margam, V. M., Jannasch, A., ...Pittendrigh, B. R. (2011). Systems-scale analysis reveals pathways involved in cellular response to methamphetamine. Insights into Methamphetamine Syndrome, 6(4), e18215.
  32. METHAMPHETAMINE • > 40% meth users had dental/oral dz1 • Almost 60% had missing teeth • IV users higher rates of dental dz compared to smoking/snorting, and to other IV drugs2 • Altered Ca utilization?3 • High intake refined CHO, high calorie carbonated beverages, increased acidity in oral cavity, GI regurgitation/vomiting4 “Meth mouth” 1. Shetty, V., Mooney, L. J., Zigler, C. M., Belin, T. R., Murphy, D., & Rawson, R. (2010). The relationship between methamphetamine use and increased dental disease. Journal of the American Dental Association, 141(3), 307-318. 2. Laslett, A., Dietze, P., & Dwyer, R. (2008). The oral health of street- recruited injecting drug users: Prevalence and correlates of problem. Addiction, 103, 1821- 1825. doi:10.1111/j.1360- 0443.2008.02339.x 3. Sun, L., Li, H., Seufferheld, M .J., Walters Jr., K. R., Margam, V. M., Jannasch, A., ...Pittendrigh, B. R. (2011). Systems-scale analysis reveals pathways involved in cellular response to methamphetamine. Insights into methamphetamine syndrome, 6(4), e18215. 4. Hamamoto, D. T., & Rhodus, N. L. (2009). Methamphetamine abuse and dentistry. Oral Diseases, 15, 27- 37. doi:10.1111/j.1601- 0825.2008.01459.x
  33. METHAMPHETAMINE • Cessation and subsequent improvements in nutrition and oral hygiene 1st line of treatment • Oral health affects capacity to consume food, therefore… • Potential impact all areas of nutrition • Interventions must be realistic! • Monitor/evaluate xerostomia, chewing ability, and taste Consumption of refined CHO • Replace with fruits/vegetables
  34. “SOCIAL DRUGS” CAFFEINE & NICOTINE • Used together for synergistic effects • Caffeine as cue for nicotine • Some treatment centers do not allow “social drugs,” others allow without any formal regulation • Often used as a breakfast substitute for individuals in recovery, which may have adverse effects in the afternoon1 1. Dekker, T. (2000). Nutrition and recovery. Toronto, CAN: Centre for Addiction and Mental Health.
  35. CAFFEINE • No longer just coffee, tea, chocolate and sodas • Energy drinks, pills • Workout supplements (>300mg) • “Caffeinism” 600-750 mg/day • >1000 mg/day defined as toxic1 • DSM-5: >250 mg can be intoxicating • Coffee/tea inhibits the absorption of iron in food • Affects duration/quality of sleep 1. Hilton, T. (2007). Pharmacological issues in the management of people with mental illness and problems with alcohol and illicit drug misuse. Criminal Behavior and Mental Health, 17, 215- 224. doi:10.1002/cbm.669
  36. Yudko, E., & McNiece, S. I., (2014). Relationship between coffee use and depression and anxiety in a population of adult polysubstance abusers. Journal of Addiction Medicine, 8(6), 438-442. • N = 69 • Mean age = 35 • Treatment center in rural Hawaii • Racially diverse • About half Pacific Islander • Coffee use associated with depression • Beck Depression Inventory • Direction of causality?
  37. NICOTINE Nicotine • Increases metabolism1 • Acts as appetite suppressant1 • Compromises senses of taste and smell2 Smokers have tendency to choose hyperpalatable snack foods, less likely to enjoy the taste of fruits and vegetables Smokers lower in plasma vitamin C and total carotenoids, independent of dietary intake3 Introducing the vape? 1. Novak, C. M., & Gavini, C. K. (2012). Smokeless weight loss. Diabetes, 61, 776-777. 2. Hatcher, A. S. (2008). Nutrition and addictions. Dallas, TX: Understanding Nutrition, PC. 3. Dekker, T. (2000). Nutrition and recovery. Toronto, CAN: Centre for Addiction and Mental Health.
  38. “SOCIAL DRUG” USE – THOUGHTS • Caffeine and nicotine can impact one’s hunger/fullness cues and lead to dysfunctional eating behavior • Dietitians in treatment settings can help patients meet reduction or cessation goals when ready • By focusing on the benefits of improved physical health, patients will be positioned to make informed choices about what they eat • Strict avoidance of caffeine during early recovery may make nutrition seem punitive vs. a helpful component of recovery • “First things first” – complete avoidance may lead to relapse • Nutrition education and counseling can become an effective adjunctive approach towards caffeine/nicotine reduction/cessation
  39. LET’S BE PRACTICAL – BIG PICTURE • Caffeine, nicotine, and hyperpalatable food may have beneficial functions in early recovery! • First issue is always to get the individual past the immediate crisis… • “Many of us have noticed a tendency to eat sweets and have found this practice beneficial.” –AA Big Book, p. 134 • Prolonged abuse after abstinence achieved may contribute to: • Comorbid conditions • Compromised quality of life • Decreased likelihood of long-term recovery • Overall healthcare burden
  40. 4. Food Addiction (FA)
  41. “ADDICTION” – DSM-5??? • Non-Substance-Related • Gambling • Behavioral Addictions? • Sex Addiction • Exercise Addiction • Shopping Addiction • Gaming Currently insufficient evidence for diagnostic criteria What about food??? Is it substance-related? Behavioral? Both?
  42. THE CONTROVERSY OF FOOD ADDICTION • Is overeating a behavioral problem or a substance related problem? • Does obesity stem from high-risk people or high-risk foods? • Abstinence from offending “drug foods”? • Risk factor for binge eating? • Or abstinence from offending behaviors? • Classic ED treatment
  43. CURRENT CLIMATE • Eating disorder (ED) clinicians uneasy about incorporating FA • Classic EDs such as AN-R do not resemble an addiction • Education about FA will cause those with restrictive EDs to deepen into their ED • Challenges the classic messages: • “All foods fit” • “Everything in moderation” • “A calorie is a calorie” • “Food is fuel” Meanwhile… Standard ED treatment is associated with high rates of relapse and poor long-term remission rates1 1. Bergh, C., Callmar, M., Danemar, S., Holcke, M., Isberg, S., Leon, M., ...Sodersten, P. (2013). Effective treatment of eating disorders: Results at multiple sites. Behavioral Neuroscience, 127(6), 878-889.
  44. MODERATION? • Perceived (vs. defined) • Self-serving biases • Justify over-consumption • Used to reduce self-conflict • Very appealing message • More part of the problem than the solution • Misinterpreted & misapplied • Big Food loves “moderation” vanDellen, M. R., Isherwood, J. C., & Delose, J. E. (2016). How do people define moderation? Appetite, 101, 156-162.
  45. DEFINING ADDICTION & FOOD American Society of Addiction Medicine (ASAM) “addiction is a primary, chronic disease of brain reward, motivation, memory, and related circuitry” ASAM recognizes food as having addictive potential Food (Wikipedia) (Noun) Any nutritious substance that people or animals eat or drink, or that plants absorb, in order to maintain life and growth. Food in it’s natural state is hardly addictive… But what about highly concentrated by- products of food? aka processed food?
  46. COCA LEAF VS. CRACK COCAINE Coca Leaf • Not highly addictive Powder Cocaine • By-product • Addictive Crack Cocaine • Further processed • Wreaks havoc on human brain
  47. POPPY PLANT VS. HEROIN Poppy Plant • Not highly addictive Raw opium • By-product • Addictive Heroin • Further processed • Highly Addictive
  48. WHEAT PLANT VS. WHITE FLOUR Wheat Plant • Not addictive Whole Wheat Flour • By-product Refined White Flour • Further Processed • “Offensive”
  49. SUGAR CANE VS. REFINED WHITE SUGAR Sugar Cane • Not addictive Raw Sugar • By-product Refined Sugar • Further Processed • “Offensive”
  50. CORN VS. HIGH FRUCTOSE CORN SYRUP (HFCS) Corn • Not addictive Corn Syrup • By-product HFCS • Further Processed • “Offensive”
  51. FOOD ADDICTION • Highly processed foods that share characteristics of abused drugs1 • High dose, high concentration • Rapid rate of absorption • Most addictive combinations typically contain1 • White flour, sugar, fat (e.g. cookie) • Abundance of addictive food assoc. w/ craving & compulsion2 1. Schulte, E. M., Avena, N. M., & Gearhardt, A. N. (2015). Which foods may be addictive? The roles of processing, fat content, and glycemic load. PLoS ONE, 10(2). 2. Potenza, M. N., & Grilo, C. M. (2014). How relevant is craving to obesity and its treatment? Frontiers in Psychiatry, 5(164).
  52. FOOD ADDICTION • Drugs addicts share many characteristics with compulsive overeaters • Brain imaging1 • Behavioral2 • “Reward” from substance • Drugs/alcohol • Hedonic food • Highly palatable food • Processed food w/ added sugars/salt/fat 1. Volkow, N. D., & Wise, R. A. (2005). How can drug addiction help us to understand obesity? Nature Neuroscience, 8(5), 555-560. 2. Davis, C., Curtis, C., Levitan, R. D., Carter, J. C., Kaplan, A. S., & Kennedy, J. L. (2011). Evidence that 'food addiction' is a valid phenotype of obesity. Appetite, 57, 711-717.
  53. YALE FOOD ADDICTION SCALE (YFAS) • Developed in 2008, both internally & externally validated1 • Abnormal desire for sweet, salty, and fatty foods documented in obese adults using YFAS2 • Diagnostic scoring based on seven symptoms in the DSM-IV-TR for substance dependence • Withdrawal • Tolerance • Use despite negative consequences • Food addiction found in 57% of obese BED patients3 1. Gearhardt, A. N., Corbin, W. R., & Brownell, K. D. (2009). Preliminary validation of the Yale food addiction scale. Appetite, 52, 430-436. 2. Davis, C., Curtis, C., Levitan, R. D., Carter, J. C., Kaplan, A. S., & Kennedy, J. L. (2011). Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite, (57), 711-717. 3. Gearhardt, A. N., White, M. A., Masheb, R. M., Morgan, P. T., Crosby, R. D., & Grilo, C. M. (2012). An examination of the food addiction construct in obese patients with binge eating disorder. International Journal of Eating Disorders, 45, 657-663.
  54. FOOD ADDICTION – CULPRITS …Sugar, Salt, Fat + dynamic contrast • The more multisensory the food the more likely a person is to crave it • Combining a cold food such as ice cream with a warm sauce such as hot fudge, and topping it off with smooth Reese’s peanut butter cups and crunchy heath bar pieces becomes irresistible
  55. FOOD ADDICTION – CULPRITS Refined grains… w/ sugar/salt/fat
  56. FOOD ADDICTION – CULPRITS What is the difference between a baked potato and French fries with ketchup? Fat…Salt…Sugar
  57. Schulte, E. M., Avena, N. M., & Gearhardt, A. N. (2015). Which foods may be addictive? The roles of processing, fat content, and glycemic load. PLoS ONE, 10(2). 1. Chocolate 2. Ice Cream 3. French Fries 4. Pizza 5. Cookie 6. Cake 7. Popcorn (Buttered) 8. Cheeseburger
  58. WHAT IS A “FOOD ENVIRONMENT”? • Collection of physical, biological, and social factors affecting eating habits/patterns • Access to food • “Food Deserts” convenience foods • Resource limitations? • Food availability at home (rehab) • Environmental causes of overeating? • Highly available “hyperpalatable” foods a risk factor for food addiction in some individuals? • “Big Food” aka The Food Industry created irresistible, yet toxic “Food Environment”?
  59. WITHDRAWAL – ANIMAL MODELS • Rats w/ access to highly palatable cafeteria diet for 40 days • When taken off, they reject standard chow! • Chronic exposure to addictive substances causes self- administration of excess in attempt to regain the same hedonic level (subjective pleasure) Cottone, P., Sabino, V., & Steardo, L. (2008). Opioid-dependent anticipatory negative contrast and binge-like eating in rats with limited access to highly preferred food. Neuropsychopharmacology, 33, 524-535.
  60. BED vs. FOOD ADDICTION Binge Eating Disorder • Ate the whole box of chocolates in one sitting • Psychological/emotional • DSM-5 clinical diagnosis, insurance reimbursement Food Addiction • Ate the whole box over several sittings • Biological/neurochemical • Not recognized or reimbursable There are more similarities than there are differences… Obesity can exist without either one!
  61. FOOD ADDICTION • Reward-responsive phenotype of obesity1 • Can exist without obesity2 • And without BED • Food becomes less rewarding and more habitual3 • Alterations in dopamine circuitry • Low levels of DA transmission linked w/ heightened propensities towards substance abuse in bulimic women4 1. Davis, Caroline (2013). Compulsive overeating as an addictive behavior: Overlap between food addiction and binge eating disorder. Current Obesity Reports, 2, 171-178. 2. Eichen, D. M., Lent, M. R., Goldbacher, E., & Foster, G. D. (2013). Exploration of "food addiction" in overweight and obese treatment- seeking adults. Appetite, 67, 22-24. 3. Guo, J., Simmons, W. K., Herscovitch, P., Martin, A., & Hall, K. D. (2014). Striatal dopamine D2-like receptor correlation with human obesity and opportunistic eating behavior. Molecular Psychiatry, 1-7. 4. Steiger, H., Thaler, L., Gauvin, L., Joober, R., Labbe, A., Israel, M., & Kucer, A. (2016). Epistatic interactions involving DRD2, DRD4, and COMT polymorphisms and risk of substance abuse in women with binge-purge eating disturbances. Journal of Psychiatric Research, 77, 8-14.
  62. REWARD DEFICIENCY SYNDROME (RDS) • Dysfunction of the dopamine D2 (DAD2) receptor in striatum • Leading to substance- seeking behavior • Alcohol, drug • Food • Concept that unites: • Addiction • Compulsivity • Impulsivity Blum, K., Sheridan, P. J., Wood, R. C., Braverman, E. R., Chen, T. J. H., Cull, J. G., & Comings, D. E. (1996). The D2 dopamine receptor gene as a determinant of reward deficiency syndrome. Journal of the Royal Society of Medicine, 89, 396- 400.
  63. REWARD DEFICIENCY SYNDROME (RDS) • Yet, recent meta- analysis found no support for link between DAD2- related RDS as mechanism underlying obesity • A1 allele • Novelty seeking • Delay discounting • Impulsivity • Avoiding neg. cons. Benton, D., Young, H. A. (2016). A meta-analysis of the relationship between brain dopamine receptors and obesity: A matter of changes in behavior rather than food addiction? International Journal of Obesity, 40, S12-S21.
  64. BRAINS OF OBESE INDIVIDUALS • Low inhibitory control • Impaired prefrontal activity leading to problems of impulse control1 • Low availability of DAD2 receptors in NAc associated w/ reduced activity in the prefrontal cortex1 • Contributing to impulsivity and poor self-control • “Reinforcement pathology” favors unhealthy behaviors that contribute to weight gain2 1. Carr, K., Daniel, T., Lin, H., & Epstein, L. (2011). Reinforcement pathology and obesity. Current Drug Abuse Reviews, 4(3), 190-196. 2. Volkow, N., Wang, G., Fowler, J., Tomasi, D., & Baler, R. (2012). Food and drug reward: Overlapping circuits in human obesity and addiction. Current Topics in Behavioral Neurosciences, 11, 1-24.
  65. REWARD SURFEIT THEORY • Individuals w/ greater reward region sensitivity to food intake at elevated risk for overeating • Habitual intake of palatable foods leads to hyper- responsivity of attention and reward valuation Val-Laillet, D., Aarts, E., Weber, B., Ferrari, M., Quaresima, V., Stoeckel, L. E., …Stice, E. (2015). Neuroimaging and neuromodulation approaches to study eating behavior and prevent and treat eating disorders and obesity. Neuroimage: Clinical, 8, 1-31.
  66. PHARMACOLOGY • Animal models: • Naltrexone reduces food intake1 • Opioid system: • Medial PFC regions • Involved in the control of feeding behavior • Key mediator of hedonic feeding • May be responsible for hyper-evaluation of highly palatable foods • Varenicline reduces sucrose consumption2 • Long-term 1. Blasio, A., Steardo, L., Sabino, V., & Cottone, P. (2013). Opioid system in the medial prefrontal cortex mediates binge-like eating. Addiction Biology, 19, 652-662. 2. Shariff, M., Quik, M., Holgate, J., Morgan, M., Patkar, O. L., Tam, V., ...Bartlett, S. E. (2016). Neuronal nicotinic acetylcholine receptor modulators reduce sugar intake. PLoS ONE, 11(3).
  67. WANTING VS. LIKING Berridge, K. C., Robinson, T. E., & Aldridge, J. W. (2009). Dissecting components of reward: ‘liking’, ‘wanting’, and learning. Current Opinion in Pharmacology, 9(1), 65-73. LEARNING: Predictive associations and cognitions
  68. 5. Disordered Eating
  69. CO-OCCURING SUBSTANCE USE DISORDER (SUD) & EATING DISORDER (ED) • HOT TOPIC (shortage of data!) • Anorexia nervosa (AN) + AUD • Alcohol use disorder (AUD) + AN • Bulimia nervosa (BN) + AUD • AUD + BN • BN + SUD • SUD + BN • Binge eating disorder (BED) + SUD • SUD + BED (often sub-threshold)
  70. BACKGROUND • Substance Use Disorders (SUD) on the rise • Eating Disorder (ED) + SUD • SUD + ED • Bidirectional associations1,2 • Most of the research conducted on females with AN and bulimia nervosa (BN) • “Drunkorexia”3 1. Baker, J. H., Mitchell, K. S., Neale, M. C., & Kendler, K. S. (2010). Eating disorder symptomatology and substance use disorders: Prevalence and shared risk in a population based twin sample. International Journal of Eating Disorders, 43, 648-658. 2. Grilo. C. M., Levy, K. N., Becker, D. F., Edell, W. S., & McGlashan, T. H. (1995). Eating disorders in female inpatients with versus without substance use disorders. Addictive Behaviors, 20(2), 255-260. 3. Hunt, T. K., & Forbush, K. T. (2016). Is "drunkorexia" an eating disorder, substance use disorder, or both? Eating Behaviors, 22, 40-45.
  71. SUD/AUD + GASTRIC BYPASS • New onset SUDs/AUDs in the post-surgical period (second year or later) • Absorption rate • Addiction transfer 1. Fowler, L., Ivezaj, V., & Saules, K. K. (2014). Problematic intake of high-sugar/low-fat and high-glycemic index foods by bariatric patients is associated with development of post-surgical new onset substance use disorders. Eating Behaviors, 15, 505-508. 2. King, W. C., Chen, J., Mitchell, J. E., Kalarchian, M. A., Steffen, K. J., Engel, S. E., Courcoulas, A. P., Pories, W. J., & Yanovski, S. Z. (2012). Prevalence of alcohol use disorders before and after bariatric surgery. Journal of the American Medical Association, 307(23), E1-E10. 3. Wiedemann, A. A., Saules, K. K., Ivezaj, V. (2013). Emergence of new onset substance use disorders among post-weight loss surgery patients. Clinical Obesity, 3, 194-201.
  72. SUD/AUD + GASTRIC BYPASS • Post-RYGB1 • Lower appeal rating of high-energy foods • Yale Food Addiction Scale (YFAS) scores • Gut microbiota? 1. Scholtz, S., Goldstone, A. P., & le Roux, C. W. (2015). Changes in reward after gastric bypass: the advantages and disadvantages. Current Atherosclerosis Reports, 17(61).
  73. SUD – DISORDERED EATING • Women in SUD treatment1 • BED and sub-threshold BED • Bulimia nervosa • Men in SUD treatment2 • First 6 months • Bingeing • Use of food to satisfy drug cravings • 7-36 months • Weight concerns, distress about efforts to lose weight 1. Czarlinksi, J. A., Aase, D. M., & Jason, L. A. (2012). Eating disorders, normative eating self-efficacy and body image self-efficacy: Women in recovery homes. European Eating Disorders Review, 20, 190-195. 2. Cowan, J., & Devine, C. (2008). Food, eating, and weight concerns of men in recovery from substance addiction. Appetite, 50, 33-42. doi:10.1016/j.appet.2007.05.006
  74. NUTRITION & ADDICTION TREATMENT • Disordered eating • Drug abuse risk factor for EDs1 • Genetic and environmental2 • Increased sugar use over time3 • Alcohol linked to bingeing/purging4 1. Krahn, D. D. (1991). The relationship of eating disorders and substance abuse. Journal of Substance Abuse, 3(2), 239-253. 2. Munn-Chernoff, M. A., Duncan, A. E., Grant, J. D., Wade, T. D., Agrawal, A., Bucholz, K. K., ... Heath, A. C. (2013). A twin study of alcohol dependence, binge eating, and compensatory behaviors. Journal of Studies on Alcohol and Drugs, 74, 664-673. 3. Levine, A. S., Kotz, C. M., & Gosnell, B. A. (2003). Sugar and fats: The neurobiology of preference [Special section]. Journal of Nutrition, 831S-834S. 4. Fischer, S., Anderson, K. G., & Smith, G. T. (2004). Coping with distress by eating or drinking: Role of trait urgency and expectancies. Psychology of Addictive Behaviors, 18(3), 269-274.
  75. BULIMIA NERVOSA (BN) + STIMULANTS • 707 undergrads1 • Nonmedical prescription stimulants • Ritalin, Adderral, Concerta • Used for appetite suppression and weight loss • Associated with greater ED symptomatology • Binge eating • Purging 1. Kilwein, T. M., Goodman, E. L., Looby, A., & De Young, K. P. (2016). Nonmedical prescription stimulant use for suppressing appetite and controlling body weight is uniquely associated with more severe eating disorder symptomatology. International Journal of Eating Disorders, Advanced online publication.
  76. BN + ADDICTION • Associated with the eating or the compensatory behaviors?1 • DSM-5 purging disorder • Overlap between BN + FA • Nutritional approach? • Reduced exposure to addictive foods?1 • Liberalize the diet? • Food restriction increases reward sensitivity, promotes rebound bingeing2 1. Muele, A., von Rezori, V., & Blechert, J. (2014). Food addiction and bulimia nervosa. European Eating Disorders Review. doi:10.1002/erv.2306 2. Avena, N., Murray, S., & Gold, M. S. (2013). Comparing the effects of food restriction and overeating on brain reward systems. Experimental Gerontology, 48, 1062-1067.
  77. Umberg, E. N., Shader, R. I., Hsu, G., & Greenblatt, D. J. (2012). From disordered eating to addiction: The "food drug" in bulimia nervosa. Journal of Clinical Pharmacology, 32, 376-389. • BN should be separated into two distinct sub-types!!! • Hyporesponsive to reward • Akin to AN • Hypersensitive reward circuitry • Akin to FA
  78. ED + FA • Patients with FA: • Lower self-directedness • More negative urgency • Lack of perseverance • Probability of FA predicted by: • High negative urgency • High reward dependence • Low lack of premeditation Wolz, I., Hilker, I., Granero, R., Jimenez-Murcia, S., Gearhardt, A. N., Dieguez, C., …Fernandez-Aranda, F. (2016). “Food addiction” in patients with eating disorders is associated with negative urgency and difficulties to focus on long-term goals. Fronteirs in Psychology, 7(61).
  79. BED + SUD • Approximately one fourth of BED patients have SUD1 • BED should be treated in a way that acknowledges the presence of a range of binge eating phenotypes2 • Including co-occurring SUD1 1. Becker, D. F., & Grilo, C. M. (2015). Comorbidity of mood and substance use disorders in patients with binge eating disorder: Associations with personality disorder and eating disorder pathology. Journal of Psychosomatic Research. Advance online publication. Retrieved from 2. Marcus, M. D., & Wildes, J. E. (2014). Disordered eating in obese individuals. Current opinion in psychiatry, 27(6), 443- 447.
  80. DISORDERED EATING • Body image issues often relevant to both AUD/SUD patients • Does not always imply presence of ED • Early recovery is stressful! • Craving, compulsivity • Relapse risk • Substance abuse linked to low distress tolerance, leading to consumption of food1 • Night Eating Syndrome 1. Kozak, A. T., & Fought, A. (2011). Beyond alcohol and drug addiction. Does the negative trait of low distress tolerance have an association with overeating? Appetite, 57, 578-581. doi:10.1016/j.appet.2011.07.008
  81. NIGHT EATING SYNDROME • Severity associated with FA1 • Higher food tolerance • Amount of food consumed • Effect of consumed food • Among psychiatric outpatients2 • Turkish sample: • Depression • Impulse control disorder • Nicotine dependency • Psych meds? 1. Nolan, L. J., & Geliebter, A. (2016). "Food addiction" is associated with night eating severity. Appetite, 98, 89-94. 2. Saracli, O., Atasoy, N., Akdemir, A., Guriz, O., Konuk, N., Sevincer, G. M., ...Atik, L. (2015). The prevalence and clinical features of the night eating syndrome in psychiatric out-patient population. Comprehensive Psychiatry, 57, 79- 84.
  82. 6. Hormones
  83. FACTORS THAT REGULATE FOOD INTAKE • Caloric requirements • Reinforcing responses • Palatability • Conditioned responses • Cues • Cognitive control • Inhibition/regulation
  84. HORMONES • Neuronal & gut hormones • “Cross-talk” via “Gut-brain axis” • Gut peptides released from enteroendocrine cells in response to pre-absorptive nutrients can reach brain1 • Indirectly • Receptors in enteric nervous system • Directly • Systemic circulation or lymphatics 1. Bauer, P. V., Hamr, S. C., & Duca, F. A. (2015). Regulation of energy balance by a gut-brain axis and involvement of the gut microbiota. Cellular and Molecular Life Sciences. doi:10.1007/s00018- 015-2083-z
  85. GUT-BRAIN AXIS • Stomach as 2nd Taste System • “Sensing receptors” • Mechanoreceptors: touch/pressure • Chemoreceptors: chemical • Thermoreceptors: temperature • Osmoreceptors: osmotic pressure • Wall of gut brain stem • Neurohormonal stimuli • Ghrelin (appetite stimulant) • “Light” versions of food detected by Gut-Brain Axis Witherly, S. A. (2007). Why humans like junk food. Lincoln, NE: iUniverse
  86. VENTRAL TEGMENTAL AREA (VTA) • Contains dopamine neurons that project to cortico-limbic structures: • Nucleus accumbens (pleasure) • Medial prefrontal cortex (cognition) • Hippocampus (memory) • Amygdala (emotional reactivity) • Direct input from hypothalamus • Governs several endocrine processes (leptin, ghrelin)
  87. HYPOTHALAMUS • Regulates energy balance • Altering energy intake & expenditure • Arcuate nucleus • Integration site for neurological & blood-borne signals • Brain reward system (midbrain) • Hedonic feeding (dopamine) • Modulated by blood-borne signals Bauer, P. V., Hamr, S. C., & Duca, F. A. (2015). Regulation of energy balance by a gut-brain axis and involvement of the gut microbiota. Cellular and Molecular Life Sciences. doi:10.1007/s00018-015- 2083-z
  88. LEPTIN • Produced/secreted by adipose tissue • Plasma leptin associated w/ fat mass • Increases metabolic rate • Initiates starvation response • Decreases food intake • Reward value of sucrose decreased by leptin via reduction in dopamine signaling1 1. De Araujo, I. E., Deisseroth, K., Domingos, A. I., Friedman, J., Gradinaru, V., & Ren, X. (2011). Leptin regulates the reward value of nutrient. Nature Neuroscience, 14, 1562-1568.
  89. LEPTIN & CRAVING • Leptin regulates homeostatic center of hypothalamus • Hedonic system1 • Subjective desires for food • Food deprivation decreases circulating leptin • Contributing to preference for highly palatable foods • “Hunger is the best sauce” • Leptin-dopamine interaction • Bi-directional2 1. Schloegl, H., Percik, R., Hortsmann, A., Villringer, A., & Stumvoll, M. (2011). Peptide hormones regulating appetite - focus on neuroimaging studies in humans. Diabetes/Metabolism Research and Reviews, 27, 104-112. 2. Leinninger, G. M. (2011). Lateral thinking about leptin: A review of leptin action via the lateral hypothalamus. Physiology and Behavior, 104(4), 572-581.
  90. LEPTIN & CRAVING • Leptin • Inhibits signaling in nucleus accumbens (VTA) • Among smokers trying to quit1 • Higher leptin, greater craving • Difficulty achieving abstinence 1. de Silva Gomes, A., Toffolo, M. C. F., van Keulen, H. V., e Silva, F. M. C., Ferreira, A. P., Luquetti, S. C. P. D., Aguiar, A. S. (2015). Influence of the leptin and cortisol levels on craving and smoking cessation. Psychiatry Research, 229, 126-132.
  91. GHRELIN • Stimulates appetite • Decreases after eating • Opposing effects with leptin • Leptin counters ghrelin • Stomach-derived • Receptors identified in VTA, hippocampus, amygdala1 • Sight of food elevates ghrelin2 • Non-obese healthy subjects 1. Dagher, A (2012). Hunger, hunger, and food addiction. In Brownell, K. D., & Gold, M. S., Food and addiction (131-137). New York, NY: Oxford University Press. 2. Schussler, P., Kluge, M., Yassouridis, A., Dresler, M., Uhr, M., & Steiger, A. (2012). Ghrelin levels increases after pictures showing food. Obesity, 20, 1212-1217.
  92. INSULIN • Peptide hormone from pancreas • Similarities to leptin: • Anorexigenic • Adiposity signal • Attenuates food reward • When low, drive for food intake increases • Works with dopamine to calibrate reward associated with feeding1 • Depresses dopamine conc. in VTA, which may suppress salience of food once satiety is reached 1. Mebel, D. M., Wong, J. C. Y., Dong, Y. J., & Borgland, S. L. (2012). Insulin in the ventral tegmental area reduces hedonic feeding and suppresses dopamine concentration via increased reuptake. Behavioral Neuroscience, 36, 2336-2346.
  93. INSULIN & LEPTIN • Insulin receptor signaling pathway interferes with leptin signaling • Insulin blocks leptin • Hyperinsulinemia contributes to the pathogenesis of leptin resistance1 • Interferes with leptin extinguishing of dopamine clearance in the nucleus accumbens2 (addiction) 1. Kellerer, M., Lammers, R., Fritsche, A., Strack, V., Machicao, F., Borboni, P., Ullrich, A., & Haring, H. U. (2001). Insulin inhibits leptin receptor signaling in HEK293 cells at the level of janus kinase-2: A potential mechanism for hyperinsulinaemia-associated leptin resistance. Diabetologia, 44, 1125-1132. 2. Lustig, R. H. (2013, October). Sugar, hormones and addiction. Symposium conducted at The Lifestyle Intervention Conference, Las Vegas, NV.
  94. Daws, L. C., Avison, M. J., Robertson, S. D., Niswender, K. D., Galli, A., & Saunders, C. (2011). Insulin signaling and addiction. Neuropharmacology, 61(7), 1123-1128. • Insulin receptors present in brain and midbrain dopamine neurons • Insulin-influenced dopamine transmission can affect the ability of drugs to exert their neurochemical and behavioral effects • Interplay between insulin signaling and drug-induced increases in extracellular dopamine may contribute to high comorbidity of eating disorders and drug abuse • Improvements in brain dopamine function by normalizing or bypassing disruptions in insulin signaling might be effective in treating addictions
  95. Ersche, K. D., Stochl J., Woodward, J. M., & Fletcher, P. C. (2013). The skinny on cocaine. Insights into eating behavior and body weight in cocaine-dependent men. Appetite. Advance online publication. Retrieved from • Cocaine-dependent men reported increased food intake, specifically foods high in fat and carbohydrate • Trend towards lower levels of circulating leptin in the cocaine group, directly interfering with metabolic processes • Overeating in cocaine-dependent individuals pre-dates recovery, with the effect masked by lack of weight gain • Taken together, cocaine abuse results in imbalance between fat intake and storage, leading to excessive weight gain during recovery
  96. HORMONES – DISCUSSION • Food and drugs compete for overlapping reward mechanisms • When substance abstinence has been achieved, likely a compensatory increased drive for food • Ravenous “rebound appetite” • Hypothalamus
  97. HORMONES – DISCUSSION • Normalizing disrupted leptin signaling cascade may be sufficient to decrease motivation for food reward • Weight gain during addiction recovery should be monitored/controlled in order to counter associated hormonal adaptions • Exposure to highly palatable
  98. 7. Gut Microbiome
  99. BURNING QUESTIONS • Why are so many of us drawn to foods that can compromise our quality of life? • Why do some of us reject foods that can heal us? • Why are educational efforts alone often not sufficient to produce sustainable behavior change? • Why is it so challenging to develop a new relationship to food? Lack of willpower? Food addiction? Restrained eating? Dieting?
  100. Over 90% of over 4,000 peer-reviewed articles on PubMed published within last 5 years In a human body, microbial cells outnumber human cells by a scale of 10
  102. DEFINITIONS • Microbiota • Microorganisms sharing human body space • Microbiome • Collective genomes of these microorganisms
  103. DEFINITIONS • Symbiosis • Interdependence/cooperation • Different species live together • Not necessarily mutualism • Commensal • One benefits, other unaffected • Pathogenic/Parasitic • Cause or produce disease • “Dysbiosis”
  104. MICROBIOTA • Bacteria • Archea • Protozoans • Fungi • Viruses Share human space Gut Microbiota • “Hidden Organ” Homeostasis or disease
  105. GUT MICROBIOTA – FUNCTIONS • Regulating gut motility • Digestion of cellulose (fiber) • Fermenting unused energy substrates • Destroying toxins • Biosynthesis: • Vitamin K • B-vitamins • Amino Acids (lysine, threonine) • Absorption of minerals Konturak et al. (2015)
  106. GUT MICROBIOTA – FUNCTIONS • New insights: • Disease development • Brain health • Attenuation • Memory • Learning Matsumoto, M., Kibe, R., Ooga, T., Aiba, Y., Sawaki, E., Koga, Y., & Benno, Y. (2013). Cerebral low-molecular metabolites influenced by intestinal microbiota: A pilot study. Frontiers in Systems Neuroscience, 7(9). Althani et al. (2015)
  107. GUT DYSBIOSIS – General • Microflora imbalanced • Symbiotic relationship lost • Inflammatory Bowel Disease1 • Irritable Bowel Syndrome1 • NAFLD1 • GI Malignancy1 • Autism2 • Crohn’s3 • Asthma3 • Allergies4 • Eczema4 • Diabetes4 • Obesity4 1. Parekh, P. J., Balart, L. A., & Johnson, D. A. (2015). The influence of the gut microbiome on obesity, metabolic syndrome and gastrointestinal disease. Clinical and Translational Gastroenterology, 6(e91). 2. Zhang, Y., Li, S., Gan, R., Zhou, T., Xu, D., & Li, H. (2015). Impacts of gut bacteria on human health and disease. International Journal of Molecular Sciences, 16, 7493-7519. 3. Davenport, E. R., Cusanovich, D. A., Michelini, K., Barreiro, L. B., Ober, C., & Gilad, Y. (2015). Genome-wide association studies of the human gut microbiota. Plos One, 10(11). 4. Villanueva-Millan, M. J., Perez-Matute, P., & Oteo, J. A. (2015). Gut microbiota: A key player in health and disease. A review focused on obesity. Journal of Physiology and Biochemistry. doi:10.1007/s13105-015-0390-3
  108. “LEAKY GUT” • Increased gut permeability • Microbial translocation • Metabolic endotoxemia • Low-grade inflammation • pro-inflammatory cytokines and free radicals • Inflammation in liver, pancreas, brain Konturek, P. C., Haziri, D., Brzozowski, T., Hess, T., Heyman, S., Kwiecien, S., Konturek, S. J., & Koziel, J. (2015). Emerging role of fecal microbial therapy in the treatment of gastrointestinal and extra-gastrointestinal diseases. Journal of Physiology and Pharmacology, 66(4), 483-491. Althani et al. (2015)
  109. MICROBIOME & BRAIN • Bi-directional communication! • Pathways:1 • Autonomic nervous system • Enteric nervous system • Neuroendocrine system • Immune system • Via: • Vagus nerve • Spinal cord • Circulatory system • Inflammatory signaling molecules2 1. Foster, J. A., & Neufeld, K. M. (2013). Gut-brain axis: How the microbiome influences anxiety and depression. Trends in Neurosciences, 36(5), 305-312. 2. Gorky, J., & Schwaber, J. (2016). The role of the gut- brain axis in alcohol use disorders. Progress in Neuro- Psychopharmacology & Biological Psychiatry, 65, 234- 241. Cryan et al. (2012)
  110. BRAIN-GUT PATHWAYS • Autonomic nervous system • Sympathetic • “Fight-or-flight” • Parasympathetic • Organ function, “rest and digest” • Hypothalamic-pituitary adrenal (HPA) axis • Corticotrophin releasing factor (CRF) directly acting on gut Keightley, P. C., Koloski, N. A., & Talley, N. J. (2015). Pathways in gut-brain communication: Evidence for distinct gut-to-brain and brain-to-gut syndromes. Australian & New Zealand Journal of Psychiatry, 49(3), 207-214. Cryan et al. (2012)
  111. BRAIN-GUT AXIS • Anxiety and depression1 • sympathetic parasympathetic • Regulates enteric nervous system • Up-regulate HPA axis • CRF & Cortisol • Stress hormones • Impair digestion • IBD & IBS both associated w/ anxiety and depression2 1. Keightley, P. C., Koloski, N. A., & Talley, N. J. (2015). Pathways in gut-brain communication: Evidence for distinct gut-to-brain and brain-to- gut syndromes. Australian & New Zealand Journal of Psychiatry, 49(3), 207-214. 2. Lyte, M. (2013). Microbial endocrinology in the microbiome-gut-brain axis: How bacterial production and utilization of neurochemicals influence behavior. PLOS Pathogens, 9(11).
  112. GUT-BRAIN AXIS • Functional GI disorders linked to anxiety & depression • Direction of causality? • GI inflammation linked to anxiety in mice1 • Is microbiota the link between poor diet & depression? • Can diet prevent depression? • Does depression promote “leaky gut”?2 vicious cycle 1. Foster, J. A., & Neufeld, K. M. (2013). Gut-brain axis: How the microbiome influences anxiety and depression. Trends in Neurosciences, 36(5), 305-312. 2. Klecolt-Glaser, J. K., Derry, H. M., Fagundes, C. P. (2015). Inflammation: Depression fans the flames and feasts on the heat. American Journal of Psychiatry, 172(11), 1075-1091.
  113. GUT BACTERIA & BEHAVIOR • GABA • Synthesized from MSG by Lactobacillus & Bifidobacterium • Norepinephrine • Produced by Escherichia coli, Bacillus, & Saccharomyces • Serotonin • Produced by Candida, Streptococcus, & Escherichia • Dopamine • Produced by Bacillus & Serratia Evrensel, A., Ceylan, M. E. (2015). The gut-brain axis: the missing link in depression. Clinical Psychopharmacology and Neuroscience, 13(3), 239-244. More than 50% of dopamine & vast majority of serotonin (90%) have an intestinal source
  114. GUT & BEHAVIOR • Other signaling neuro-active molecules synthesized or mimicked by gut microbiota:1 • Acetylcholine • Histamine • Melatonin • All serve as clear implication that gut bacteria influence brain function & behavior 1. Petra, A., I., Panagiotidou, S., Hatziagelaki, E., Stewart, J. M., Conti, P., & Theoharides, T. C. (2015). Gut- microbiota-brain axis and its effect on neuropsychiatric disorders with suspected immune dysregulation. Clinical Therapeutics, 37(5), 984-995.
  115. ARTIFICIAL SWEETENERS (AS) • Interfere with gut microbiota1 • Beneficial bacteria • Pass through SI, but enter LI • Induce glucose intolerance1,2,3 • glycemic response after CHO • Elevated fasting glucose (rats) • “Metabolic derangements”2 • “Metabolic abnormalities”3 “…directly contributed to enhancing the exact epidemic that they themselves were intended to fight.” 1. Pepino, M. Y. (2015). Metabolic effects of non- nutritive sweeteners. Physiology & Behavior. physbeh.2015.06.024 2. Swithers, S. E. (2013). Artificial sweeteners produce counterintuitive effect of inducing metabolic derangements. Trends in Endocrinology Metabolism, 24(9), 431-441. 3. Suez, J., Korem, T., Zeevi, D., Zilberman- Schapira, G., Thaiss, C. A., Maza, O., ...Elinav, E. (2014). Artificial sweeteners induce glucose intolerance by altering the gut microbiome. Nature. doi:10.1038/nature13793
  117. GUT-LIVER AXIS • Liver = largest immune organ • Primary site for EtOH metabolism • Responds to pathogen-derived signals1 • Bile acids as communicators • Modulates microbiome (and vice versa) • Ex: conjugated bile acids secreted into duodenum modified by bacteria & sent back to liver2 • Chronic EtOH bile acid in stool3 • Cirrhotic bile acid in stool3 1. Szabo, G. (2015). Gut-liver axis in alcoholic liver disease. Gastroenterology, 148(1), 30-36. 2. Hartmann, P., Seebauer, C. T., & Schnabl, B. (2015). Alcoholic liver disease: The gut microbiome and liver cross talk. Alcoholism: Clinical and Experimental Research, 39(5), 763-775. 3. Kakiyama, G., Hylemon, P. B., Zhou, H., Pandak, W. M., Heuman, D. M., Kang, D. J., ...Bajaj, J. S. (2014). Colonic inflammation and secondary bile acids in alcohol cirrhosis. American Journal of Physiology - Gastrointestinal and Liver Physiology, 306, G929-G937
  118. GUT-LIVER AXIS • Intestinal oxidation of EtOH • Acetaldehyde • Alters intestinal permeability • EtOH consumption • Intestinal epithelial barrier • Zinc deficiency?1 • Bacterial translocation • Intestinal dysbiosis Progression of alcoholic liver disease (ALD)2 1. Zhong, W., McClain, C. J., Cave, M., Kang, Y. J., & Zhou, Z. (2010). The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. The American Journal of Physiology- Gastrointestinal and Liver Physiology, 298, G625-G633. 2.Szabo, G. (2015). Gut-liver axis in alcoholic liver disease. Gastroenterology, 148(1), 30-36.
  119. Hartmann et al. (2015)
  120. ALCOHOL & GUT MICROBES • Small intestinal bacterial overgrowth (SIBO)1 • Also large intestine • May explain GI symptoms • Diarrhea • Nausea • Abdominal pain • Impact nutrient absorption? • B-vitamin deficiency?2 1. Hartmann, P., Seebauer, C. T., & Schnabl, B. (2015). Alcoholic liver disease: The gut microbiome and liver cross talk. Alcoholism: Clinical and Experimental Research, 39(5), 763-775. 2. Chen, P., & Schnabl, B. (2014). Host-microbiome interactions in alcoholic liver disease. Gut and Liver, 8(3), 237-241. Hartmann et al. (2015)
  121. ALCOHOL & GUT LEAKINESS • Persists into abstinence1 • Alcoholics with gut leakiness2 • At 3 weeks sober, had higher scores of: • Depression • Anxiety • Alcohol craving • Dysbiosis during abstinence can be long-lasting 1. Mutlu, E. A., Gillevet, P. M., Rangwala, H., Sikaroodi, M., Naqvi, A., Engen, P. A., ...Keshavarzian, A. (2012). Colonic microbiome is altered in alcoholism. American Journal of Physiology- Gastrointestinal and Liver Physiology, 302, G966-G978. 2. Leclercq, S., Matamoros, S., Cani, P. D., Neyrinck, A. M., Jamar, F., Starkel, P., ...Delzenne, N. M. (2014). Intestinal permeability, gut-bacterial dysbiosis, and behavioral markers of alcohol-dependence severity. Proceedings of the National Academy of the Sciences. Retrieved from
  122. ALCOHOL WITHDRAWAL • Decrease in protective colonies?1 • Increase in pathogenic colonies?1 • Inflammatory signaling • Cytokine release • Both correlated to depression and alcohol craving2 • Gut dysbiosis • Gut-Brain Axis • Neuroinflammation1 • Amygdala (emotion)1 • Corticotropin releasing factor1 Withdrawal behavior/symptoms 1. Gorky, J., & Schwaber, J. (2016). The role of the gut-brain axis in alcohol use disorders. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 65, 234-241. 2. Leclercq, S., Matamoros, S., Cani, P. D., Neyrinck, A. M., Jamar, F., Starkel, P., ...Delzenne, N. M. (2014). Intestinal permeability, gut- bacterial dysbiosis, and behavioral markers of alcohol-dependence severity. Proceedings of the National Academy of the Sciences. Retrieved from Gorky & Schwaber (2016)
  123. OPIATES & MICROBIOME Animal Data: Morphine Treatment • Gut epithelial barrier dysfunction1 • Disrupted tight junction organization • Inflammation in small intestine • potential pathogenic bacteria2 • Enterococcus faecalis 100x • Decreased microbial diversity • Bile acid metabolism greatly affected2 • Naltrexone (opioid receptor antagonist) reversed effect on bile acid metabolism 1. Meng, J., Yu, H., Ma, J., Wang, J., Banerjee, S., Charboneau, R., ...Roy, S. (2013). Morphine induces bacterial translocation in mice by compromising intestinal barrier function in a TLR-dependent manner. PloS One, 8(1), e54040. 2. Wang, F. (2015). Temporal modulation of gut microbiome and metabolome by morphine. (Doctoral dissertation). Wang (2015)
  124. 8. Nutrition Therapy
  125. NUTRITION INTERVENTIONS – GOALS • Primary goal is to support recovery by any means necessary • Complete abstinence from all illicit mind-altering substances • Nutrition therapy emphasizing correction of nutrient deficiencies • Lab data to warrant aggressive interventions
  126. NUTRITION INTERVENTIONS – GOALS • Immediately bombarding an addict entering treatment with pills and other supplements may fail to support behavioral aspects of recovery • If individuals begin using again, efforts to correct nutritional deficiencies are futile, and are likely to redevelop!
  127. SUPPLEMENTS VS. FOOD • Supplements may give patients the idea that as long as they take pills, they do not need to improve their eating habits • Street drugs exert tremendous strain on liver supraphysiological doses of nutrients may actually conflict with healing process • Eating behavior FIRST, supplements SECOND
  128. IDEAL TIMELINE – NUTRITION THERAPY • 6 hours • Complete diet liberalization • Micronutrient supplementation • 6 days • Targeted nutrition education • Diet liberalization (goal: improvement) • 6 weeks • Reduce intake of sugar and refined CHO • 6 months • Cessation of supplementation
  129. SO WHAT ARE YOU SAYING? • Liberalized diet including abnormal amounts of sugar during first weeks of abstinence can assuage painful symptoms of withdrawal • Consumption behavior should be monitored and eventually sugar use should be reduced • Assessed individually
  130. NUTRITION INTERVENTIONS • “Western Diet” – PROBLEM • Low in fiber • High in sugar and/or AS • High in inflammatory fats • Omega-6 and certain saturated fats • Nutrition in Recovery – SOLUTION • High in fiber • Low in sugar, no AS • High in anti-inflammatory omega-3s • Lower in pro-inflammatory omega-6 Priority #1 Transitions are typically gradual & progressive. Gut will hardly allow for anything else!
  131. THE IMPORTANCE OF FIBER • Gradual/progressive reintroduction • Low fiber tolerance creates significant barriers for nutrition therapy involving fruits, vegetables, whole grains, beans • Increase 2-4 g/week to meet recs: • 38 g/day men, 25 g/day women • Ages 14-50 Focus on improved gut health • Optimal absorption of AAs, vits/mins
  132. INTERVENTIONS – FIBER • Get fiber from food, not from fiber supplements! • Fruits • Vegetables – emphasize raw • Whole grains • Beans • Nuts/seeds – emphasize raw • Eat a wide range of plant foods on a daily basis • F or V with every meal/snack Every time you eat: Fiber Fat Protein
  133. OPERATION: HEAL THE GUT! • Gut-Brain Communication1 • Brain-Gut (Bi-Directional) “Psychological treatments are known to improve functional gastrointestinal disorders, the next wave of research may involve preventative microbiological gut based treatments for primary psychological presentations…” 1. Keightley, P. C., Koloski, N. A., & Talley, N. J. (2015). Pathways in gut- brain communication: Evidence for distinct gut-to-brain and brain-to-gut syndromes. Australian & New Zealand Journal of Psychiatry, 49(3), 207- 214.
  134. INTERVENTIONS – BEVERAGES • Eliminate artificial sweeteners • And artificial colors • Stop consuming sweetened beverages. Yes, all of them! • Beverage list: • Water • Chia water • Tea (unsweetened) • Black coffee? • Milk (organic only) • Alt. milk? (unsweet, carrag. free) Negative impact of (short- term) artificial sweeteners on gut microbiota reversed w/in 2-8 weeks1 1. Suez, J., Zilberman-Schapira, G., Segal, E., & Elinav, E. (2015). Non-caloric artificial sweeteners and the microbiome: Findings and challenges. Gut Microbes. Retrieved from Fresh Juice?
  135. INTERVENTIONS – GRAINS • Reduce/eliminate refined grains • White flour, white rice • Processed cereals, etc. • Only eat 100% whole grains • Quinoa • Brown rice • Oats • Buckwheat • Farro • Barley • Ancient grains…
  136. INTERVENTIONS – FATS • Minimize exposure to omega-6 • Sunflower • Corn • Soybean • Grapeseed • Sesame • Peanut • Use nut oils instead: • Almond, walnut, pistachio Use avocado, coconut, olive oils Most fat in our diets should come from food NOT from refined oils! Eat these: Nuts, seeds Avocado, coconut, olives Animal products Organic dairy
  137. INTERVENTIONS – ANIMAL PROTEIN • Is human gut dysbiosis linked to consistent exposure to low dose antibiotics from animal agriculture? YES • Look for: • No Antibiotics • Raised Without Antibiotics • If we demand change, it can totally happen
  138. INTERVENTIONS – FERMENTED FOODS • Kefir • Unsweetened, organic, full-fat • Other cultured dairy products • Raw sauerkraut, raw kimchi • Sodium can be very high • Lots of commercial fermented beverages, tonics, and foods on the market (buyer beware)
  139. INTERVENTIONS – TIMING • “Never hungry, never full” • Eat every 2.5 - 4.5 hours • Reduce potential for hormonal extremes • Avoid the “crash”
  140. NUTRITION THERAPY – PROTOCOLS Wiss, D. A., & Waterhous, T. S. (2014). Nutrition therapy for eating disorders, substance use disorders, and addictions. In Brewerton, T. D., & Dennis, A. B., Eating disorders, substance use disorders, and addictions (pp. 509-532). Heidelberg, Germany: Springer Publishing.
  141. RECS – POLY-SUBSTANCE ABUSE INVOLVING ALCOHOL • MVI (low metal) • Additional B-vitamins primarily thiamine (for EtOH) • Omega-3 supplement DHA rich • Diet rich in vits A, C, E, Se, Fe • Probiotics if GI distress
  142. RECS – OPIATES • Liquid MVI (low metal) • Additional vit. B6 • Additional calcium and vit. D • Digestive enzymes, probiotics • Fiber if constipated (Chia!) • Higher caloric needs? • Diet rich in vits A, C, E, Se, Fe
  143. RECS – COCAINE • MVI (low metal) • Omega-3 supp DHA rich • Protein-rich diet • Diet rich in vits A, C, E, Se, Fe • Gradual weight gain1 • Not drastic/immediate 1. Ersche, K. D., Stochl, J., Woodward, J. M., & Fletcher, P.C. (2013). The skinny on cocaine. Insights into eating behavior and body weight in cocaine-dependent men. Appetite. Advance online publication. Retrieved from
  144. RECS – METHAMPHETAMINE • MVI (low metal, no Fe) • Omega-3 supp DHA rich • Protein-rich diet • Diet rich in vits A, C, E, Se • Lower refined CHO intake
  145. OTHER RECS – NUTRITION THERAPY • 50% of fruits and vegetables should be raw • Vs. cooked, canned, frozen, dried • Minimal fruit juice • Spotlight on fiber! “Zen Nutrient”1 • Gut bacteria • Beans, nuts, seeds! • Brazil nuts (Se) 1. Hoffinger, R. (2012). The recovery diet. Avon, MA: Adams Media.
  146. OTHER RECS – NUTRITION THERAPY • Oily fish • Plant-based omega-3’s • Flax seeds, walnuts • Chia seeds! • Dairy choices (go organic!) • Milk, yogurt, cottage cheese • Low protein high-fat cheeses and processed cheeses used sparingly • Alternative milks • Calcium, vitamin D
  147. PROBIOTICS • Effects highly strain dependent • Reversal of behavior problems1 • Normalization of:1 • Immune response • Norepinephrine levels in brain • Gut-Brain axis • Lactobacillus casei strain Shirota relieves stress-associated symptoms2 hypersecretion of cortisol 1. Evrensel, A., Ceylan, M. E. (2015). The gut- brain axis: the missing link in depression. Clinical Psychopharmacology and Neuroscience, 13(3), 239-244. 2. Takada, M., Nishida, K., Kataoka-Kato, A., Gondo, Y., Ishikawa, H., Suda, K., …Rokutan, K. (2016). Probiotic Lactobacillus casei strain Shirota relieves stress-associated symptoms by modulating the gut-brain interaction in human and animal models. Neurogastroenterology and Motility, doi:10.1111/nmo.12804 “Live organisms that confer a beneficial health effect on host when administered in proper amounts” – INTL def.
  148. PROBIOTICS & WEIGHT • Lactobacillus species received most attention for obesity and metabolic syndrome1 • Commercial probiotics appear to favor production of butyrate and proprionate2 • Beneficial effect associated w/ restoration of A. municiphila2 • Inversely correlated w/ wt. gain • Reduced levels of cortisol3 1. Lecomte, V., Kaakoush, N. O., Maloney, C. A., Raipuria, M., Huinao, K. D., Mitchell, H. M., & Morris, M. J. (2015). Changes in gut microbiota in rats fed a high fat diet correlate with obesity-associated metabolic parameters. PLoS ONE, 10(5). 2. Alard, J., Lehter, V., Rhimi, M., Mangin, I., Peucelle, V., Abraham, A., ...Grangette, C. (2016). Beneficial metabolic effects of selected probiotics on diet- induced obesity and insulin resistance in mice are associated with dysbiotic gut microbiota. Environmental Microbiology. doi:10.1111/1462- 2920.13181 3. Bull, M. J., & Plummer, N. T. (2015). Part 2: Treatments for chronic gastrointestinal disease and gut dysbiosis. Integrative Medicine, 14(1), 25-33. GUT HEROES? L. plantarum? L. rhamnosis?
  149. PROBIOTICS • May be useful in:1 • Diarrhea • Gastroenteritis • IBS • IBD • Cancer • Infant allergies • Failure-to-thrive • Hyperlipidemia • Hepatic diseases • H. pylori infections (ulcers) • Mental health!!! 1. Scavuzzi, B. M., Miglioranza, L .H., Henrique, F. C., Paroschi, T. P., Lozovoy, M. A. B., Simao, A. N. C., & Dichi, I. (2015). The role of probiotics on each component of the metabolic syndrome and other cardiovascular risks. Expert Opinion on Therapeutic Targets, 19(8). Malaguarna et al. (2015)
  150. PROBIOTICS – MECHANISMS • Displacement of pathogens • Competition with hostile bacteria • Production of bacteriocins • Alteration of microbial enzyme activities • Inhibition of bacterial translocation • Enhancement of mucosal barrier function • Effects on Ca-dependent K channels • In intestinal sensory neurons • Induction of opioid and cannabinoid receptors • In intestinal epithelial cells • Modulation of the immune system • Through signals on epithelial cells • Increasing antibody levels Bravo, J. A., Julio-Pieper, M., Forsythe, P., Kunze, W., Dinan, T. G., Bienenstock, J., & Cryan, J. F. (2012). Communication between gastrointestinal bacteria and the nervous system. Current Opinion in Pharmacology, 12, 667-672.
  151. SUMMARY – NUTRITION THERAPY • Ideal macro breakdown • 45-50% CHO • 25-30% protein • 20-30% fat • Of CHO consumed: • 75% unrefined • Whole grain, fruits, vegetables • Dairy (if tolerant) • Some leeway for sugar and refined grains in early recovery
  152. SUMMARY – NUTRITION THERAPY • Nutritional deficiency lowers antioxidant potential of cells • Increased potential for cell damage • Increased need for antioxidant vitamins A, C, E, selenium • Higher protein needs than the general population • Promote neurotransmitter synthesis
  153. WHAT ABOUT EXERCISE? Lifestyle interventions involving both diet and exercise • Exercise supported in treatment of mental illness1 with profound impacts on cognitive abilities2 • Aerobic activity transforms not only body but mind2 • Exercise can help rebuild brain cells killed by alcohol- ten min. of exercise could blunt an alcoholic’s craving2 • Other benefits: • Increased self-esteem, self-efficacy • Elevated mood • Improved energy and concentration • More relaxing sleep • Relief of tension • NORMALIZE HORMONES Integration of exercise along w/ nutrition critical for full recovery from substance abuse 1. Forsyth, A., Deane, F. P., & Williams, P. (2009). Dietitians and exercise physiologists in primary care: Lifestyle Interventions for patients with depression and/or anxiety. Journal of Allied Health, 38(2), e-63-68 2. Ratey, J. J., & Hagerman, E. (2008). Spark. New York, NY: Little, Brown and Company.
  154. EXERCISE IN RECOVERY • 15 minutes of brisk walking reduces urge for sugary snacks in overweight individuals1 • Benefits of exercise in alcohol recovery2 • Provide pleasurable states • Reduce depressive symptoms • Increase self-efficacy • Provide positive alternatives • Decrease stress reactivity • Decrease urges to drink 1. Ledochowski, L., Ruedl, G., Taylor, A. H., & Kopp, M. (2015). Acute effects of brisk walking on sugary snack cravings in overweight people, affect and responses to a manipulated stress situation and to a sugary snack cue: A crossover study. PLoS ONE, 10(3). 2. Brown, R. A., Abrantes, A. M., Read, J. P., Marcus, B. H., Jakicic, J., Strong, D. R., ...Gordon, A. A. (2009). Aerobic exercise for alcohol recovery: Rationale, program description, and preliminary findings. Behavior Modification, 33(2), 220-249.
  155. EXERCISE PROTOCOLS • Strength training • GI tract is made of muscles • Twice/week • Cardio • Outdoors whenever possible • Twice/week • Yoga • Aids in digestion (parasympathetic nervous system) • Basically helps with EVERYTHING • Twice/week
  156. BIG PICTURE – GOALS • Not necessarily weight loss • Relapse prevention • Disease prevention • Focus on overall health • Body, mind, spirit • Behavior change & self-efficacy • “Sanity restoration” • “Recovery” • Can be difficult to measure Eventually developing a relationship w/ food & exercise that is intuitive/personal • Avoid “quick fix” whenever possible
  157. BIG PICTURE – GOALS • Cooking Classes • Mandatory part of treatment! • Life Skills • Grocery shopping • Food safety • Meal planning • Kitchen cleaning • Challenge the entitlement
  158. FOOD ADDICTION • Recent meta-analysis1 • 20% of all subjects tested for FA met criteria • No well-accepted treatment • Abstinence from addictive food? • Mindfulness? Intuitive Eating? • Health at Every Size? • Psychiatric interventions? • Surgical interventions? 1. Pursey, K. M., Stanwell, P., Gearhardt, A. N., Collins, C. E., Burrows, T. L. (2014). The prevalence of food addiction as assessed by the Yale food addiction scale: A systematic review. Nutrients, 6, 4552-4590.
  159. GOOD VS. BAD FOODS? • As an eating disorder specialist, this simplistic distinction can cause more harm than good • Cognitive distortion • HOWEVER, we can start to discern between: • Real food vs. processed food • Non-addictive vs. addictive food • Gut healing vs. gut harming • If it has the potential to promote dysbiosis, think twice! “Everyone knows how important the brain is. We have all sorts of educational protocols in place for the brain. But what about the second brain? If the gut truly is the second brain, we need educational protocols for the gut.” David Wiss MS RDN Nutrition in Recovery
  160. ABSTINENCE FROM OFFENDING FOODS??? • Some food addicts do benefit from restricting added sugars, refined grains, fried foods… • Beware of rebound bingeing vs. • Disordered thinking patterns • “Orthorexia”
  161. HOW TO END FOOD ADDICTION Take Care of Yourself: • Regular meals/snacks • Plenty of water • Minimal caffeine • Daily exercise • Something you enjoy • Modulates reward pathway • Sufficient quality sleep • Support system • Give up on perfectionism
  162. HOW TO END FOOD ADDICTION • Reconnect with food • Intuitive Eating • Attuned Eating • Mindful Eating • Stop multitasking at meals • Only eat table • Pay attention (non-judgmentally) • Focus on each mouthful • Chew and savor • Put down cutlery between bites • Quality not quantity • Prepare your own food
  163. INTERVENTIONS – “INTUITIVE EATING” • Can we trust our body wisdom? • Near gut homeostasis • Low addictive symptomatology • Hormonal milieu relatively stable • Mindfulness training YES – in sync with intuition • Gut dysbiosis • Addiction/withdrawal/craving • Hormonal extremes • Mindless eating NO – addiction running the show Guarner et al. (2003)
  164. 9. Conclusions
  165. CONCLUSIONS • Restoration of nutritional status in SUD should look beyond vitamin/mineral status and body weight! • Goals should include BEHAVIORS: • Gut (HOT TOPIC!!!) • Brain chemistry • Hormones Minimize spikes/drops in insulin
  166. NUTRITIONAL TREATMENT • Must consider biology: • A calorie is NOT a calorie • It is “about the food” • Food industry continues to deny responsibility, always stressing individual responsibility for eating, and pointing to lack of exercise • Psychological interventions alone are not sufficient • Educational efforts alone are not sufficient (just like drug addiction) Gut, brain, endocrine system
  167. TREATMENT-BASED EVIDENCE • Most people report that eating less “processed foods” & more “whole foods” improves wellness & mood • Impact more pronounced in some • But we never really knew WHY... UNTIL NOW? • Many highly processed foods have ingredients that negatively impact gut microbiota!
  168. THE ROLE OF THE DIETITIAN • Dietary intake • Nutritional needs • Regular feeding patterns • Healthy weight goal • Food fears, restrictions, rules • Feelings/emotions around food • Medical nutrition therapy
  169. WHAT IS YOUR FOOD PHILOSOPHY? “All foods fit. But not all foods fit for all people. And just because the food industry manufactures and sells it, does not mean we have to include it.”
  170. WHAT CAN THE RDN DO AS A MEMBER OF THE TREATMENT TEAM? Every patient who walks into substance abuse treatment should be assessed by a dietitian!!! • Screen for ED and other dysfunctional/disordered food behaviors • Request nutrition-related labs for high-risk patients • Run groups and offer individual counseling (Nutrition Therapy) • Collect data and publish findings (that means YOU!) • Develop educational curriculum, life skills experiential therapies • Plan special events ex: Supermarket Tours • Attend treatment planning and staff meetings • Work w/ doctors/therapists/counselors to help achieve treatment goals • Nutrition/exercise interventions to facilitate behavior change favorable to long-term recovery and improved quality of life • Audit the menu and suggest substitutions within the budget • Food service and food safety improvements • Work with the chef to improve the “food environment”
  171. WHAT’S NEXT? • RDN integrated member of the treatment team! • Individual counseling • Educational groups • Approves all food/beverage • Meal/snack planning • Supermarket tours & meal outings • Treatment planning
  173. “Food for thought is no substitute for the real thing.” ~ Walt Kelly

Editor's Notes

  1. CHO contributes to production of serotonin (drowsy) Protein contributes to production of dopamine, norepinephrine (alert)
  2. A major reason people take drugs is because they like what it does to their brain. In the beginning it is to “feel good” and eventually it is to “feel better”. Dopamine activity increases for drugs, food, sex, and other rewarding events.
  3. Phenylalanine relatively widespread in food
  4. Major brain chemical involved in addiction Highly palatable foods, as well as sex and other rewarding events
  5. Wrong kind of fat in membranes
  6. GI discomfort includes both diarrhea and constipation
  7. NAC reduced cocaine-seeking behavior in animal models NAC appears to restore levels of glutamate in the nucleus accumbens, leading to reductions in drug-seeking behavior Protein: meat, fish, dairy, nuts
  8. Fe supplementation contraindicated
  9. Xerostomia = dry mouth
  10. White flour rapid mouth meltdown, rapidly becomes sugar.
  11. And for some people: refined grains Dynamic Contrast
  12. AN + AUD: Alcohol to impact hunger-fullness cues, adds empty calories AUD + AN: Alcoholic anorexia BN + AUD: use alcohol to induce vomiting AUD + BN: other forms of purging (diuretics, laxatives, diet pills) BN + SUD: stimulants such as meth for purging SUD + BN: meth probably most common BED + SUD: use drugs but real issue is food SUD + BED: binge eat when no drugs around
  13. Common for individuals recovering from SUD to experience additional psychiatric symptoms
  14. More sensing receptors than oral cavity Dieting causes a rise in ghrelin. Protective mechanism against starvation. Brain AND gut have a memory of foods eaten in the past, including taste AND calories.
  15. None of the male participants reported losing weight or appetite suppression as a reason for using cocaine (unlike many females) Higher fat intake, less fat storage Decreased plasma leptin with a high fat diet suggests an impaired energy balance (leptin inhibition). This imbalance is what leads to weight gain. Dysfunctional eating predates beginning of use for many as well
  16. Focusing on single vitamins and amino acids is futile
  17. Not to mention hypervitaminosis Beware of individuals who make outrageous claims related to the efficacy of vitamin and amino acid therapy.
  18. Nutrition education should emphasize what to eat, not what not to eat. 6 months: assuming balanced diet
  19. Nutrition should be introduced as a helpful rather than punitive part of the recovery process
  20. Fiber supplements can be used to maintain gradual and progressive weekly increases if oral intake is poor As always, increased water intake should accompany increased fiber with a goal of 2-3 L/day
  21. Higher caloric needs for leptin restoration
  22. Weight gain should be gradual as opposed to immediate.
  23. Again, gradual weight gain compared to drastic.
  24. Many patients with SUD have an aversion to processed foods because it acts on their brain similarly to drugs, leading to overconsumption Ginger bread house “exposure therapy” not necessary
  25. Corporate wellness for treatment staff