The document proposes a new model called the Food and Weight Unit Spectrum Model (FWUSM) to conceptualize and treat eating disorders that incorporates recent data on food addiction. It explores the relationship between eating disorders and addictions, noting similarities between processed foods high in sugar, fat and salt and addictive drugs in their ability to hijack the brain's reward system. Food addiction, as measured by the Yale Food Addiction Scale, has been found in a significant percentage of obese and binge eating disorder patients. The document suggests some eating disorders and obesity may be a form of addiction driven by alterations in dopamine and opioid neurotransmitter systems that regulate reward, motivation and hedonic aspects of eating. The proposed FWUSM aims to map

1. INCORPORATING FOOD ADDICTION
INTO DISORDERED EATING:
The Food and Weight Unit Spectrum
Model (FWUSM)

2. OBJECTIVES
• Explore the relationship between eating
disorders (EDs) and addictions
• Propose a new model of conceptualizing
and treating EDs that incorporates recent
data on food addiction (FA)
• Introduce the Food and Weight Unit
Spectrum Model (FWUSM)

3. SECTIONS
1. Background
2. Food Addiction
3. Systems Influencing Intake
4. Anorexia Nervosa
5. Bulimia Nervosa
6. Binge Eating Disorder
7. Current Controversies
8. FWUSM
9. Conclusions

4. Frank, G. W. F. (2015). Recent advances in neuroimaging to
model eating disorder neurobiology. Eating Disorders, 17(22)
“…moving away from contrasting ill groups with
controls toward a dimensional approach that
identifies neurobiological underpinnings of
psychiatric disease based on specific behavioral
constructs may help eventually develop more
accurate models of EDs and identify empirically
more specific and effective biological treatments.”

5. 1. Background

6. BACKGROUND – ED
• Classic ED model designed for
middle class young female with
anorexia nervosa (AN)
• Recent data1
• Both genders
• All ages
• All income levels
Increased awareness, changing
societal values, targeted research
• Evolving American diet?
1. Mitchison, D., Hay, P., Slewa-Younana, S., &
Mond, J. (2014). The changing demographic profile
of eating disorder behaviors in the community.
BMC Public Health, 14(943).

7. BACKGROUND – SUD
• Substance Use Disorders (SUD)
on the rise
• ED + SUD
• SUD + ED
• Bidirectional associations1,2
• Most of the research conducted
on females with AN and bulimia
nervosa (BN)
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.

8. SUBSTANCE USE DISORDER (SUD)
• Early recovery:
• Bingeing to satisfy cravings1
• Unhealthy/undesirable wt. gain2
• Cocaine dependent men:3
• Altered fat regulation
• Lower circulating leptin
1. Cowan, J., & Devine, C. (2008). Food, eating, and
weight concerns of men in recovery from substance
addiction. Appetite, 50, 33-42.
2. Emerson, M. H., Glovsky, E., Amaro, H., Nieves, R.
(2009). Unhealthy weight gain during treatment for
alcohol and drug use in four residential program for
Latina and African American women. Substance Use
and Misuse, 44, 1553-1565.
3. 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, 71(100), 75-80.

9. 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.

10. 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)

11. BACKGROUND – 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.

12. 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).

13. 2. Food Addiction

14. 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?

15. COCA LEAF VS. CRACK COCAINE
Coca Leaf
• Not highly
addictive
Powder Cocaine
• By-product
• Addictive
Crack Cocaine
• Further processed
• Wreaks havoc on
human brain

16. POPPY PLANT VS. HEROIN
Poppy Plant
• Not highly
addictive
Raw opium
• By-product
• Addictive
Heroin
• Further processed
• Highly Addictive

17. WHEAT PLANT VS. WHITE FLOUR
Wheat Plant
• Not addictive
Whole Wheat
Flour
• By-product
Refined White
Flour
• Further
Processed
• “Offensive”

18. SUGAR CANE VS. REFINED WHITE SUGAR
Sugar Cane
• Not addictive
Raw Sugar
• By-product
Refined Sugar
• Further Processed
• “Offensive”

19. CORN VS. HIGH FRUCTOSE CORN SYRUP (HFCS)
Corn
• Not addictive
Corn Syrup
• By-product
HFCS
• Further Processed
• “Offensive”

20. 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).

21. 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

22. 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.

23. FOOD ADDICTION (FA)
• 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.

24. 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
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.

25. DOPAMINE
• Catecholamine neurotransmitter
• Dopamine is the major brain
chemical involved in addiction
• Important in:
• Movement (muscle control)
• Motivation and attention
• “Reward”
• Well-being

26. 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.

27. 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.

28. 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.

29. 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.

30. OPIOID SYSTEM
• Animal models1
• Naltrexone reduces
food intake
• 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
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.

31. WANTING VS. LIKING
For more info see:
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.
http://ocw.mit.edu/courses/experimental-study-group/es-s10-drugs-and-the-brain-spring-2013/handouts/MITES_S10S13_addictionwk4.pdf

32. 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.

33. 3. Systems Influencing Intake

34. SYSTEMS INFLUENCING FOOD INTAKE
• Homeostatic System
• Post-consummatory
• Post-absorptive
• Hedonic/Pleasure-Reward System
• Consummatory
• Interaction Between Homeostatic
and Hedonic Mechanisms

35. HOMEOSTATIC SYSTEM
• Key Components:
• Hypothalamus
• Adiposity Signals
• Leptin
• Insulin
• Appetite-regulating
gastrointestinal (GI) hormones
• Orexigenic (appetite enhancing)
• Anorexigenic (suppressing)
• Nutrient-related signals
• Vagus nerve

36. 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

37. 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)

38. FOOD ADDICTION – HORMONES
• Leptin-deficient individuals
could be classified as meeting
criteria for FA1
• Hyperinsulinemia may be
contributing to leptin
resistance2
• Ghrelin (gut-derived) may alter
the set point of dopaminergic
neurons in the VTA enhancing
ability of rewarding substances
to activate midbrain dopamine3
1. Albayrak, O., Wolfle, S. M., & Hebebrand, J. (2012).
Does food addiction exist? A phenomological
discussion based on the psychiatric classification of
substance-related disorders and addiction. Obesity
Facts, 5, 165-179.
2. 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.
3. Dickson, S. L., Egecioglu, E., Landgren S., Skibicka,
K. P., Engel, J. A., & Jerlhag (2011). The role of central
ghrelin system in reward from food and chemical
drugs. Molecular and Cellular Endocrinology, 340, 80-
87.

39. 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

40. SHORT CHAIN FATTY ACIDS (SCFA)
• From microbial mediated
degradation of dietary fiber
calories to the host
• Constitute approximately
10% of energy source in
healthy people1
• Microbiota in lean patients
produces larger amounts of
SCFAs1
1. Tilg, H., & Adolph, T. E. (2016). Influence of the human
intestinal microbiome on obesity and metabolic dysfunction.
Current Opinion in Pediatrics, 27(4).
Jesus Raposo et al. (2016)

41. SCFAs
• Fermentation byproducts:
• Butyrate
• 4-carbon; byproduct of Firmicutes
• Propionate
• 3-carbon, byproduct of Bacteroidetes
• Acetate
• 2-carbon, byproduct of Bacteroidetes
• All have protective effects
• Promote healthy body weight1
• Synergistic effects
1. 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

42. SCFAs & METABOLISM
• Promotion of increased
uptake of monosaccharides
• Storage of triglyceride
• Digestion of dietary fiber
• Synthesis of
hormonal precursors Jayasinghe, T. N., Chiavaroli, V., Holland, D. J., Cutfield, W. S., &
O'Sullivan, J. M. (2016). The new era of treatment for obesity
and metabolic disorders: Evidence and expectations for gut
micbrobiome transplantation. Frontiers in Cellular and
Infection Microbiology, 6(15).

43. SCFAs & HORMONES
• SCFAs as modulators of the
enteric neuroendocrine system
• Stimulate anorexigenic hormones1
• Glucagon-like peptide (GLP-1)2
• Secretion of peptide YY (PYY)2
• Increase synthesis of leptin1
1. Chakraborti, C. K. (2015). New-found link
between microbiota and obesity. World Journal
of Gastrointestinal Pathopsysiology, 6(4), 110-
119.
2. Belizario, J. E., & Napolitano, M. (2015).
Human microbiomes and their roles in dysbiosis,
common diseases, and novel therapeutic
approaches. Frontiers in Microbiology, 6(1050).

44. HORMONES – FIBER
• Fiber-rich diet improve
insulin sensitivy1
• SCFAs may activate
adipose tissue to reduce
uptake of fatty acids &
glucose2
utilization by other tissues
ENERGY BALANCE
1. Ling, Q. L., Ting, L. H., Lei, Z., Chen, F. Q., & Ping, J. W. (2015).
Effect of the gut microbiota on obesity and its underlying
mechanisms: an update. Biomedical and Environmental Science,
28(11), 839-847.
2. Janssen, A. W. F., & Kersten, S. (2015). The role of the gut
microbiota in metabolic health. The FASEB Journal, 29.

45. 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

46. 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…

47. 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

48. 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

49. 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)

50. IN THE LAY PRESS…
http://www.theatlantic.com/health/archive/2014/08/your-gut-bacteria-want-you-to-eat-a-cupcake/378702/

51. 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

52. • Generating cravings:
“Chocolate desiring” vs.
“chocolate indifferent”1
• Different microbial
metabolites in urine
• Despite identical diets
• “Microscopic
puppetmasters”
1. Rezzi, S., Ramadan, Z., Martin, F. P., Fay, L. B., van Bladeren, P., Lindon J. C.,
…Kochar, S. (2007). Human metabolic phenotypes link directly to specific
dietary preferences in healthy individuals. Journal of Proteome Research, 6(11),
4469-4477.

53. • Possible mechanisms:
• Microbes modulate host
receptor expression
• Influence on food preference
• Changes in taste receptor expression
and activity reported after gastric
bypass surgery
• Influence via neural mechanisms
• Hijacking nervous system
• Via vagus nerve
• Via adrenergic neurochemicals
• Catecholamines (dop/epi/norepi)

54. CONCLUSIONS
• Microorganisms are competing for nutritional resources
• Evolutionary conflict between host & microbiota may lead
to cravings and cognitive conflict regarding food choice
• Exercising self-control over eating may be partly a matter of
suppressing microbial signals that originate in the gut
• Acquired taste may be due to acquisitions of microbes
that benefit from that food
• One way to change eating behavior is by intervening on the
microbiota FOCUS ON INCREASING DIVERSITY

55. 4. Anorexia Nervosa

56. ANOREXIA NERVOSA (AN)
• DSM-5
• Restriction of intake
• Intense fear of gaining weight
• Persistent behaviors preventing
weight gain (even at low weight)
• Body image disturbance
• Non-weight related
appearance concerns
• Skin, nose, body hair, teeth…

57. AN + SUD/AUD
• AN-Restricting Type
• Less likely to have SUD than binge-
eating/purging type1
• May be due to higher rates of
impulsivity associated with bulimia2
• Women with AN may use
substances to control weight3
• Women with BN may turn to
drugs/alcohol to subdue bulimic
urges3
1. Root, T. L., Pinheiro, A. P., Thornton, L.,
Strober, M., Fernandez-Aranda, F., Brandt, H.,
...Bulik, C. M. (2010). Substance use disorders
in women with anorexia nervosa. International
Journal of Eating Disorders, 43, 14-21.
2. Bulik, C. M., Klump, K. L., Thornton, L.,
Kaplan, A. S., Devlin, B., Fichter, M. M., ... &
Kaye, W. H. (2004). Alcohol use disorder
comorbidity in eating disorders: a multicenter
study. Journal of Clinical Psychology, 65(7),
1000-1006.
3. 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.

58. AN + ADDICTION
• Of all EDs, AN-R is the least
compatible with SUDs1,2
• Restricting AN:1
• Ability to consistently abstain
• Less likely to exhibit cravings
• May not experience impaired
behavioral control
• AN it is less so “about the
food” and more so related to
underlying psychological factors
(unrelated to addiction)
1. Brewerton, T. D. (2014). Are eating disorders
addictions? In Brewerton, T. D., Dennis, A. B..
Eating disorders, addictions, and substance use
disorders (pp. 267-299). Heidelberg, Germany:
Springer Publishing.
2. Peterson, C. B., Pisetsky, E. M., Swanson, S. A.,
Crosby, R. D., Mitchell, J. E., Wonderlich, S. A.,
…Crow, S. J. (2016). Examining the utility of
narrowing the anorexia nervosa subtypes for
adults. Comprehensive Psychiatry, 67, 54-58.

59. 5. Bulimia Nervosa

60. BULIMIA NERVOSA (BN)
• Has similarities to AN, but there
are some clear differences:
• Ability to consistently control
food intake
• Compensatory behavior
• Reward circuitry in the
dopaminergic brain system1
• Are bulimics in the normal
weight range food addicts?2
1. 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.
2. Muele, A. (2012). Food addiction and body-
mass-index: A non-linear relationship. Medical
Hypotheses, 79, 508-511.

61. BULIMIA NERVOSA (BN) – DSM-5
A. Recurrent episodes of binge eating, characterized by:
1. Eating amount definitely larger than normal w/in 2-hour period
2. Sense of lack of control over eating during the episode
B. Recurrent inappropriate compensatory behavior in order
to prevent weight gain (vomiting, laxatives, diuretics,
medications, fasting, exercise)
C. Binge eating and compensatory behavior occur (on
average) at least once a week for 3 months
D. Self-evaluation is unduly influenced by body shape and
weight
E. The disturbance does not occur exclusively during
episodes of anorexia nervosa

62. BN + SUD/AUD
• Associations linked to
genetic influences1
• BN + SUDs more so
genetic than
environmental2
• Alcohol reducing food
craving in BN:3
• Increased satiety
• Reduced attention to
eating-related urges
• Improving mood
1. Slane, J. D., Burt, S. A., & Klump, K. L. (2012). Bulimic behaviors and
alcohol use: Shared genetic influences. Behavior Genetics, 42, 603-613.
2. 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.
3. Bruce, K. R., Steiger, H., Israel, M., Ng Ying Kin, N. M. K., Hakim, J.,
Schwartz, D., Richardson, J., & Mansour, S. A., (2011). Effect of acute
alcohol intoxication on eating-related urges among women with bulimia
nervosa. International Journal of Eating Disorders, 44, 333-339.

63. 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.

64. 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.

65. 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

66. 6. Binge Eating Disorder

67. BINGE EATING DISORDER (BED) – DSM-5
A. Recurrent episodes of binge eating, characterized by:
1. Eating amount definitely larger than normal w/in 2-hour period
2. Sense of lack of control over eating during the episode
B. Episode has 3 or more:
1. Eating much more rapidly than normal
2. Eating until feeling uncomfortably full
3. Eating large amounts when not physically hungry
4. Eating alone because of embarrassment
5. Feeling disgusted/depressed/guilty
C. Marked distress
D. Occurrence of once per week for at least 3 months
E. No compensatory behavior (i.e. “purge”)

68. BED OVERLAP WITH SUD
• Using larger than
intended amounts
• Continuing to use despite
negative consequences
• Reducing other
pleasurable activities

69. 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
http://dx.doi.org/10.1016/j.psychores.2015.01.016
2. Marcus, M. D., & Wildes, J. E. (2014). Disordered eating in
obese individuals. Current opinion in psychiatry, 27(6), 443-
447.

70. BED SIMILAR TO AN & BN
• Body dissatisfaction1
• Shame1
• Severe self criticism1
• Social comparison2
• Maladaptive
emotional regulation
• Food fears
• Restrictive eating
1. Duarte, C., Pinto-Gouveia, J., Ferreira, C. (2014). Escaping from body
image shame and harsh self-criticism: Exploration of underlying
mechanisms of binge eating. Eating Behaviors, 15, 638-643.
2. Duarte, C., Ferreira, C., & Pinto-Gouveia, J. (2016). At the core of eating
disorders: Overvaluation, social rank, self-criticism and shame in anorexia,
bulimia and binge eating disorder. Comprehensive Psychiatry, 66, 123-131.

71. Aloi, M., Rania, M., Caroleo, M., Bruni, A., Palmieri, A., Cauteruccio, M. A., De Fazio,
P., & Segura-Garcia, C. (2015). Decision making, central coherence and set-shifting: A
comparison between binge eating disorder, anorexia nervosa and healthy controls.
BMC Psychiatry, 15(6).
• BED + AN
• Neurocognitive differences
• AN
• Rigidity
• Attention to detail
• BED
• Lack of attention
• Difficulty adapting to changes
We need different interventions!

72. BED vs. FOOD ADDICTION
Binge Eating Disorder
• Ate the whole box of
chocolates in one sitting
• Emotional disturbance
• DSM-5 clinical diagnosis,
insurance reimbursement
Food Addiction
• Ate the whole box over
several sittings
• Physiological response
• Not recognized or
reimbursable
There are more similarities than there are differences…
Obesity can exist without either one!

73. BED + FA
• Consumption of highly
processed palatable foods1
• To forget worries
• Alleviate negative feelings
• When there is both, obesity
is likely the result2
• Obesity + BED leads to a
lower quality of life than if
either of those conditions
exist alone3
1. Boggiano, M. M., Burgess, E. E., Turan, B., Soleymani, T.,
Daniel, S., Vinson, L. D., Lokken, K. L., Wingo, B. C., & Morse, T.
(2014). Motives for eating tasty foods associated with binge-
eating. Results from a student and a weight-loss seeking
population. doi:10.1016/j.appet.2014.08.026
2. 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.
3. Perez, M., & Warren, C. S. (2012). The relationship between
quality of life, binge-eating disorder, and obesity status in an
ethnically diverse sample. Obesity, 20, 879-885.

74. AN EATING CONTINUUM
• Homeostatic eating
• Passive overeating
• No psychopathology
• Mild and intermittent “loss-of-
control” eating
• Compulsive, episodic binges
• Binge Eating Disorder (BED)
• Severe BED with addictive
disorder
• Compulsive psychopathology

75. CURRENT CLIMATE – BED TREATMENT
• The debate of weight
• Treatment with AN-Rs???
• Liberalize the diet?
• Moderation?
• Effective when there is not
addictive symptomatology
• Eating pathology stems from
psychological (e.g. trauma) rather
than biological issues
• Obesity similar to opioid
addiction (vs. other addictions)1
• BED + FA needs different food
plans than AN-R!!!
1. Karlsson, H. K., Tuominen, L., Tuulari, J. J., Hirvonene, J.,
Parkkola, R., Helin, S., …Nummenmaa, L. (2015). Obesity is
associated with decreased μ-opioid but unaltered dopamine
D2 receptor availability in the brain. The Journal of
Neuroscience, 35(9), 3959-3965.

76. CURRENT CLIMATE – BED TREATMENT
• Hallmarks of BED:
• Low self-esteem experiences
• Weak therapeutic alliance
• Low mastery and clarification
experiences
• Predicting:
• Treatment dissatisfaction
• Early discontinuation of care
Amianto, F., Ottone, L., Daga, G. A., & Fassino, S. (2015).
Binge-eating disorder diagnosis and treatment: A recap in
front of DSM-5. BMC Psychiatry, 15(70).

77. 7. Current Controversies

78. 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

79. 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”

80. CURRENT CLIMATE
• ED professionals 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.

81. 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
vanDellen, M. R., Isherwood, J. C., & Delose, J. E. (2016). How
do people define moderation? Appetite, 101, 156-162.

82. FA 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

83. 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!

84. 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

85. 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)

86. 8. Food and Weight Unit
Spectrum Model (FWUSM)

88. FOOD & WEIGHT UNIT SPECTRUM MODEL
• Bottom half of FWUSM
• Classic ED treatment
• “Not about the food”
• Big picture treatment goals:
• Make peace with food
• Liberalize the diet
• Make peace with body
• Therapy and/or medications
(big picture foundation)
• Nutrition as medicine/fuel
• Movement?

89. FOOD & WEIGHT UNIT SPECTRUM MODEL
• Upper half of FWUSM:
• Clear signs of addiction
• Tolerance, withdrawal…
• Biological underpinnings
• “About the food”
• Big picture treatment goals:
• Stabilize the body (gut, hormones)
• Heal dysfunctional brain circuitry
• Reduced exposure to highly palatable
foods; caloric upper limits
• Restricting the excess/undesirable
• Nutrition/exercise (foundation)
• Therapy/medication

90. FWUSM
• Weight status reflected by
movement towards corners:
• Upper left = obesity
• Bottom right = underweight
• Useful to specify severity:
• Mild
• Moderate
• Severe
• Extreme

91. FWUSM – THE REALITY
• What about the patients near
the mid-section of the diagram?
• Combination of treatment
approaches, determined by
clinical staff
• Example:
• BED patient mid-section but lower
half: dessert four times/week
• BED patient mid-section but
upper half: dessert twice/week
• BED patient at top: no dessert

92. 8. Conclusions

93. CONCLUSION
• Treatment for EDs should vary
based on individual assessment
and diagnosis
• Food Addiction is a valid
construct that should be
incorporated into the spectrum
of disordered eating,
particularly those with BN, BED,
and co-occurring addictive
disorders (FA, SUD/AUD)

94. 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.”

96. QUESTIONS?