David Wiss MS RDN discusses the importance of nutrition in addiction recovery and the rationale for the Registered Dietitian Nutritionist to be a member of the treatment team. Topics include:
Food and Mood
Food Addiction
Disordered Eating
Hormones
Nutrition Therapy
2. OBJECTIVES
1. Discuss the impact of addictive substances on
nutritional status and links to chronic disease
2. Explore disordered and dysfunctional eating
patterns in addicted populations
3. Propose nutrition therapy guidelines for specific
substances and for poly-substance abuse
5. 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
http://www.substanceabusepolicy.com/content/2/1/12
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.
6. 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
7. 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
8. Verzar, F. (1955). Nutrition as a factor against addiction. The
American Journal of Clinical Nutrition, 3(5), 363-374.
“The dangerous effects of starvation in
contributing to personality deterioration,
together with the additional dangers of
addiction, might be abolished, and a
problem that is mainly psychological might
thus be solved by better nutrition”
• Chewing coca leaves (South America),
association between cocaine and
inhibition of hunger
• Improvements in nutrition of coca-
addicted populations may abolish
addictive habit of coca chewing
9. ACADEMY OF NUTRITION AND DIETETICS
• Formerly the American Dietetic Association (ADA)
• Position paper (1990) supporting need for nutrition intervention in
treatment/recovery from addiction
• Registered Dietitians (RDs) essential members of the treatment team
• Nutrition care integrated into the protocol rather than “patched on”
• Nutrition professionals urged to “take aggressive action to ensure
involvement in treatment and recovery programs.”
American Dietetic Association (1990, September). Position of the American Dietetic
Association: Nutrition intervention in treatment and recovery from chemical
dependency. Journal of the American Dietetic Association, 90(9), 1274-1277.
10. SO WHAT HAPPENED???
…Little progress incorporating dietitians
into drug rehabilitation programs despite
continued explosion of drug abuse
• Lack of interest from RDs
• Difficulties conducting research on this
population
• Non-collaboration between public and
private sector
• Limited funding for new initiatives
• Associated stigmas of drug abuse
11. WHAT WE KNOW FOR SURE…
• Individuals in recovery will benefit from
learning new behaviors with respect to
food & nutrition
• Increasing body of evidence that suggests
nutrition interventions in substance abuse
treatment lead to improved outcomes1,2,3
Dysfunctional eating patterns and
nutritional interventions in the SUD
population require further investigation
1. Barbadoro, P., Ponzio, E., Pertosa, M. E.,
Aliotta, F., D’Errico, M. M., Prospero, E., &
Minelli, A. (2011). The effects of educational
intervention on nutritional behaviour in
alcohol-dependent patients. Alcohol and
Alcoholism, 46(1), 77-79.
doi:10.1093/alcalc/agq075
2. Grant, L. P., Haughton, B., & Sachan, D. S.
(2004). Nutrition education is positively
associated with substance abuse treatment
program outcomes. Journal of the American
Dietetic Association, 104(4), 604-610.
3. Cowan, J. A., & Devine, C. M. (2012).
Process evaluation of an environmental and
educational intervention in residential drug-
treatment facilities. Public Health Nutrition,
15, 1159-1167.
doi:10.1017/S1368980012000572
12. TO BE CLEAR…
• The most substantial health burden arising
from drug addiction lies not in the direct
effects of intoxication but in the secondary
effects on physical health
• Given that weight gain following abstinence
from drugs is a source of major personal
suffering, there is a pressing need for a
more detailed understanding of the effects
of drug addiction on dietary intake
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
http://dx.doi.org/10.1016/j.ap
pet.2013.07.011
13. WHY DO RECOVERING ADDICTS GAIN WEIGHT?
• “Drugs exert such a strong
reinforcing influence on the
pathways in the brain that
weaker reinforcing signals,
such as those from food, are
ignored and fail to motivate
behavior”
• Appetite and taste returns
in the post-drug state
Blumenthal, D. M., & Gold, M. S. (2012).
Relationship between drugs of abuse and
eating. In Brownell, K. D., & Gold, M. S., Food
and addiction (pp. 254-265). New York, NY:
Oxford University Press.
17. FOOD & MOOD – Carbohydrates
• Is a low-carb diet the answer? NO
• Need minimum of 100-150 g CHO/day
• Glucose brain, CNS function
• 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 – Carbohydrates
• Serotonin
• Feel calm, centered
• Recognition due to popularity of
SSRI anti-depressants
• Stress
• Depletes serotonin availability
• Carb cravings can be caused by
serotonin deficiency
• Serotonin reduces cravings for CHO
• You don’t have to take an
antidepressant to boost serotonin
Leyse-Wallace, R. (2008). Linking
nutrition to mental health.
Lincoln, NE: iUniverse.
19. 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.
20. DOPAMINE
• Catecholamine neurotransmitter
• Dopamine is the major brain
chemical involved in addiction
• Important in:
• Movement (muscle control)
• Motivation and attention
• Reward
• Well-being
22. 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?
23. FOOD & MOOD – Fat
• Essential fatty acids (EFAs):
• Linoleic (omega-6)
• Linolenic (omega-3) EPA, DHA
• Eicosanoid production
• Inflammatory processes
• Cell membrane integrity
• 55%-60% dry wt of brain is lipid
• 35% composed of PUFA Fortuna, J. L. (2009). Nutrition for the focused
brain. Mason, Ohio: Cengage Learning.
24. 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 now 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
25. ADDICTION & MENTAL HEALTH
• Addictive substances strip brain of essential fats, and
impair absorption/utilization of AA’s necessary for
neurotransmitter synthesis1
• Controlled studies have linked essential fatty acid
deficiency to anxiety as well as relapse2,3
• ***Nutrient deficiencies/imbalances may cause behavior
resembling dual diagnosis clinical diagnoses should be
postponed until nutritional issues have been addressed***
• “Better collaboration among treatment professionals is
needed in order to serve the multifaceted needs of
chemical dependent patients, and reduce prescriptive care
contraindicated in the condition of substance abuse.”4
1. Grotzkyj-Giorgi, M. (2009). Nutrition
and addiction – can dietary changes
assist with recovery?. Drugs and
Alcohol Today, 9(2), 24-28.
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:10.1097/01.jcp.0000246214.49271.
fl
3. 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
4. Kaiser, S. K., Prednergast, K., & Ruter,
T. J. (2008). Nutritional links to
substance abuse recovery. Journal of
Addictions Nursing, 19, 125-129.
27. 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.
28. 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
29. POLY-SUBSTANCE ABUSE
• > ½ detox patients deficient in
either iron or vitamins,
particularly A and C1
• Low K associated w/ alcohol-
dependence
• Prevalence of malnutrition
likely underestimated
• Oral MVI & parenteral thiamine
upon admission
1. 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.
doi:10.1016/j.nut.2011.11.003
30. POLY-SUBSTANCE ABUSE
• Significantly low vit. A, C, E levels
compared to non-addict controls1
• Antioxidant vitamins
• Increased copper2,3
• Inflammation?
• Increased zinc2
• Acute fasting?
• Immune regulation?
• Decrease in iron2,4
• Malnutrition?
• Role of other lifestyle factors?
1. 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.
2. 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
http://www.substanceabusepolicy.com/content/2/1/1
2
3. 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
4. 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.
doi:10.1016/j.nut.2011.11.003
31. 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
32. Nakah, A. E., Frank, O., Louria, D. B., Quinones, M. A., Baker, H. (1979). A vitamin
profile of heroin addiction. American Journal of Public Health, 69(10), 1058-1060.
• Classic heroin study
• n = 149
• 45% deficient in vitamin B6
• Replicated in 19811
• 37% deficient in folate
• Replicated in 20042
• 19% deficient in thiamine
• Elevated Mg and Phos in
methadone patients2
1.Heathcote, J., & Taylor, K. B. (1981). Immunity
and nutrition in heroin addicts. Drug and alcohol
dependence, 8, 245-255
2. 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. doi:10.1038/sj.ejcn.1601827
33. 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
34. Varela, P., Marcos, A., Santacruz I., Ripoll, S., & Requejo A. M. (1997). Human
immunodeficiency virus infection and nutritional status in female drug addicts
undergoing detoxification: anthropometric and immunologic assessments.
American Journal of Clinical Nutrition, 66, 504S-508S.
• Malnutrition present in all 36 heroin
addicted females prior to quitting
• After 6 months detoxification: adequate
recovery of nutrition status, including
those with HIV
• Authors recommend nutrition education
as early as possible to help patients get
free of drug habits, and contribute
significantly to an improved quality of life
35. OPIATES – TREATMENT RESEARCH
• Methadone-treated patients1
• Higher consumption of sweets
• Higher eagerness to consume
sweet foods
• Willingness to consume larger
quantities desired by controls
• Qualitative research on heroin
users confirmed2
• Dysfunctional eating patterns
1. Nolan, L. J., & Scagnelli, L. M. (2007).
Preference for sweet foods and higher
body mass index in patients being treated
in long-term methadone maintenance.
Substance Use and Misuse, 42, 1555-1566.
doi:10.1080/10826080701517727
2. 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
36. STIMULANTS
• Many ED patients gravitate towards
their use (appetite suppression)
• Daily users more likely to snack than
eat meals
• Post-using (“come down”) binge-
eating behavior
• Use again as compensatory purge
• ED vs. SUD vs. Dual-Diagnosis
37. 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.
38. COCAINE
• Low levels of omega-3 and omega-6
linked to relapse1
• May stem from increased anxiety
associated w/ low PUFA2
• Omega-3 PUFAs used in treatment for
depression3
• Addiction stripping brain EFAs4
• Impaired utilization of AAs for NT
synthesis (dopamine, serotonin)
• 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:10.1097/01.jcp.0000246214.49271.fl
3. Ross, B. M., Seguin, J., & Sierwerda, L. E. (2007).
Omega-3 fatty acids as treatments for mental
illness: Which disorder and which fatty acid?
Lipids in Health and Disease, 6(21),
doi:101.1186/1476-511X-6-21
4. 1. Grotzkyj-Giorgi, M. (2009). Nutrition and
addiction – can dietary changes assist with
recovery?. Drugs and Alcohol Today, 9(2), 24-28.
39. COCAINE – AMINO ACID THERAPY?
• N-acetylcysteine (NAC)
• Proposed pharmacological treatment for
relapse prevention1
• 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.
40. 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.
41. 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
42. 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
43. METHAMPHETAMINE
• Animal models:
• Antioxidant Se plays
protective role in meth-
induced neurotoxicity1
• Co-Q10 shown to
attenuate meth and
cocaine neurotoxicity2
1. Imam, S. Z., & Ali, S. F. (2000). Selenium, an
antioxidant, attenuates methamphetamine-
induced dopaminergic toxicity and peroxynitrite
generation. Brain Research, 855, 186-191.
2. Klongpanichapak, S., Govitrapong, P., Sharma,
S. K., & Edabi, M. (2006). Attenuation of cocaine
and methamphetamine neurotoxicity by
coenzyme Q10. Neurochemical Research, 31, 303-
311. doi:10.1007/s11064-005-9025-3
45. “ADDICTION”* – DSM-5
• “Substance-Related and
Addictive Disorders”
• Alcohol-Related
• Caffeine-Related
• Cannabis-Related
• Hallucinogen-Related
• Inhalant-Related
• Opioid-Related
• Sedative-, Hypnotic, or Anxiolytic-Related
• Stimulant-Related
• Tobacco-Related
• Non-Substance-Related
Specify current severity:
Mild (2-3 symptoms)
Moderate (4-5 symptoms)
Severe (6 or more symptoms)
Specify descriptive features:
In early remission
In sustained remission
On maintenance therapy
In a controlled environment
*The word “addiction” is omitted from
the official DSM-5 substance use
disorder diagnostic terminology
because of its uncertain definition and
its potentially negative connotation
46. “ADDICTION” – DSM-5
• Non-Substance-Related
• Gambling
• Behavioral Addictions?
• Sex Addiction
• Exercise Addiction
• Shopping Addiction
Currently insufficient
evidence for diagnostic criteria
What about food???
Is it substance-related?
Behavioral?
Both?
49. 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
50. ACADEMY OF NUTRITION AND DIETETICS ON
FOOD ADDICTION
• “Total Diet Approach”1
• Rejects labeling foods as “good”
and “bad” because it is believed to
foster unhealthful eating behaviors
• Unless contraindicated by
extenuating circumstances
• “Sugar addiction present in
humans has not been proven”2
1. Academy of Nutrition and Dietetics
(2013). Position of the American Dietetic
Association: Total diet approach to
communicating food and nutrition
information. Journal of the American
Dietetic Association, 113(2), 307-317.
2. Academy of Nutrition and Dietetics
(2012). Position of the Academy of
Nutrition and Dietetics: Use of nutritive
and nonnutritive sweeteners. Journal of
the Academy of Nutrition and Dietetics,
112(5), 739-758.
51. 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?
52. COCA LEAF VS. CRACK COCAINE
Coca Leaf
• Not highly
addictive
Powder Cocaine
• By-product
• Addictive
Crack Cocaine
• Further processed
• Wreaks havoc on
human brain
53. POPPY PLANT VS. HEROIN
Poppy Plant
• Not highly
addictive
Raw opium
• By-product
• Addictive
Heroin
• Further processed
• Highly Addictive
54. WHEAT PLANT VS. WHITE FLOUR
Wheat Plant
• Not addictive
Whole Wheat
Flour
• By-product
Refined White
Flour
• Further
Processed
• “Offensive”
55. CORN VS. HIGH FRUCTOSE CORN SYRUP (HFCS)
Corn
• Not addictive
Corn Syrup
• By-product
HFCS
• Further Processed
• “Offensive”
56. 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.
57. FOOD ADDICTION
• Endogenous opioid release1
• Dopamine activity in brain2
• Gut-brain dopamine axis3
• Site of convergence
• Metabolic/hormonal
• Regulate eating behavior
1. Yeomans, M. R., & Gray, R. W. (2002). Opioid
peptides and the control of human ingestive
behaviour. Neuroscience and Biobehavioral Reviews,
26, 713-728.
2. Stice, E., Spoor, S., Bohon, C., & Small, D. M.
(2008, October). Relation between obesity and
blunted striatal response to food is moderated by
TaqIA A1 allele. Science, 332, 449-452.
3. De Araujo, I. E., Ferreira, J. G., Tellez, L. A., Ren, X.,
& Yeckel, C. W. (2012). The gut-brain dopamine axis:
A regulatory system for caloric intake. Physiology
and Behavior, 106(3), 394-399.
58. 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.
59. FOOD ADDICTION – CULPRITS
… Sugar, Salt, Fat
• 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
61. FOOD ADDICTION – CULPRITS
What is the
difference between a
baked potato and
French fries with
ketchup?
Fat…Salt…Sugar
62. 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
63. 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”?
64. FOOD ADDICTION
• Stressing “moderation” to addicts is a moot
point because the prefrontal cortex function is
severely impaired1
• The message of “get it together”, “stop eating
so much”, and “just become an intuitive eater”
is not helpful2
• “Food can act on the brain as an addictive
substance. Certain constituents of food, sugar
in particular, may hijack the brain and override
will, judgment, and personal responsibility, and
in so doing create a public health menace.”3
• “Food addiction” versus “food and addiction”3
1.Goldstein, R. Z., & Volkow, N. D.
(2011). Dysfunction of the prefrontal
cortex in addiction: Neuroimaging
findings and clinical implications.
Nature Reviews Neuroscience,
12(11), 652-669.
2. Peeke, P. (2012). The hunger fix.
New York, NY: Rodale.
3. Brownell, K. D., & Gold, M. S.
(2012). Food and addiction. New
York, NY: Oxford University Press.
66. 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.
67. AUD – DISORDERED EATING
• Sobriety time was positively
associated with increased
sugar use1
• Documented preferences for
sweets in abstinent alcoholics2
• “The use of sweets was often
helpful, of course depending
upon a doctor’s advice.” –AA
Big Book, p. 133
1. Levine, A. S., Kotz, C. M., & Gosnell, B. A.
(2003). Sugar and fats: The neurobiology of
preference [Special section]. Journal of Nutrition,
831S-834S.
2. Krahn, D., Grossman, J., Henk, H., Mussey, M.,
Crosby, R., & Gosnell, B. (2006). Sweet intake,
sweet-liking, urges to eat, and weight change:
relationship to alcohol dependence and
abstinence. Addictive Behaviors, 31, 622-631.
doi:10/1016/j.addbeh.2005.05.056
68. 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
69. 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 (psych meds?)
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
70. 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)
71. 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
72. 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”)
73. 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!
75. DISORDERED EATING IN MALES
• More commonly in pursuit of a
lean, muscular physique
• Role of the fitness industry
• Similar to the fashion industry
• Unrealistic body types
• Photoshop
Body dissatisfaction
77. ED & SUD – MALES
• Men w/ BED greater frequency
of SUD1
• Many men uncover symptoms
of EDs during addiction
treatment2 (hiding out?)
• SUD not limited to street drugs
may include3
• Fat burners
• Anabolic androgenic steroids
• Performance-enhancing drugs
1. Barry, D. C., Grilo, C. M., &
Masheb, R. M. (2002). Gender
differences in patients with binge
eating disorder. International
Journal of Eating Disorders, 31,
63-70.
2. Stanford, S. C., & Lemberg, R.
(2012). Measuring eating
disorders in men: Development of
the eating disorder assessment for
men (EDAM). Eating Disorders:
The Journal of Treatment and
Prevention, 20(5), 427-436.
3. Eisenberg, M. E., Wall, M., &
Neumark-Sztainer, D. (2012).
Muscle-enhancing behaviors
among adolescent girls and boys.
Pediatrics, 130(6), 1019-1026.
78. STEROIDS & SUD
• 35% of male steroid abusers
met lifetime criteria for SUD1
• Dependence syndromes
• Progression to other recreational
drugs, including stimulants2
• Significant percentage of male
heroin addicts living in a
treatment facility used opioids
to counteract associated
depression and withdrawal
following steroid abuse3
1.Kanayama, G., Hudson, J. I., &
Pope Jr., H. G. (2008). Long-term
psychiatric and medical
consequences of anabolic-
androgenic steroid abuse. Drug and
Alcohol Dependence, 98(1-2), 1-12.
2. Hildebrandt, T., Langenbucher, J.
W., Lai, J. K., Loeb, K. L., &
Hollander, E. (2011). Development
and validation of the appearance
and performance enhancing drug
schedule. Addictive Behavior,
36(10), 949-958.
3. Arvary, D. & Pope Jr., H. G. (2000).
Anabolic-androgenic steroids as a
gateway to opioid dependence.
New England Journal of Medicine,
342(20), 1532.
79. EXERCISE DEPENDENCE
• Describing the related
phenomenon of compulsive
physical activity1
• Originally did not involve
muscle development, only
aerobic
• Now linked to drive for
muscularity2
• May partially explain the
phenomenon of steroid
addiction
1. Veale, D. (1987). Exercise
dependence. British Journal of Addiction,
82, 735-40.
2. Hale, B. D., Roth, A. D., DeLong, R. E.,
& Briggs, M. S. (2010). Exercise
dependence and the drive for
muscularity in male bodybuilders, power
lifters, and fitness lifters. Body Image, 7,
234-239.
84. WHY PEOPLE LIKE JUNK FOOD
• Stomach as 2nd Taste System
• “Sensing receptors”
• Mechanoreceptors
• Chemoreceptors
• Thermoreceptors
• Osmoreceptors
• 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
85. 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.
86. LEPTIN
• Low levels lead to higher reward
value of food
• Body perceives hungry state,
enhancing motivation for food
• When satiated, dopamine
release/firing inhibited in
nucleus accumbens
• Interestingly…
• High levels have no pronounced
effect on metabolism/feeding1
1. Pandit, R., de Jong, J. W.,
Vanderschuren, L. J. M. J., & Adan, R. A. H
(2011). Neurobiology of overeating and
obesity: The role of melanocortins and
beyond. European Journal of
Pharmacology, 660, 28-42.
87. LEPTIN & VTA
• Leptin regulates homeostatic
center of hypothalamus
• Hedonic system1
• Subjective desires for food
• Food deprivation decreases
circulating leptin
• Contributing to preference for
highly palatable foods
• 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),
88. 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.
89. GHRELIN & VTA
• Obese subjects1
• Ghrelin low
• Post-meal ghrelin remains higher
• Injection of ghrelin into VTA and
nucleus accumbens increases
feeding behavior2
• VTA direct target site for
ghrelin’s action on sweet food
motivation3
• Enhanced intake of saccharin4
1. English, P. J., Ghatei, M. A., Malik, I. A.,
Bloom, S. R., & Wilding, J. P. H. (2002).
Food fails to suppress ghrelin levels in
obese humans. The Journal of Clinical
Endocrinology and Metabolism, 87(6),
2984-2987.
2. Naleid, A. M., Grace, M. K., Cummings,
D. E., & Levine, A. S. (2005). Ghrelin
induces feeding in the mesolimbic reward
pathways between the ventral tegmental
area and the nucleus accumbens.
Peptides, 26, 2274-2279.
3. Skibicka, K. P., Hansson, C., Alvarez-
Crespo, M., Friberg, P. A., & Dickson, S. L.
(2011). Ghrelin directly targets the
ventral tegmental area to increase food
motivation. Neuroscience, 180, 129-137.
4. Disse, E., Bussier, A., Veyray-Durebex,
C., Deblon, N., Pfluger, P. T., Tschop, M. H.,
...Rohner-Jeanrenaud, F. (2010).
Peripheral ghrelin enhances sweet taste
food consumption and preference,
regardless of its caloric content.
Physiology and Behavior, 101, 277-281.
90. GHRELIN & VTA
• Ghrelin alters set point of
dopaminergic neurons1
• Anticipatory physiological
responses to scheduled meals2
• Opioid receptor pathways3
• Regulation of food incentive and
hedonics
• Motivational effects on feeding4
1. 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.
2. Pandit, R., Mercer, J. G., Overduin, J., la
Fleur, S. E., & Adan, R. A. H. (2012). Dietary
factors affect food reward and motivation
to eat. Obesity Facts, 5, 221-242.
3. Kawahara, Y., Kaneko, F., Yamada, M.,
Kishikawa, Y., Kawahara, H., & Nishi, A.
(2013). Food reward-sensitive interaction
of ghrelin and opioid receptor pathways in
mesolimbic dopamine system.
Neuropharmacology, 67, 395-402.
4. Overduin, J., Figlewicz, D. P., Bennet-Jay,
J., Kittleson, S., & Cummings, D. E. (2012).
Ghrelin increases motivation to eat, but
does not alter food palatability. The
American Journal of Physiology -
Regulatory, Integrative and Comparative
Physiology, 303, R259-R269.
91. INSULIN
• Peptide hormone from pancreas
• Similarities to leptin:
• Adiposity signal
• Anorexigenic
• 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.
92. 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.
93. INSULIN & GHRELIN
• Similar to ghrelin, receptors in1
• Hypothalamus
• VTA
• Hippocampus
• Amygdala
• Secretion decreased by ghrelin2
• Vice versa3
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. Broglio, F., Arvat, E., Benso, A., Gottero,
C., Mucciolo, G., Papotti, M., ... Ghigo, E.
(2001). Ghrelin, a natural GH secretatogue
produced by the stomach, induces
hyperglycemia and reduces insulin
secretion in humans. The Journal of Clinical
Endocrinology and Metabolism, 86(10),
5083-5086.
3. Broglio, F., Gottero, C., Prodam, F.,
Destesfanis, S., Gauna, C., Me, E., ... Ghigo,
E. (2004). Ghrelin secretion is inhibited by
glucose load and insulin-induced
hypoglycaemia but unaffected by glucagon
and arginine in humans. Clinical
Endocrinology, 61, 503-509.
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-influenced dopamine transmission can affect the
ability of drugs to exert their neurochemical and behavioral
effects
• Insulin receptors present in brain and midbrain dopamine
neurons
• 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. ALCOHOL & GHRELIN
• Rewarding properties of alcohol
require ghrelin1
• Ghrelin increases during withdrawal2
(changes in hunger?)
• Alcoholic beverage before a meal?
(stimulates appetite)
• Key role in alcohol-seeking behavior3
• Dopamine neurobiology
• Hyperghrelinemia related to
addiction?1 Innovative treatment?3
1. Jerlhag, E., Egecloglu, E.,
Landgren, S., Salome, N., Hellg,
M., Moechars, D., ... Engel, J. A.
(2009). Requirement of central
ghrelin signaling for alcohol
reward. Proceedings of the
National Academy of Sciences,
106(27), 11318-11323.
2. Kraus, T., Reulbach, U.,
Bayerlein, K., Mugele, B.,
Hillemacher, T., Sperling, W., ...
Bleich, S. (2004). Leptin is
associated with craving in
females with alcoholism.
Addiction Biology, 9, 213-219.
3. Leggio, L., Ferrulli, A.,
Cardone, S., Nesci, A., Miceli,
A., Malandrino, N., ...
Addolorato, G. (2011). Ghrelin
system in alcohol-dependent
subjects: Role of plasma ghrelin
levels in alcohol drinking and
craving. Addiction Biology, 17,
452-464.
96. METHAMPHETAMINE
• Linked to eating disorders1
• Food restriction enhances
rewarding effect2
• Ghrelin required for reward3
• Hyperghrelinemia observable in
SUD patients raises important
questions about ghrelin + meth3
1. Neale, A., Abraham, S., & Russell, J.
(2008). "Ice" use and eating disorders: A
report of three cases. International Journal
of Eating Disorders, 42, 188-191.
2. Cabeza de Vaca, S., & Carr, K. D. (1998).
Food restriction enhances the central
rewarding effect of abused drugs. The
Journal of Neuroscience, 18(8), 7502-7510.
3. Jerlhag, E., Egecioglu, E., Dickson, S. L., &
Engel, J. A. (2010). Ghrelin receptor
antagonism attenuates cocaine- and
amphetamine-induced locomotor
stimulation, accumbal dopamine release,
and conditioned place preference.
Psychopharmacology, 211, 415-422.
97. COCAINE
• PET brain imaging: deficits in
dopamine signaling similar for
cocaine-addicted and obese rats1
• Human addicts prefer highest
preference of sucrose offered2
• Reinforces depleted reward
pathways
1. Michaelides, M., Thanos, P. K., Kim, R.,
Cho, J., Ananth, M., Wang, G., & Volkow,
N. D. (2012). PET imaging predicts future
body weight and cocaine preference.
Neuroimage, 59, 1508-1513.
2. Levandowski, M. T., Viola, T. W.,
Tractenberg, S. G., Teixeira, A. L., Brietzke,
E., Bauer, M. E., & Grassi-Oliveira, R.
(2013). Adipokines during early
abstinence of crack cocaine in dependent
women reporting childhood
maltreatment. Psychiatry Research, 210,
536-540.
98. COCAINE
• Ghrelin modulates
reinforcement and reward1
• Female crack users2
• Low leptin in early abstinence
• Increasing during
detoxification
• Improved diet, weight gain
1. Clifford, P. S., Rodriguez, J., Schul, D., Hughes,
S., Kniffin, T., Hart, N., ... Martinez, J. (2012).
Attenuation of cocaine-induced locomotor
sensitization in rats sustaining genetic or
pharmacologic antagonism of ghrelin
receptors. Addiction Biology, 17(6), 956-963.
2. Michaelides, M., Thanos, P. K., Kim, R., Cho,
J., Ananth, M., Wang, G., & Volkow, N. D.
(2012). PET imaging predicts future body
weight and cocaine preference. Neuroimage,
59, 1508-1513.
99. 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
http://dx.doi.org/10.1016/j.appet.2013.07.011
• 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
100. OPIATES
• Ghrelin likely more responsible
than leptin for inducing
increases in drug-taking and
drug-seeking behaviors1
• However, treatment with a
ghrelin receptor agonist had
no effect on reinstatement of
heroin-seeking in rats1
1. Maric, T., Sedki, F., Ronfard, B., Chafetz, D.,
Shalev, U. (2012). A limited role for ghrelin in
heroin self-administration and food
deprivation-induced reinstatement of heroin
seeking in rats. Addiction Biology, 17(3), 613-
622.
101. METHADONE
• Basal leptin and adiponectin
significantly decreased, resistin
increased1
• Independent of BMI, body fat, and insulin
sensitivity
• Lower serum leptin may contribute to
immune dysfunction2
• Proposed trials involving gene therapy
aimed at reinstating leptin circuitry in
drug addicts3
1. Housova, J., Wilczek, H., Haluzik, M.
M., Kremen, J., Krizova, J., & Haluzik, M.
(2005). Adipocyte-derived hormones in
heroin addicts: The influence of
methadone maintenance treatment.
Physiological Research, 54, 73-78.
2. Sanchez-Margalet, V., Martin-Romero,
C., Santos-Alvarez, J., Goberna, R., Najib,
S., & Gonzalez-Yanes, C. (2003). Role of
leptin as an immunomodulator of blood
mononuclear cells: mechanisms of
action. Clinical and Experimental
Immunology, 133(1), 11-19.
3. Kalra, S. P. (2012). Leptin gene
therapy for hyperphagia, obesity,
metabolic diseases, and addiction. In
Brownell, K. D., & Gold, M. S., Food and
addiction (131-137). New York, NY:
Oxford University Press.
102. 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
103. 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
105. “SOCIAL DRUGS”
CAFFEINE AND 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.
106. 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
107. 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 e-cig?
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.
108. “SOCIAL DRUG” USE – CONCLUSIONS
• 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
109. LET’S BE PRACTICAL – BIG PICTURE
• Much like tobacco and caffeine, 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
110. 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
111. ABSTINENCE FROM OFFENDING FOODS???
• Some binge eaters (highly dysregulated) benefit
from restricting added sugars and refined grains
• Beware of rebound bingeing
• Disordered thinking patterns
• “Orthorexia”
However, SUD patients should NOT be
forced to eat highly palatable refined foods under
the guise of protection from potential ED
112. NUTRITION INTERVENTIONS – GOALS
• Primary goal is to support
recovery by any means necessary
• Complete abstinence from all mind-
altering substances
• Nutrition therapy emphasizing
correction of nutrient deficiencies
• Lab data to warrant aggressive
interventions
113. 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!
114. SUPPLEMENTS VS. FOOD
• Supps may give pts 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
115. SUPPLEMENTATION
• Compromised GI function may create
barriers for absorption of vitamins
• Liquid forms useful
• Meal replacement drinks
• MVI w/ low metal content
• Antioxidant supps?
• Co-Q10, alpha lipoic acid, resveratrol,
flavonoid polyphenols
116. 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
117. EATING REGULARLY
• Provides the body with
continuous supply of energy
• Eat every 2-4 hours
• Stabilize energy levels, stable BG
• Avoid the “crash” by limiting sugar,
refined grains, and caffeine
• Prevent cravings for sweets
• Prevent cravings for alcohol/drugs
118. 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
119. 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
120. 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
121. 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
http://dx.doi.org/10.1016/j.appet.2013
.07.011
122. 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
123. 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.
124. 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
125. 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
126. 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
general population
• Promote NT synthesis
129. 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.
130. 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
132. CONCLUSIONS
• Restoration of nutritional status
in SUD should look beyond
vitamin/mineral status and body
weight!
• Goals should include:
• Gut (HOT TOPIC)
• Brain chemistry
• Hormones
Minimize spikes/drops in insulin
Normalize leptin, prevent hyperghrelinemia
133. 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
134. 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 curriculum
• 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”
135. TREATMENT INDUSTRY LEADERS
• Florida Recovery Center (FL)
• Hazelden (MN)
• Betty Ford (CA)
• Treatment models that include measures
to prevent post-detoxification overeating
• Provide patients with access to dietitians
• Emphasize exercise
• Help patients to plan for expected
changes in eating and the reinforcing
effects of food
136. BREATHE LIFE HEALING CENTERS
• RDN integrated member of the
treatment team!
• Individual counseling
• Educational groups
• Approves all food/beverage
• Meal/snack planning
• Supermarket tours
• Meal outings
Eating becomes as elective an activity as socializing or performing community service
Hypothalamus (appetite center in the brain) “wakes up” and appetite can be ravenous
Non-diabetics
Reactive vs. primary hypoglycemia (e.g. anorexia or starvation)
Has anyone attempted a low-carb diet?
SSRI = selective serotonin reuptake inhibitor (ex: Prozac)
Anyone eat in response to stress? What do you eat? (Probably not chicken breast)
“Self-medication with food”
CHO contributes to production of serotonin (drowsy)
Protein contributes to production of dopamine, norepinephrine (alert)
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.
Phenylalanine relatively widespread in food
Phenylalanine in diet soda
Major brain chemical involved in addiction
Highly palatable foods, as well as sex and other rewarding events
GI discomfort includes both diarrhea and constipation
Mg and Phos related to bone health
Easier to collect data from methadone patients
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
Fe supplementation contraindicated
Academy of Nutrition and Dietetics is in the pocket of Big Food
White flour rapid mouth meltdown, rapidly becomes sugar.
And for some people: refined grains
Dynamic Contrast
Prefrontal cortex: executive function
“Addict” associated with social stigma. Food AND addiction has policy implications.
Common for individuals recovering from SUD to experience additional psychiatric symptoms
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
Food industry never uses the term “addiction”. Loyal customers are referred to as “heavy users” at the Coke headquarters in Atlanta.
Big Food uses terms like “crave-able”, “likeable”, and “snackable”
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.
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
Nutrition should be introduced as a helpful rather than punitive part of the recovery process
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
Focusing on single vitamins and amino acids is futile
Not to mention hypervitaminosis
Beware of individuals who make outrageous claims related to the efficacy of vitamin and amino acid therapy.
It is unknown if copper-chelating agents would be a useful intervention
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
Nutrition education should emphasize what to eat, not what not to eat.
6 months: assuming balanced diet
Higher caloric needs for leptin restoration
Weight gain should be gradual as opposed to immediate.
Again, gradual weight gain compared to drastic.
Corporate wellness for treatment staff
Betty Ford recently acquired by Hazelden
So many treatment centers fail to address the biological needs of patients.