The Badly Behaving Brain: How Ultra-Processed Food Addiction Thwarts Sustained Weight Loss

Abstract

Global obesity rates continue to rise, despite billions spent annually on weight loss. Sustained success is rare; recidivism is the most common feature of weight loss attempts. According to the DSM-5 criteria for substance use disorders, the pattern of ultra-processed food (UPF) overconsumption is best characterized as an addiction. There is significant overlap in how UPF and drugs of abuse impact many brain systems. Over time, neurological changes result in overpowering cravings, insatiable hunger, and a willpower gap. The Yale Food Addiction Scale 2.0 is a validated and widely used tool for the diagnosis of UPF addiction. Research on treatment is nascent, but two weight loss approaches that directly target addiction, GLP-1 agonists and Bright Line Eating, both decrease hunger and cravings and result in significantly greater sustained weight loss than other methods. Addressing addiction is an avenue to weight loss that warrants further study.

1. Introduction

The World Health Organization declared obesity to be a global epidemic in 1997 [1]. In 2013, the Member States of the World Health Assembly unanimously agreed to adopt the target that rises in childhood, adolescent, and adult obesity should be halted at 2010 levels by 2025 [2]. But the rise has not abated; instead, we are on pace to see a doubling of obesity by 2025 [3]. It is now projected that by 2035, one half of all people worldwide will be living with overweight or obesity [4]. Co-occurring with this rise in obesity has been a steady increase in UPF consumption [5]. Mounting evidence indicates that these trends are related [6, 7, 8].

Meanwhile, sustained weight loss is rare [9]. Dieters repeatedly “fall off” and “get back on” the wagon just like smokers and others with a substance use disorder who are trying to quit [10]. The extremely poor results of nearly every type of weight loss approach do not make sense, given how motivated people are to not be overweight [11] and how much time and money they spend to lose weight [12]. Even people attempting to lose weight for a needed surgery or to avoid a second limb amputation due to type 2 diabetes are not likely to be successful [13, 14]. Many researchers are concluding that addiction is the framework that best explains this pattern of behavior [15].

Since there is little consensus, currently, regarding whether the proper term should be “food addiction,” “processed food addiction,” “ultra-processed food addiction,” or something else (like “eating addiction”), in this article we will use these terms interchangeably, while defaulting to “ultra-processed food addiction” or UPFA. Irrespective of the term used, the reality is, as one group of researchers put it, that “the neurological evidence for overeating as an addiction is extensive” [15]. In this chapter we will review this evidence, and the implications it has, both for a person trying to lose weight and a global society trying to support people in being healthy.

First, we will discuss new research on the relationship between UPF and weight gain. Then we will outline the many brain changes that co-occur with repeated intake of all drugs of abuse, including UPF. We will discuss fMRI research that sheds light on the specific elements of UPF that are driving the addictive response, versus those contributing to overeating more broadly. Then we will outline the three main phenomena that impact people trying to lose weight, which together hijack sound reasoning and create the “badly behaving brain” that thwarts long-term adherence to a healthy eating regimen: overpowering cravings, insatiable hunger, and the willpower gap.

The second half of the chapter will explore the diagnosis and treatment of UPFA, beginning with a review of the diagnostic criteria for substance use disorders in the DSM-5 and the evidence that excess food consumption meets these criteria. We will discuss research on the Yale Food Addiction Scale 2.0 and data showing the extent to which UPFA correlates with BMI, various eating disorders, and type 2 diabetes. Then we will discuss treatment options for those afflicted. Interestingly, the two current weight loss approaches that most directly target addiction, GLP-1 weight loss drugs and Bright Line Eating, are the two non-surgical approaches with the highest rates of sustained weight loss. Finally, we will explore eight distinct reasons why UPFA is uniquely challenging and difficult to overcome.

2. Ultra-processed food addiction (UPFA)

The question of whether UPF consumption is a causal contributor to the obesity pandemic is logically distinct from the question of whether UPF is addictive. Research shows that both are true [6, 16], and, of course, because many of the features of addiction—like an inability to control consumption, including difficulty quitting or moderating—drive UPF overconsumption, these phenomena are deeply related. We will first address the relationship between the processing of food and its impact on human weight.

2.1 UPF and weight gain

Until recently, it was unclear that the processing of food was a driver of human weight gain, separate and apart from its energy density, sugar content, lack of fiber, or the like. But in 2019, Hall and colleagues published a randomized controlled trial of ad libitum food intake in 20 weight-stable adults (average BMI 27) who spent 4 weeks in a metabolic ward [17]. They were randomly assigned to eat either an ultra-processed diet or a diet of entirely unprocessed foods for 2 weeks; the groups switched diets for the remaining 2 weeks. Importantly, the diets were matched for presented calories, energy density, protein, carbohydrate, fat, sugar, sodium, and fiber. Subjects could eat as much as they wanted from the diet they were on, in a structured setting of meals and snacks. Over the 2 weeks, subjects on the ultra-processed diet ate an average of 508 extra calories daily and gained significant weight, while subjects on the unprocessed diet lost significant weight. Subjects did not report preferring the ultra-processed diet nor enjoying it over the unprocessed diet [17, 18]. Despite the small sample size, the tightly controlled conditions of this experiment shed light on the power of food processing, in and of itself, to drive overconsumption and weight gain. Further evidence of the impact of UPF consumption on weight gain can be found in the increase of overweight and obesity as fast food outlets and snack foods become more available within a population [18, 19].

The impact of UPF consumption on weight is sobering, considering that two-thirds of the calories that children and adolescents consume in the USA today are UPF [20, 21] and that the prevalence of UPF is rapidly increasing worldwide [19]. For example, in China alone, over 2000 new McDonalds, Pizza Hut, and KFC outlets opened over the most recent calendar year (2023)—an average of one new fast food restaurant every 5 hours [22]. Given that the constraints of food delivery and storage result in ultra-processing being required to optimize profits, these trends are not likely to decline anytime soon [18].

2.2 UPF and addiction

The earliest studies on the dopamine response curve and addiction in rats did not use alcohol, opioids, stimulants, caffeine, or tobacco as the addictive agent, they used glucose [23]. Results showed that dopamine receptor downregulation occurred after repeated exposure, resulting in cravings. Thereafter, cues that predicted the addictive reward caused a spike in dopamine, while actual delivery of the addictive agent produced less and less of an effect [23, 24]. Sweet taste alone drives an addictive response: consumption of a sweet beverage activates dopaminergic neurons in the midbrain and then the ventral striatum, wiring the brain to remember the cues associated with that reward [25]. Rats, when not hungry nor thirsty, who are offered a forced-choice between a bolus of cocaine or some sips of sweetened water (whether sweetened with saccharin or sucrose) so strongly prefer the sweet taste that they nearly ignore the cocaine [26].

In humans, an fMRI study with a crossover design explored whether it was sugar, fat, or both, that drives the addictive response in the brain. Subjects were given a sample of a chocolate milkshake matched for flavor but containing high vs. low sugar and high vs. low fat in a 2x2 design. The presence of high sugar, but not fat, activated the insula and the associated reward centers of the brain [27]. Salt drives passive overconsumption of calories but not an addictive response [28]. But foods containing flour, and other forms of glucose unmitigated by significant fiber (like potato chips or popcorn), repeatedly score among the most addictive foods [29]. Combinations of ultra-processed carbohydrates and fats appear to be the most rewarding [30].

As with all addictions, key features of the neurological changes associated with UPFA include dopamine receptor downregulation [31, 32, 33] as well as opiate [34, 35, 36], endocannabinoid [37, 38], and serotonin [39, 40] receptor downregulation. People with a substance use disorder tend to experience reduced inhibition around their drug of choice, and this holds true for UPFA and UPF [41]. People with a drug addiction experience an increased stress response, specifically heightened release of corticotropin releasing factor; this same response has been found in those addicted to UPF [42]. Many entire textbooks and review articles catalog the broad and consistent body of literature, now totaling thousands of articles, accepting that UPF is addictive and is associated with the same pattern of neurological and behavioral changes as drugs of abuse [16, 43, 44, 45, 46].

Heightened cue reactivity, especially in early abstinence, is another common feature of both drug addiction and UPFA [47]. Much like addictive drug use, the consumption of UPF sensitizes dopaminergic systems [48]. Thus, environmental cues associated with UPF can both evoke cravings and initiate episodes of binge consumption [49]. In studies examining the neural response to food cues, the brain areas known to be involved in cue reactivity in response to drugs showed higher activation with UPF compared to minimally processed foods [50]. In addition, studies using MRI revealed that both food and smoking cues were associated with increased activation in almost identical areas—namely the left amygdala, bilateral insula, bilateral orbitofrontal cortex, and striatum [51, 52]. A wide and heavily replicated literature shows that the cue reactivity and cue-induced cravings produced by drug and food cues are nearly identical [53].

Finally, specific impairments in cognitive function are found with extensive use of both addictive drugs and UPF. For example, exposure to UPF early in life predicts long-term deficits in both learning and memory [54]. In addition, childhood obesity is associated with cognitive deficits that may last into adulthood [55, 56, 57]. In adults, UPF consumption impairs cognition [58, 59], and binge eating is associated with deficits in attention, memory, and inhibition [60].

3. The badly behaving brain

Millions of people are spending time, money, and significant effort trying to lose weight, only to fail repeatedly. The average dieter makes four or five new attempts each year [61]. Many experience the strange phenomenon where they launch a new attempt with confidence and excitement, watch it work awhile, and then find themselves heavier than they were before, without a clear idea of what made it all unravel [62]. Three phenomena—all related to UPF consumption and how it impacts the brain—are driving this pattern of behavior and experience. We call them overpowering cravings, insatiable hunger, and the willpower gap.

3.1 Overpowering cravings

Dopamine downregulation is the neural substrate of cravings [63]. Initial exposure to an addictive substance causes a spike in dopamine [64]. The dopamine response to UPF is not as large as the dopamine response to heroin or cocaine; it’s more like the response to alcohol or tobacco [65]. Yet, it is larger than the dopamine response to broccoli or blueberries [66, 67, 68], and, over time, it causes downregulation of the dopamine receptors [69]. This, combined with the downregulation of serotonin, endocannabinoid, and opiate receptors that also occurs with UPFA [34, 35, 36, 37, 38, 39, 40], leaves a person in a state of discomfort and malaise unless and until they consume more UPF to get relief [70]. In other words, cravings are both an effort, driven by positive reinforcement, to experience the release of dopamine, and an effort, driven by negative reinforcement, to seek relief from a now-unpleasant baseline state [71, 72]. Behavioral examples of such cravings are: driving across town for a specific food to scratch a specific itch or wandering through grocery store aisles (or scrolling through food delivery apps or staring into the refrigerator) wondering what will “hit the spot.”

What makes the cravings “overpowering” is that, with the development of UPFA, decision making is impaired [58, 59] and inhibition is reduced [41], leaving the prefrontal cortex unable to effectively counteract the urges generated by the reward centers of the midbrain [73]. In addition, as addiction develops, the wanting of UPF increases while the liking of it decreases [74], leaving a person in a chronic state of yearning that is never satisfied. Over time, as UPF consumption leads to depression and increased days of poor mental health [75, 76], this pattern becomes increasingly difficult to break.

3.2 Insatiable hunger

Hunger is thought of as a helpful physiological drive, a signal that more fuel is needed. Someone starts a meal hungry, and over the course of the meal, the hunger diminishes or perhaps goes away entirely [77, 78]. The modern hunger that accompanies UPFA, however, is “insatiable” precisely because it does not go away over the course of a meal [79, 80, 81]. People eat an entire dinner and then, still wanting more, sit on the couch with a family-sized bag of chips. Chips gone, they go to the freezer for ice cream. This is insatiable hunger.

Under normal circumstances, leptin triggers the ventromedial nucleus of the hypothalamus to signal that adequate fuel has been consumed, effectively regulating energy homeostasis [82]. Both current consumption of fuel and overall increased adiposity trigger leptin release from fat cells [83]. Several factors result in leptin resistance, the inability of the hypothalamus to sense circulating leptin and register its signal: high baseline insulin levels [84], high triglycerides [85] and inflammation, especially of the ventromedial nucleus of the hypothalamus [86]. Since UPF consumption causes all three [87, 88, 89], regular UPF consumption, with or without addiction, can result in insatiable hunger. This is confirmed by clinical experience—many people in modern society report that they never, or rarely, feel full [90, 91].

UPF also often delivers a mismatch between what it promises in the mouth and what it delivers to the stomach, with non-nutritive sweeteners signaling a big bolus of calories that never arrives and flavor profiles cueing the stomach to expect, for example, large amounts of fat from a fat-free product. Over time, this disparity also contributes to insatiable hunger [92, 93].

When leptin was discovered in 1994, pharmaceutical companies spent small fortunes attempting to patent the perfect leptin pill or injection that would take away the desire to eat [94]. But because the problem is leptin resistance, not leptin deficiency, no amount of exogenous leptin produces satiety [95]. Very low levels of leptin signal starvation, an urgent situation causing a cascade of hormonal changes that compels the consumption of large amounts of fuel [96]. Given that leptin resistance mimics this state in the brain [97], the resulting insatiable hunger makes perfect sense. Furthermore, leptin does not just act on the hypothalamus, it also acts on the brain stem [98], making prolonged calorie restriction in the face of insatiable hunger about as doable as holding your breath while slowly climbing a long flight of stairs.

3.3 The willpower gap

In an experience sampling study published in 2012, Hofmann and colleagues concluded that people are resisting temptations an average of 4 hours per day, that they give in to their temptations about half the time, and that the urge to eat is the number one temptation people are trying to resist [99]. Further, resisting temptations, making decisions, and regulating emotions all require effective functioning of the anterior cingulate cortex [100], which after 15 minutes of effort is depleted to the point of significantly diminished functioning [101, 102], resulting in a marked inability to restrain impulses—a willpower gap. This willpower gap impacts people without an addiction to UPF (and may help to explain the significant rates of overweight and obesity, and dieting recidivism, in those populations), but for people with UPFA, several additional factors are operative. First, as previously discussed, both inhibition [41] and decision making are significantly impaired [58, 59], widening the willpower gap. And second, cue reactivity is stronger, especially during early abstinence [47], making the person with UPFA extra sensitive to the myriad temporal, spatial, visual, auditory, and olfactory cues to eat in the modern obesogenic environment [103], greatly increasing the frequency of encountering the willpower gap throughout the day. Astute bariatric surgeons, dieticians, and general practitioners have sensed for decades that increased information or education alone is not the solution to the obesity pandemic, as they have little lasting effect [104]. When it comes to weight loss, the willpower gap helps explain the chasm between knowledge and volition on the one hand, and sustained execution on the other.

4. The diagnosis of ultra-processed food addiction

For both individuals wanting support and clinicians trying to help them, effective and accurate diagnosis is the first step in the treatment journey. There are dozens, if not hundreds, of online quizzes and self-assessments to help someone get a sense of whether they have an addictive relationship with sugar, UPF, or food more generally, but there is currently only one validated diagnostic tool: the Yale Food Addiction Scale (YFAS) [105], now in its second iteration (YFAS 2.0) [106], discussed in greater detail below. The YFAS 2.0 is based on the diagnostic criteria for substance use disorders in the DSM-5 section on Substance-Related Addictive Disorders [107, 108], which we will review next.

4.1 The DSM-5 criteria for substance use disorders

In the DSM-5, there are 11 criteria for a substance use disorder. Diagnosis is given along a continuum, with the presence of 2–3 symptoms indicating a mild disorder, 4–5 symptoms a moderate disorder, and 6 or more symptoms a severe disorder. In each case, however, the pattern of use must also lead to “clinically significant impairment or distress” [108]. Research shows that the use and abuse of UPF meets each of these 11 criteria, with examples and prevalence as follows.

4.1.1 Criterion 1: consuming more than intended

UPF is eaten in larger amounts or over a longer period than was intended.

Consuming more UPF than intended is a common, perhaps even universal, experience [109]; in fact, irresistibility and overconsumption are features that UPF manufacturers tout, as with the Lay’s potato chip slogan, “Betcha can’t eat just one!” With UPFA, this overconsumption can reach levels that cause significant impairment and distress [76, 110]. Increases in diagnosis of UPFA correlate with increases in the frequency of binge episodes [106]. Because UPFA is associated with gradually impaired impulse control [41, 60], this symptom is progressive [16]. Prevalence: in the general population, 19.3% of people have this symptom [106].

4.1.2 Criterion 2: desiring yet unable to cut down, stop, or stay stopped

There is a persistent desire or unsuccessful efforts to cut down or control UPF consumption.

On the surface, this criterion seems easily met by the vast majority of people, as it is plausible to imagine that most everyone, at one time or another, has attempted to diet or control their food intake. However, very few diets require abstinence from all UPF; indeed, the sale and distribution of branded UPF is a core component of many diets. Further, attempting to stop consuming an addictive, injurious substance is not the same as attempting to lose weight [111, 112]. Yet, market research shows that the average dieter makes four or five new attempts each year, highlighting the difficulty people have in staying “on the wagon” once they stop eating certain foods [61]. The evidence is clear that UPF is not only difficult to resist, it is also specifically engineered to enhance palatability and desire [113]. Prevalence: in the general population, 25% of people have this symptom [106].

4.1.3 Criterion 3: significant time spent

A great deal of time is spent in activities necessary to obtain UPF, consume UPF, and recover from its effects.

Clearly, if the average dieter is making four or five attempts to lose weight each year, they are spending significant time (and likely significant money) preparing for, launching, failing at, and recovering from their attempts to control their food consumption [61]. People also report spending a lot of time driving to get specific foods, significant time eating certain foods throughout the day, and a lot of time feeling tired and sluggish from overeating [114]. In the later stages of UPFA, the impact can expand to nearly 24 hours each day if disrupted sleep and night eating infiltrate the overnight hours and mental obsession with procuring and consuming UPF and managing weight and health symptoms dominate during the day [115]. Even among those with UPFA who do not have a weight problem, the time spent obsessing about what they have eaten or not eaten, what they plan to eat or not eat, and whether they are on their food plan or off their food plan can nearly consume the day [116]. Prevalence: in the general population, 18.7% of people have this symptom [106].

4.1.4 Criterion 4: craving

Craving, or a strong desire or urge to consume UPF.

Of all food, UPF has the highest likelihood of being consumed in an addictive manner and the highest likelihood of being craved [117]. Not only does the experience of craving UPF parallel the experience of craving drugs of abuse, but the activation pattern in neural structures associated with craving shows significant overlap across various addictive substances, including UPF [52, 118]. In self-reported data, overeating is linked to more intense and frequent instances of food craving among individuals with binge eating disorder, bulimia nervosa, and obesity [119]. Similarly, food addiction, as gauged by the Yale Food Addiction Scale, correlates with elevated self-reported food craving [120]. Thus, the criterion of frequently experiencing craving or a strong urge to consume a substance can be extended to UPF and represents an observable symptom in the context of UPFA. Prevalence: in the general population, 20.3% of people have this symptom [106].

4.1.5 Criterion 5: failure to fulfill roles

Recurrent UPF consumption resulting in a failure to fulfill major role obligations at work, school, or home.

There is a significant literature confirming that obesity hampers people’s ability to fulfill their role obligations at work, school, and home [121], and given the correlation between UPFA and obesity [106, 122], some of that impact is likely stemming from addiction. But even people who are not carrying excess weight can struggle to perform their major role obligations due to the impact of food obsession and the negative consequences of overconsuming UPF such as remorse, shame, sluggishness, and a desire to isolate [123]. In the general population, the prevalence of this symptom is 21.5% [106], which means that more than one in five people is agreeing that, over the prior 12 months, “My overeating got in the way of me taking care of my family or doing household chores” and “I didn’t do well at work or school because I was eating too much” [124].

4.1.6 Criterion 6: use despite social or interpersonal problems

Continued UPF consumption despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of UPF.

Social and interpersonal challenges manifest distinctly within the realm of eating behavior. Notably, obese individuals report heightened levels of social isolation compared to those with normal weight [125]. While this can be attributed to weight gain accompanying excess consumption of UPF, research indicates a significant connection between interpersonal problems—such as distrust, social insecurity, or hostility—and binge eating behavior, independent of body mass [125, 126]. Experimental research focusing on UPFA and social or interpersonal problems is just emerging and future studies are needed to establish a causal link between the two. Preliminary data indicate that others’ disapproval of food choices and eating behaviors contributes to interpersonal conflict [117]. Prevalence: in the general population, 19.4% of people have this symptom [106], which means they agree that they have problems with family and friends because of how much they overeat and their friends and family worry about how much they overeat [127].

4.1.7 Criterion 7: important activities given up

Important social, occupational, or recreational activities are given up or reduced because of UPF consumption.

As noted above, individuals with obesity often report heightened levels of social isolation that may be attributed to body weight, but also to eating behaviors [125]. Disordered eating can also lead to decreases in exercise and other physical activities [128]. Recent findings demonstrate that the obesity epidemic is a direct result of the prevalence of UPF in our diets [129]. Regardless of BMI, people with UPFA endorse statements like: “I eat certain foods so often or in such large amounts that I stop doing other important things like working or spending time with family or friends” and “I avoid work, school, or other activities because I’m afraid I will overeat there” and “I felt so bad about overeating that I didn’t do other important things like working or spending time with family or friends” [130]. Prevalence: in the general population, 11.9% of people have this symptom [106].

4.1.8 Criterion 8: hazardous use

Recurrent UPF consumption in situations in which it is physically hazardous.

The symptom of hazardous use typically pertains to the risks associated with intoxication, such as driving or using heavy machinery, or even simpler situations such as crossing a busy street on foot. Clearly, eating does not involve the same level of intoxication as alcohol or opiates. However, a parallel can be drawn with tobacco, where the DSM-5 suggests that this criterion may encompass smoking in bed, posing a fire risk. Extending this analogy, the hazards of UPF consumption include eating while driving, which is known to impair performance and increase crash risks [131, 132, 133]. Indeed, approximately one in four people agree that, over the past 12 months, they have been so distracted, either by thinking about food or by eating food, that they could have been hurt (e.g., when driving a car, crossing the street, or operating machinery) [106, 134]. Prevalence: in the general population, 24.8% of people have this symptom [106].

4.1.9 Criterion 9: Use despite physical or emotional consequences

UPF consumption is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by UPF.

This particular criterion involves continued excess consumption of UPF despite an acute health condition exacerbated by UPF. This is a relatively widespread phenomenon, as individuals with diabetes often continue to consume excessive sugar despite knowing that it is injurious [135, 136] and individuals who have recently had a medical procedure (such as bariatric surgery) often continue to overeat despite the contraindications [137]. In fact, of people who have just had a limb amputated due to unmanaged type 2 diabetes, 55% will have a second limb amputated within 2 years [14]. Additionally, persons with both UPFA and certain eating disorders with psychologically harmful comorbidities are seen to persist in detrimental eating, resisting dietary recommendations that could potentially reduce their symptoms and accompanying psychological distress [138]. In short, physical and psychological problems are often not sufficient to reduce the consumption of UPF. Prevalence: in the general population, 23.5% of people have this symptom [106].

4.1.10 Criterion 10: tolerance

Tolerance, as defined by either of the following:

1. A need for markedly increased amounts of UPF to achieve intoxication or desired effect.

2. A markedly diminished effect with continued use of the same amount of UPF.

Individuals with UPFA report diminished enjoyment of UPF over time [113]. Considering that psychological changes, as well as physiological and behavioral changes, accompany tolerance [139], a decrease in the subjective reward value of UPF over time is a marker of the development of tolerance. In the general population, 17.4% of people have this symptom [106], which means they agree with statements like, “eating the same amount of food did not give me as much enjoyment as it used to” and, “I needed to eat more and more to get the feelings I wanted from eating” [140].

4.1.11 Criterion 11: withdrawal

Withdrawal, as manifested by either of the following:

1. The characteristic withdrawal syndrome for UPF.

2. UPF (or closely related substances) are taken to relieve or avoid withdrawal symptoms.

Mounting evidence indicates that withdrawal effects are indeed observed with UPF [10, 141]. Specific foods, particularly those highly processed with added sweeteners and fats, exhibit heightened addictive potential [44, 70]. While both behavioral and substance-related factors play significant roles in the addictive process for food, UPFA symptoms more closely align with the criteria for substance use disorder [141], and withdrawal symptoms are a defining feature. Classic withdrawal symptoms such as anxiety, headaches, irritability, and unstable mood appear for many individuals upon decreasing or stopping consumption of UPF [142]. In addition, the time-scale of withdrawal symptoms is the same as for tobacco, opiates, stimulants, and alcohol [142]. Prevalence: in the general population, 29.7% of people have this symptom [106].

4.1.12 The requirement of significant impairment or distress

In the general population, the average person has 2.38 of these 11 symptoms, which would qualify them for a diagnosis of mild UPFA, except that only 12.5% of people in the mild symptom range meet the criteria for a pattern of use that causes “clinically significant impairment or distress,” which is also required for diagnosis. In the moderate range of 4–5 symptoms, only 19.6% of people meet this threshold, while in the severe range of 6 or more symptoms, 61.5% of people have significant impairment or distress [106].

There is a significant implication of the “impairment or distress” requirement on weight gain and weight loss trends. The data show that most people in Western society can be said to have an addictive relationship with food, as evidenced by manifesting multiple symptoms of UPFA [106], but they will not meet the criteria for an addiction diagnosis because it is not bothering them badly enough or inhibiting their functioning to a significant extent [106]. However, the addictive symptoms may very well be contributing to their weight gain and hindering their efforts to lose weight—and to maintain that weight loss once it is achieved. This would help to explain abysmal weight loss results [9] and widespread diet recidivism [10]. It would also predict that weight loss approaches taking an abstinence-based approach to UPFA, rather than building consumption of UPF into their plans, would be significantly more successful than average. This turns out to be the case, and is the subject of Section 5.

4.2 The Yale food addiction scale

The original Yale Food Addiction Scale (YFAS) to diagnose food addiction was released in 2009 by Yale University’s Rudd Center for Food Policy and Obesity [105]. It was a 25-item self-report Likert-scale questionnaire examining eating behaviors over the prior 12 months, based on the DSM-4 criteria for substance dependence. A shorter, modified YFAS (mYFAS) with only 9 items was released in 2014 and was shown to yield similar results to the original [143]. In 2013, a version for children, the YFAS-C, was released [144].

In May of 2013, the DSM-5 was published with significant updates to the DSM-4. The section on Substance Use Disorders was renamed Substance-Related and Addictive Disorders. Substance abuse and substance dependence were combined, and the new substance use disorders diagnosis could now be made along a continuum: mild (2–3 symptoms), moderate (4–5 symptoms), or severe (6–11 symptoms). The symptom of legal consequences was removed and the symptom of craving was added. In 2016, the YFAS 2.0 was released to conform to the new DSM-5 structure and thereby update the instrument to reflect the latest thinking in substance use diagnosis [106]. Shortly thereafter, the mYFAS 2.0 and mYFAS-C 2.0 were released to offer an updated shorter screening tool and an updated version suitable for children, respectively [145, 146].

The YFAS 2.0 was shown to have convergent validity by measuring associations with scores on other instruments assessing problematic eating behaviors such as the Three Factor Eating Questionnaire (TFEQ) disinhibition, TFEQ hunger, current BMI, highest BMI, and frequency of binge eating episodes [106]. Food addiction scores increase with BMI [106]. Discriminant validity was shown by demonstrating that YFAS 2.0 scores are not significantly correlated with TFEQ dietary restraint, as food addiction and dietary restraint are unrelated [106, 147]. Incremental validity was shown using hierarchical multiple regression, looking at YFAS 2.0 scores and binge eating frequency as predictors of BMI. YFAS 2.0 scores predicted BMI above and beyond the contributions of binge eating frequency [106].

A meta-analysis reviewing 6425 abstracts of studies assessing food addiction using the YFAS and its derivatives and including 272 studies in its analysis showed a weighted mean prevalence of food addiction diagnosis of 20% [122], meaning that, in the general population, about 20% of people likely qualify for a diagnosis of UPFA.

4.3 Correlations with eating disorders and weight

Numerous studies show that UPFA is related to, but distinct from, eating disorders [106, 122, 148]. Although the standard deviation is large as findings vary widely, a meta-analysis that calculated weighted pooled averages showed that the prevalence of UPFA, according to the YFAS and its derivatives, is roughly 44% among people with a clinical diagnosis of anorexia nervosa, 48% among people with a clinical diagnosis of bulimia nervosa, and 55% among people with a clinical diagnosis of binge eating disorder [122].

Importantly, UPFA is distinct from obesity and the propensity to gain weight [106, 122]. While UPFA is positively correlated with weight [106], according to a meta-analysis [122], the pooled prevalence of UPFA among people with no weight disorder is 17%, among people with overweight is 24%, among people with obesity is 28%, and among those who have had bariatric surgery is 28%. UPFA is a contributor to weight gain but not the sole driver. In addition, UPFA is strongly associated with type 2 diabetes in a dose-response like manner [149].

5. The treatment of ultra-processed food addiction

The scientific literature on the neurobiological similarity between addictive drugs and UPF as substances of abuse is large [150]. The literature on diagnosis is robust as well [122]. Between the two, several hundred new studies are being published every year, and that number has been increasing dramatically and linearly since 2010 [122]. In comparison, there are still relatively few published studies evaluating the treatment of UPFA [16]. One factor is that it is difficult to treat a condition that is still not formally recognized by the DSM or the ICD, especially since proper treatment, like treatment for drug or alcohol addiction, can be expensive, and governments and insurance companies typically will not cover it. Studies on treatment are also expensive and time consuming. But avenues of treatment do exist, and there is a nascent literature attempting to evaluate the results, which we review below. In addition, there are weight loss approaches that, intentionally or unintentionally, target addiction, and it turns out that they are significantly more effective than other weight loss approaches. We will cover those findings in the following sections as well.

5.1 Treatment centers and food addiction professionals

Perhaps the longest running treatment center for UPFA is Shift Recovery by Acorn, which was founded in the United States in 1993 and offers online and in-person intensive treatment programs for UPFA [151]. Bitten Jonsson Center opened in Sweden in 1999 and offered an inpatient UPFA treatment program until 2005 [152]. MFM in Iceland was founded in 2006 and offers outpatient UPFA treatment [153]. And in the United States, Milestones in Recovery [154] and Turning Point of Tampa [155] both offer inpatient treatment for individuals with co-occurring eating disorders and UPFA.

In 2016, the International School for Food Addiction Counseling and Treatment (INFACT) was established to train professionals in the core functions, clinical guidelines, and best practices of food addiction treatment. Graduates are certified in Europe by the European Certification Board and in the USA by the Addiction Professionals Certification Board as Certified Food Addiction Professionals [156]. The Food Addiction Institute (FAI) aims to advance awareness [157] and the Food Addiction Professionals Network (FAPN) provides clinicians ongoing education and peer support. In addition, many 12-step programs, such as Food Addicts in Recovery Anonymous (FA) offer comprehensive recovery programs for people with UPFA [158]. An individual looking for treatment could reach out to any of these organizations to get help.

Until recently, there was either no data or very little published data on the efficacy of these programs and approaches. But a multi-center study is underway, and their preliminary findings are promising. Across 103 participants receiving treatment from Certified Food Addiction Professionals offering online treatment group programs based in North America, Sweden, and the United Kingdom, results showed that, over 10–14 weeks of treatment, food addiction symptoms went significantly down (as measured by the YFAS 2.0 and the CRAVED instrument which measures symptoms according to the ICD-10 criteria), weight went down slightly (weight loss was not a focus of treatment), and well-being went significantly up [159]. Monthly follow-up sessions are a part of these treatment protocols, and future publications will analyze longer-term data.

5.2 Bariatric surgery

Bariatric surgery is not intended as a treatment for UPFA, but studies have shown that most post-surgical patients do experience initial remission of UPFA symptoms [160, 161]. Unfortunately, practitioners in the field do not typically observe sustained remission, though no long-term data have yet been published [162]. Studies show that significant weight regain 5–6 years post-operatively affects as many as three-quarters of surgical patients [163] and revision surgery is becoming increasingly common [164]. Two of the most common causes of weight regain post-surgery are thought to be out-of-control eating and a return to previous eating habits [163], indicating that lasting remission of UPFA symptoms after bariatric surgery is not the norm.

5.3 GLP-1 weight loss drugs

Science declared GLP-1 therapies for obesity to be the 2023 Breakthrough of the Year, for both their weight loss results and additional health benefits like reduction in heart attacks, strokes, and liver disease [165]. GLP-1 agonists such as semaglutide (marketed as Ozempic for diabetes and Wegovy for weight loss in the USA) not only help regulate blood sugar in people with diabetes and curb appetite in people with obesity, but they decrease cravings for UPF, cigarettes, alcohol, and other drugs of abuse as well. Over 100 studies in both humans and rodents have demonstrated the effects of GLP-1s on the reward pathways of the brain [166]. These drugs both decrease activity to the left insula, reducing the anticipated reward from eating UPF, and improve activity deficits in the insula, hypothalamus, and orbitofrontal cortex [166].

Clinical trials show that patients taking semaglutide lose approximately 15% of their bodyweight within 1 year [167] and maintain that weight loss at 2 years [168]. Drug use must be continued, or an average of two-thirds of lost weight will be regained within 1 year [169]. The combination of suppressed appetite and reduced addictive cravings on GLP-1 drugs produces weight loss results that are far larger than what standard weight loss approaches produce.

5.4 Bright line eating

Bright Line Eating (BLE) is an online weight-loss program within a food addiction recovery framework that teaches clients to abstain from UPF, eat three meals a day, and engage in ongoing education and peer support [170]. Research shows that, from weeks two through eight on the program, participants’ hunger and cravings decrease linearly, reaching an average rating of just 1.4 (on a Likert scale of 1 through 5, with 5 being high) at 8 weeks [171]. The average eight-week weight loss result on BLE is 7.8% of initial body weight [170], the average one-year weight loss result is 16.8% [172], and the average two-year weight loss result is 14.3% [172].

Interestingly, studies show that the process of mastication releases GLP-1 and thus contributes to satiety [173]. UPF is manufactured to require minimal chewing [18, 174] while raw vegetables and many of the other whole foods on the BLE food plan require significant chewing. Research also shows that fiber releases GLP-1 and peptide YY, another satiety hormone [175]. These factors together may play a role in the semaglutide-like appetite-suppression effects of a whole-foods, zero UPF approach to eating.

5.5 The impact of treating UPFA on weight loss

There are relatively few peer-reviewed studies on commercial weight loss programs, and even fewer randomized clinical trials. Results are notoriously poor, so there is little commercial benefit to documenting the results [176]. A direct comparison of the studies that do exist is both difficult and problematic due to differences in design, methods, variables measured, and lack of randomized assignment of participants to conditions across studies. However, despite these significant issues, a visual comparison of the weight loss data that do exist yields an interesting pattern. With these caveats in mind, Figure 1 aggregates data from 12 published papers on commercial weight loss programs and demonstrates a clear demarcation between approaches that allow (or even encourage) the consumption of UPF versus the two approaches that target addiction, whether behaviorally or pharmacologically [167, 168, 170, 172, 177, 178, 179, 180, 181, 182, 183, 184].

Figure 1.

A comparison of data from twelve peer-reviewed studies reporting weight loss results from semaglutide and various commercial weight loss programs [167, 168, 170, 172, 177, 178, 179, 180, 181, 182, 183, 184]. (No studies reporting two-year % weight loss data were found for Noom, SlimFast, Atkins, Nutrisystem, or Zone diets).

6. The hardest addiction?

UPF does not deliver a dopamine reward comparable with opiates or stimulants [185], nor are the withdrawal symptoms from UPF as severe as the withdrawal symptoms from most drugs [10, 70], yet, for eight distinct reasons, it could be argued that UPFA is uniquely difficult to overcome.

First, for no other substance addiction is the average age of first exposure so young, nor the rate of early exposure so frequent. Infant formula is UPF, so babies who are formula-fed are exposed to UPF multiple times a day, from birth or shortly thereafter. Even breastfed babies are typically exposed to UPF at around 6 months of age, as UPF cereal is the most commonly recommended first baby food [186]. Regular exposure continues from there, with research showing that 60.6% of infants and 98.3% of toddlers in the USA are consuming added sugars every day [187].

Second, UPFA is the result of a hijacking of neural circuits whose original function was to make the procurement and consumption of calories an organism’s top priority. Every other substance addiction hijacks these same circuits, but no organism’s brain prioritizes the procurement of alcohol, cocaine, or tobacco the way it prioritizes the consumption of energy dense, highly rewarding food.

Third, UPFA is a substance addiction [188] that has so many features of a behavioral addiction (such as shopping or gambling) that it is often categorized as such [189], meaning that the process of eating is rewarding and cue-laden enough to carry the addiction on its own. One could effectively argue that UPFA is actually both a substance addiction and a behavioral addiction, as people addicted to UPF often eat excessive quantities of regular foods and demonstrate an addiction to the process of eating itself [190].

Fourth, and perhaps most perniciously, UPFA is unique among all addictions in causing a health-deteriorating side effect (excess weight) that, when addressed, re-triggers the original addiction. Alcohol causes liver damage, but when the liver heals, it does not release a cascade of hormones that cause intense cravings for alcohol. Smoking causes lung damage, but when the lungs heal, nicotine cravings are not a direct result. But weight loss causes a barrage of hormonal changes that lead to overeating and weight regain [191], meaning the person with UPFA who is carrying excess weight is caught in a pernicious cycle unlike anything else in the addiction-recovery landscape.

Fifth, unique among all substance addictions, we cannot simply stop eating. People addicted to alcohol, nicotine, caffeine, or drugs can abstain completely, and feel highly confident that they are successfully abstaining, as the category definitions are quite clear. But the person addicted to UPF must continue eating on a daily basis, which raises the question, at every eating opportunity, of whether a specific food is likely to trigger an addictive response. The NOVA definition for UPF is many pages long [192] and has poor inter-rater reliability [193], highlighting that even experts find it difficult to articulate or agree on the category definition. Furthermore, some foods like peanut butter, made from just peanuts and salt, routinely trigger overconsumption [194], illustrating that, once the addiction is established, abstinence from all UPF may not be sufficient for full recovery. Lack of certainty about where to draw the line of abstinence creates a slippery slope that heightens the likelihood of relapse.

Sixth, the multi-trillion-dollar UPF industry is highly invested in our ongoing addiction, and there are currently very few limits on their reach. They use fMRI to ensure their snack formulations and commercials optimally stimulate the mesolimbic reward pathways [195]. Brains healing from addiction are extra-sensitive to these cues, especially in early recovery [47, 49, 50, 51, 52], and the bombardment of commercials, billboards, jingles, and logos for UPF can make living in modern society torturous. Certainly, decades ago, before limits on alcohol and cigarette advertising, or in a hypothetical world where drug cartels had free reign to advertise their products, we might imagine a quasi-comparable situation, but in actual modern-day society, UPF is unique in the magnitude of the advertising dollars promoting it.

Seventh, UPF consumption occurs in more locations, and more frequently throughout the day, than the use of any other addictive substance. This is significant, because relapse is often based on a specific temporal or location-based cue, as any former smoker walking out of a movie theater can attest. Most people start eating within minutes of first waking up and consume their final calories mere minutes before falling asleep [196]. From the temptation to put a scoop of sugar or packet of non-nutritive sweetener into the first morning cup of coffee, to the drive-through on the way to work, to the doughnuts in the break room, to the vending machine outside the office, to the pizza and chips in the lunch line, living an average day means encountering literally hundreds of temporal and location-based cues to consume UPF [103]. And quitting means facing all of those same cues and being well-resourced enough to not succumb, each and every time.

Eighth and finally, the social pressures to eat [197, 198], and to not consider food of any sort to be an addiction [199], are immense. The person addicted to stimulants or opiates can get out of rehab and form myriad associations where no one uses drugs and there is zero pressure to return to their addiction; even the person addicted to alcohol who misses pub culture can form plentiful associations with groups who do not blend alcohol consumption with their fellowship. But the person addicted to UPF will find that nearly every gathering of every sort involves the consumption of food and that the pressure to eat all things in moderation is immense [200]. Furthermore, bonding over food is, and always has been, woven into our very ways of experiencing togetherness and community [201].

For all these reasons, recovery from UPFA, especially if it coincides with a desire to lose weight, is especially difficult and will require an intensive and multifaceted approach.

7. Conclusion

Years ago, the construct of UPFA was hotly debated [202] and the words “food addiction” nearly always had quotes around them or were qualified with adjectives like “controversial” and “purported.” Indeed, such qualifiers will likely persist until UPFA receives official standing as a diagnosis in the DSM and the ICD. It is difficult to predict when that will be, but applications to these committees for official diagnoses are in progress.

However, during the late 2010s and early 2020s, the rate of published papers on the topic of food addiction escalated dramatically [122] and in the thousands of papers published on this topic over the past several years, two trends are marked. First, the neurobiological evidence substantiating the impact of UPF as an addictive drug in the brain, across multiple structures and impacting many cognitive functions, has become very convincing [16]. Second, there is great utility and empirical productivity in applying the DSM-5 criteria for a substance use disorder to UPF consumption [106, 122]. In a word, it fits.

More research is needed, especially controlled trials on each of the 11 criteria for a substance use disorder as applied to UPF, and also, perhaps most urgently, more research in the domain of treatment. Research shows that 30% of people receiving treatment for an eating disorder are not improving with the current standard of care [203]. Studies examining whether those individuals are more likely to have undiagnosed UPFA, and randomized, controlled trials exploring whether an abstinence-based treatment approach (rather than an all-foods-fit-for-all-people treatment approach) would help them, are badly needed. These studies are likely to be conducted over the next few years, as the field is maturing now quite rapidly.

While many will wait for an official diagnosis in the DSM or the ICD to drop the quotes and stop using the word “controversial,” the reality is that the existence of UPFA will long precede any official seal of validation. No longer is the question, “Is UPF addictive like alcohol, tobacco, stimulants, and opiates?” but rather, “How can we best treat UPFA?” and, “What are the implications?”

Clearly, as is true for alcohol, caffeine, nicotine, and all drugs, not everyone is equally susceptible to the addictive pull of UPF. But the average person has at least some degree of addictive susceptibility [106]. Two weight loss approaches—GLP-1 drugs for weight loss and Bright Line Eating—that each target UPFA directly and both decrease hunger and cravings, offer promise for people wanting to lose weight and health care practitioners looking to help them. But the average person with obesity is likely aiming for far better results than merely losing 15% of their current body weight. Perhaps if a pharmacological solution was paired with an abstinence-based approach to eating, much higher average weight loss percentages could be achieved.

We must remember that the “badly behaving brain” is performing exquisitely well, for the conditions in which it evolved. But the food environment has changed dramatically. There are good reasons why fewer than 1% of those living with obesity have reached a normal BMI within any given year [204]. Until just recently, there were no weight loss approaches that targeted UPFA. But today there are, and we now know that addressing UPFA results in far greater weight loss than ignoring it. That is important, because as our collective body mass continues to rise, we need a framework to reinvent how we approach weight loss in the twenty-first century.

Acknowledgments

Dr. Mark Goetting, Dr. Cynthia Prehar, and Joseph Fleischman provided detailed feedback and excellent copy edits of this chapter. It was a better manuscript because of their contributions.

Conflict of interest

Susan Peirce Thompson is the founder and CEO of Bright Line Eating. Andrew Kurt Thaw declares no conflict of interest.