Pillars of Change. Obesity & Addiction – Does Substance, Behavior, or Both Determine Diagnosis & Treatment?

Food Addiction

By Heather Hamilton, PhD.| ©2024BreakThrough!

Behavioral Change – Obesity & Addiction

According to the World Obesity Federation (WOF), every country is failing to meet 2025 WHO targets for addressing obesity.  Deficits include a lack of comprehensive solutions, treatment programs, and shared accountability.  Citing the CEO of WOF, “The absence of a comprehensive view of obesity has translated into fragmented health systems, weak policies and poor translation of medical knowledge into widely available resources for care and prevention.”

In the U.S. alone, annual estimates of healthcare costs associated with obesity hover around 190 Billion (anticipated to exceed 800 billion by 2030) with an additional 327 billion associated with diabetes disorders (CDC, 2014; ADA, 2020).

Addiction & Food

To address comprehensive solutions we don’t need to reinvent the process of care. As a community, we simply need to talk openly about addiction to food and use the same definitions, criteria, and evidence-based behavioral modifications from successful substance abuse recovery resources.

Addiction is typically defined as a brain disorder caused by the repetitive use of various chemicals, which alter the normal functioning of the central nervous system with consequent behavioral abnormalities [51]. There’s no question that  use of the term “addiction” in the context of food and eating behavior has been controversial and often miss-associated with binge eating disorder. However, if we compare the criteria for substance dependence with over-consumption of food there are striking similarities in behaviors and consequences.

  • There’s repeated consumption of unhealthy substances despite negative consequences to one’s health
  • Increased expenses and consequences: long-term medical expenses and hospitalization associated with Metabolic Disorder
  • Shame, remorse, and feelings of hopelessness
  • Stigma related to body image being overweight; social isolation
  • Increase likelihood of developing anxiety and depression disorders
  • Recurring desires to consume (excess carbs & fats) even after a lengthy period of abstinence [52]

What’s shocking, is that if a diagnosis for obesity (BMI > 30) was treated in accordance with existing ASAM guidelines for substance addiction treatment, nearly 50% of the US population would qualify for structured and intensive intervention.

Addiction Education in Practice

For nearly eight years, session four (90 min) of the BreakThrough! program has been devoted to teaching our clients about the disease model of addiction as it pertains to food. Benefits to this approach include:

  • Honesty in discussions regarding dysfunctional relationships with food
  • The use of standard terminology and diagnostic criteria from decades of addiction research
  • Discussions of brain functioning, cravings, tolerance, mood disturbance, & relapse
  • Building on existing evidence-based practices that facilitate recovery from other addiction disorders
  • A foundation for integrated treatment discussions across behavioral and primary health care environments.

To meet the global goal of comprehensive integrated treatment, we can start by sharing a common language that supports the implementation of evidence-based treatments for individuals and communities alike recovering from addiction to food.

For examples of what Team BreakThrough! teaches our clients, please continue reading.

What We Teach Clients – Select Topics from the BreakThrough! Course Text & Workbook

 When Food is the Drug of Choice

The development of addiction includes several changes within the structure of the brain that (depending on the substance or event) can occur over a period of days or years. There’s no single area of the brain that’s responsible for addiction. Rather, it’s thought that the brain is affected progressively top-down from outer cerebral areas inwards to the denser subcortical limbic structure [54, 55]. Three circuits in the brain are key to understanding the cycle of addiction: [58]

  • A drug-seeking circuit (compulsive) circuit
  • A drug reinforcement circuit (reward and stress)
  • A drug and cue-induced reinstatement (craving) neurocircuit [91]

The neurotransmitter dopamine is involved in all facets of substance dependence including motivation, reward circuitry, craving, seeking behaviors, and actual use. The release of dopamine in response to an event creates a learned response to the event and at the same time, encodes a positive or negative motivational significance to the event. The first time we eat chocolate we have a dopamine response. It’s through experience or events that we develop our fear or pleasure-based responses. These responses can be strengthened any time we re-experience the stimulus. After a while, if we learn we really like chocolate, we experience (motivating) dopamine responses in anticipation of driving to the store and buying it.

If we enjoy a dessert once we encode a pleasurable response. If the dessert is the same or even better the next time, this response is strengthened. We may start going to a certain restaurant more frequently just to eat that particular dessert. When we’re stressed thoughts of the dessert may soothe us. Eventually, we may get to the point where we call ahead to make sure they have or hold our favorite dessert. We may even stop going to restaurants or engaging in activities where dessert (or other foods) aren’t served. Without getting too complicated, by this stage, we think we need the dessert to relieve distress. However, once adaptation takes place, the intensity of our response to this dessert may diminish significantly. We drive to the restaurant out of habit, but now we only experience fleeting, momentary pleasure and consider ordering a second dessert to try and recapture the initial “high.”

The positive rewarding effects of nearly all substances are associated with activation and higher concentrations of dopamine in our limbic brain [92]. This effect is extremely relevant in that what we’re most likely to reach for depends on how fast we feel its effects. Pleasurable effects occurring soon after consumption (caffeine, sugar, nicotine etc.) are more likely to trigger the chain of events that lead us to compulsive consumption [81]. People with fewer dopamine receptors in the brain or reduced activity (depression) are less sensitive to the reward value of a substance. For them to achieve ‘pleasure” they’ll likely have to consume more. [59]

With repeated consumption, cellular adaptions occur in the brain which make it more difficult to manage cravings [82]. We can actively challenge our responses and cravings. If our cravings are a stress response, then practicing stress reduction techniques will help us down-regulate cortisol levels and override impulsive responses. Taking command of our thought processes (US) is key to extinguishing or moderating our fear or pleasure seeking responses.

Wanting & Liking

There’s a significant difference between “wanting” and “liking” something but often we use these terms interchangeably. It’s important to identify the difference because there are separate “wanting” and “liking” neural pathways in the brain [60]. For this chapter “wanting” is defined as desire (mesolimbic incentive salience). The “wanting” pathways in our brain are driven by the powerful dopamine system that motivates us to obtain and consume what we “want” (even when we know it may be an unhealthy choice) [94]. Essentially this system integrates aspects of motivational, cognitive and sensorimotor functions involved in goal-directed action. Cues and situations trigger urges that motivate us to obtain and consume our “wants”. The intensity of our urge or desire depends on two things; the state of dopamine activity in our brain and our perception of how the “reward” will make us feel. [94].

When we see (or smell) fries most of us experience a sudden urge to eat them – especially when they’re on someone else’s plate. Why? Because if you’re anything like me…they’re experiencing pleasure that’s right fully mine! We reach across the table because we feel like we’re missing out. Or are we? Let’s separate “want/desire” from like. To retrain our brain to pay attention to “like” we have to explore our “wants” with conscientious effort. In short, “likes” have to become more important to us than “wants”. Most of us “like” fitting into our clothes. We’ll cringe however at the thought of drinking vegetable oil. If we think about what fries are, our “want” diminishes rapidly. When we take the time to separate unconscious “want” from what we “like”…we’ll leave the fries alone.

The same distinction holds true for substances like cocaine and alcohol. Most of us are repelled by the odor of high powered solvents. However the sharp acrid smell (a motivational cue) triggers desire for someone who has previously enjoyed the stimulant effects of meth or cocaine. Similarly, we learn to “want” alcohol based on the effect it has in our brain. We train ourselves to tolerate the taste of poison until we enjoy it. For anyone suffering with an addiction, no matter the substance of choice; state-dependent changes in dopamine amplify the desire to consume. For us, that means that stress, depression, and other changes in brain activity will push us toward relapse. When we’re feeling down and the donut stand’s ahead; it’s less likely we’ll walk past. For some people, places or situations may be even more triggering than the consumption of actual substances. Places (like sports bars) become associated with the satisfaction of “wants”. While we’re developing Resistance, we may need to consider finding new activities, places or situations to reduce temptation.

The “liking: system is anatomically a much smaller system of interactive hedonic hotspots. These hot spots (less than a cubic centimeter) are nested within structures in the brain. They exist in the prefrontal cortex, and other parts of the brain that code sensory pleasures. Because the system is smaller, it stands to reason that our feelings of intense pleasure may be less frequent and shorter in duration. Advertising and social media influences aside, it’s not realistic to think that we can sustain intense feelings of pleasure.

The reinstatement of “seeking” behavior, which precedes relapse requires reactivation of the prefrontal cortex and amygdala through dopamine release [52]. When we’ve crossed the threshold of addiction to a substance or activity (gaming/electronic devices), we’re hyper-responsive (highly reactionary) to low hypodopaminergic (mood) states. If we extinguish or reduce dopamine driven responses through re-conditioning, we lessen our chances of following through to relapse.

At this point, we recognize that stimulus or cue driven responses are simply the re-activation of old associations driven by learned responses that can be challenged. After several years, people who initially struggled (and bitched) through quitting smoking, may recoil from the smell or taste of a cigarette. They’ve successfully overridden (or extinguished) the original addiction response mechanism and developed Resilience. Their PFC recognizes the cigarette and smoke as harmful rather than pleasurable. Unfortunately, sometimes withdrawal and abstinence from one substance results in an increased use of another as a compensatory mechanism. Many people turn to sweets (oral reward) which likely explains the initial weight gain (or fears) for people who choose to stop smoking or drinking [61].

Binge Eating

Binge eating is described as episodes of compulsive and excessive food consumption that is associated with cravings, persistence, and loss of control despite negative consequences [52]. While these are features of addiction, there’s an important distinction we need to keep in mind. From the perspective of evolution, binge eating was a positive adaptive survival behavior that allowed humans to gorge on food in order to survive times of scarcity [62]. In our modern context, binge eating typically results from physiological deprivation (extreme starving) or the frequent exposure to and consumption of food in the absence of hunger or deficit in energy [1].

Binge eating has its roots in the dysregulation of neurotransmitters. The flood of endorphins from eating large amounts of food temporarily alters the neurochemistry of the brain, providing brief periods of relief from emotional distress [96]. Over time, the amount of food required to achieve this effect increases. Cycles of binge eating result in imbalances in dopamine, serotonin, and norepinephrine. This has a cascade effect on other systems and organs. When we do indulge we experience satisfaction, but it’s temporary. Soon, we start wishing we had more to satisfy our cravings. These hedonic cravings, despite just eating, suggest that when the feeling of fullness begins to diminish we’re already in withdrawal.

In withdrawal, we enter a hypodopaminergic (low) state that decreases the activity, levels, and size of dopamine neurons. This state has a duration that outlasts the physical symptoms of withdrawal and may be reversed with use of the substance [81]. Avoidance of withdrawal can become a maladaptive, motivational state. Without overriding cognitive intervention, withdrawal easily transitions to goal-oriented consumption.


Tolerance is a feature of addiction whereby it’s necessary to consume greater amounts of a substance to achieve satisfaction. For the alcoholic one drink isn’t enough; they finish the bottle and look for another. With food, two cookies aren’t enough; we may eat twenty-two and then move on to ice cream. Tolerance has been observed for almost all substances in both rodent and human studies. With tolerance higher quantities are required to try to (re)capture the initial high until the “breaking point” is achieved. For some substances, the breaking point will result in severe incapacitation, lasting impairment, hospitalization, or premature death.

The Stigma of Addiction

The medical and mental health communities define addiction as a chemical imbalance in the brain. Despite overwhelming evidence, the medical community hasn’t been able to overcome moral or social condemnation of people who suffer from compulsive substance use or addiction. Remarks and judgments like these perpetuate bias and stigma: “They’re just weak” or “They could cut-down if they wanted” or “Why can’t they just ____ normally?” Even when participants in a study of Binge-Eating Disorder clearly endorsed diagnostic criteria for addiction, they were reluctant to accept or embrace the concept of being a “food addict [63].”

This reluctance speaks to the social stigma associated with being an “addict” in general. In our society, addiction doesn’t stand on its own as a medical diagnosis like “diabetes” or “hypothyroidism”. If someone says, “I’m a diabetic” we express concern or empathy. We don’t immediately add negative associations such as homelessness, domestic violence, and crime that we do for the “alcoholic” or “addict.” Unfortunately, until we acknowledge the scope and impact of addiction to food, many may refrain from seeking treatment for fear of ridicule, shame, or condemnation.

With the power of education and choice, patients have the opportunity to heal the relationship between their minds and bodies and make goal-oriented choices to achieve wellness. We don’t have to wait for more dire statistics; we can do our part by just talking openly and honestly about addiction to food.

We hope you have enjoyed this article from The BreakThrough! Program.

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References & Related Topics

51. Melis, M., Spiga, S., & Diana, M. (2005). The dopamine hypothesis of drug addiction: hypodopaminergic state. International review of neurobiology, 63, 101-154.

52. Volkow, N., & Li, T.-K. (2005). The neuroscience of addiction. Nature Neuroscience, 8(11), 1429-143

54. Tarter, R.E. and Van Thiel, D. (eds.) Alcohol and the Brain. Plenum Press, New York 139-182.

55. Tomberg, C. (2011). Cognitive Effects of Acute Alcohol Consumption and Addiction. Journal of psychophysiology.

58. Galanter M, & Kleber, H.D. The American Psychiatric Publishing Textbook of Substance Abuse Treatment, eds. (American Psychiatric Publishing, Arlington, VA), 4th Ed.

59. Koob, G. F. (1992). Neural mechanisms of drug reinforcement. In P. W. Kalivas & H. H. Samson (Eds.), Annals of the New York Academy of Sciences: Vol. 654. The neurobiology of drug and alcohol addiction (pp. 171-191). New York, NY, US: New York Academy of Sciences.

60. Berridge K.C., Robinson, T.E. (2016). Liking, wanting, and the incentive-sensitization theory of addiction. Am Psychol. 2016 Nov;71(8):670-679.

63. Curtis, C., & Davis, C. (2014). A Qualitative Study of Binge Eating and Obesity from an Addiction Perspective. Eating Disorders, 22(1), 19-32 14p. doi:10.1080/10640266.2014.857515

81. Mason, T. B., & Lewis, R. J. (2014). Reducing obesity among lesbian women: Recommendations for culturally tailored interventions. Psychology Of Sexual Orientation And Gender Diversity, 1(4), 361-376. doi:10.1037/sgd0000074

82. Prewett D., & Hamilton, H. (2014). A New Path: Personality Styles and Recovery from Addiction. College Park, GA: http://dprewett.com/newpathhandbook/

91. Chrisler, J. (2017). Weapons of mass destruction: Confronting sizeism APA 2017 Symposium, Washington, D.C.

92. Berkeley Media (2011). The new age of food marketing.http://www.bmsg.org/resources/publications/the-new-age-of-food-marketing-how-companies-are-targeting-and-luring-our-kids-and-what-advocates-can-do-about-it/

By Heather Hamilton, PhD., LMHC, NCC, DCC  |  ©2022BreakThrough!
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