Neuroscience and psychology
Sugar, cocaine and food "addiction"
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MPH, MSc
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In this article, we analyze why highly palatable foods can produce reward and impulsive or compulsive eating patterns. However, addiction is not just about reward or dopamine in a neurobiological sense; it also involves behavior, learning, context, individual vulnerability, and loss of control. Therefore, we offer a somewhat complex reflection on all of these factors.
Rather, we could say that certain ultra-processed, high-calorie, and highly palatable products can encourage greater consumption, and in some people with more vulnerable traits, even disinhibit more impulsive consumption (more driven by hedonic incentives) or compulsive consumption (more driven by learning and negative reinforcement). Calorie-dense food is more reinforcing than food with lower caloric density; that is, it produces a greater reward signal in the brain due to its higher energy density. Neuroevolutionarily, this suggests that the reward system prioritizes obtaining foods that provide more energy, as well as associated signals such as sweetness or saltiness, which anticipates sodium, essential for organisms. This is compatible with evolutionary logic. Organisms evolved in an aquatic environment rich in salts, and animal physiology has depended from very early on on ionic gradients, especially of sodium, potassium, and chloride. Therefore, when organisms colonized terrestrial environments, obtaining sodium became a significant problem.
Certain combinations of macronutrients produce a stronger reward signal (refined carbohydrates and fat, salt, even a touch of sugar, and additives such as flavor enhancers and others to improve mouthfeel, etc.). However, this alone does not produce "food addiction."
One difference is that some substances have a pharmacological component that could be considered sufficient to produce addictive behavior, for example, through the simple passive administration of the substance, without any additional behavioral or contextual factors. In other words, some substances can create neuroadaptations that result in addictive behavior, produced at a "purely pharmacological" level. However, in most addictions considered "pharmacological," there is a behavioral and contextual component: a ritual of administration, operant learning, conditioning to environmental cues, etc., including "hard drugs" (Escohotado comes to mind, of course). That is to say, many classically addictive substances are not addictive solely due to their pharmacological and passive effects. Some studies show that the active administration of a substance, compared to the passive administration of the same substance, can be more reinforcing, depending on the model, contingencies, and context. This implies that there is more than just the substance: a behavioral and contextual component also participates in reinforcement, producing learning in response to stimuli, reinforced operant responses, etc. Ultimately, biological addiction requires a pharmacological administration model that eliminates other causes of reinforcement and contingencies, something that doesn't happen directly with food in the nervous system. Intragastric infusions of glucose or nutrients can condition taste preferences or increase intake, showing that glucose can have reinforcing value beyond the cephalic phase (without enjoying its taste, etc.), but this differs from inducing sufficiently reinforcing behavior through passive administration to be considered addictive.
It has been claimed that sweets are more addictive than cocaine, generally referring to a well-known study (Lenoir et al., 2007). However, there is actually an experimental preference task in which rats more often chose the sweet stimulus than cocaine, a finding that also occurred with saccharin-sweetened water. The study does not suggest neuroadaptations, neurotoxicity, or more severe sugar withdrawal compared to cocaine; rather, it simply shows that sweetness won the behavioral choice over cocaine. This demonstrates that sweetness is a significant incentive for the nervous system, but addictive patterns related to saccharin intake are not typically observed. In other words, the reward associated with ingestion mechanisms is not systematically negated by the consumption of drugs like cocaine when other relevant sensory stimuli are available. Cocaine, however, produces higher presynaptic dopamine levels than sweetness, and despite this, even rats previously conditioned to cocaine showed a preference for accessing saccharin water, leading to an interesting conclusion regarding the neurobiological inevitability of addiction. Cocaine clearly produces a stronger increase in presynaptic dopamine than food; however, striatal opioid signaling may influence this preference despite the dopamine-related presynaptic dopamine.
Nevertheless, other studies show that animals prefer different rewards for different substances, not only saccharin water or various drugs, but also other rewards, such as social ones, like simply the opportunity to spend time with other rats. Although biological models of addiction produce a purely "chemical-centric" view, the evidence in animals and humans is much more nuanced. A central problem is the tendency toward a largely biological model of addiction, heavily focused on very specific signals like dopamine. Experimental models of addiction in animals often present the problem of forced choices. That is, in many cases, the animals spend 24 hours a day alone and isolated, with practically only one behavioral element available in their environment: pulling a lever that automatically administers a substance. The very act of pulling that lever depends, first and foremost, on creating a behavioral and vital amputation in the animal, forcing it into that experimental choice. Therefore, various researchers began conducting studies in less constrained environments, where animals have a variety of stimuli and rewards, allowing them to develop more flexible behavior and greater freedom of choice in their responses. In these models, the choice of drugs over other alternative behavioral options tends to decrease.
Without denying the existence of biological aspects, addiction also involves contextual and behavioral factors. This is applicable to research in humans. In real-life situations, a person is not faced with an experimental choice of "cocaine or nothing," but rather with a choice within a broader context: cocaine and work, relationships, play, food, romantic relationships, family, exploration, and so on. Many animal models of addiction begin by conditioning a rat, which has nothing to do for 24 hours a day except pull a lever that dispenses a substance-something far removed from an ecological framework compatible with the various rewards and choices available in real life. This leads to viewing addiction as a problem of choice, conditioned by two fundamental levels: neurocognitive (the individual's capacity to make decisions, evaluate consequences, alternatives, etc., a highly executive function) and environmental (the possibilities offered by an environment). The increase not only in screen time, but also in the rise of compulsive behaviors such as self-harm in children and adolescents, is largely due to the artificial life offered by computers and the lack of free time and physical play.
The concept of food addiction would be problematic and would have more contextual and behavioral components, making it more accurately described as an "addiction to the behavior of consuming calorie-dense and/or highly palatable foods." Despite this, the term addiction would still be too strong. Food is reinforcing, as well as a reward signal; it generates a certain procedural learning that we could call habit (self-gratification can become somewhat automatic). Some people may be more sensitive to reward, have certain difficulties with inhibitory control, or simply have a tendency towards hyperphagia and find a high availability of calorie-dense food. All these people cannot be lumped under the same category of "food addiction." Another difference between food and other substances is that biological aspects such as reinforcement, but also craving or dependence, are integrated and depend on other physiological processes: hunger, satiety, energy reserves, hormonal and neuroendocrine signals, food incentives, etc., making it a physiology more integrated into energy homeostasis. A pharmacological substance is an exogenous agent, so its neurobiological action, unlike food, is more independent of human metabolism in a homeostatic-nutritional sense.
The concept of food addiction is also problematic as a nosological entity, presenting all the usual psychometric problems in mental health, in addition to concerns about overdiagnosis. That is, we cannot create diagnostic categories for every specific behavior: food addiction, electric scooter addiction, Pac-Man addiction, etc. Creating a diagnosis for every behavior we consider peculiar, perseverative, excessive, etc., is highly problematic. The various manifestations of behavior do not constitute "illnesses" in themselves, but rather are ways in which behavior is expressed. Even when excessive, this "excessiveness" alone is not enough to imply "mental health problems" or to produce diagnostic categories. A distinction must be made between the fact that a construct is measurable and that, by virtue of being measurable, it implies the need to create a diagnostic entity assuming an etiological logic, or that it is clinically or socially useful enough to become a formal diagnosis. Moreover, it distorts the human experience of oneself, one's health, morally acceptable behavior, etc. On the other hand, the construct of food addiction overlaps with traits such as impulsivity, affective dysregulation, obesity, and even eating disorders, so its lack of unidimensionality is also problematic for justifying it as a concrete category at a strictly psychometric level.
We have briefly discussed pop psychology concepts such as "emotional hunger" and similar terms elsewhere.
Pop psychology concepts like "emotional hunger" and similar ones we have briefly discussed them elsewhere
FOOD ADDICTION
It has been claimed that ultra-processed foods generate "addiction" in the same way that substances such as nicotine, cocaine, or alcohol do. Many ultra-processed products are directly designed to maximize the reward signal with a combination of caloric density, texture, fat-sugar-salt ratio, additives, etc. This can produce certain neuroadaptations in reward circuits and, in some cases, difficulties with inhibitory control that partially overlap with those observed in "classic" addictions, where a pharmacological component is experimentally administered, producing more pronounced neuronal adaptations.Rather, we could say that certain ultra-processed, high-calorie, and highly palatable products can encourage greater consumption, and in some people with more vulnerable traits, even disinhibit more impulsive consumption (more driven by hedonic incentives) or compulsive consumption (more driven by learning and negative reinforcement). Calorie-dense food is more reinforcing than food with lower caloric density; that is, it produces a greater reward signal in the brain due to its higher energy density. Neuroevolutionarily, this suggests that the reward system prioritizes obtaining foods that provide more energy, as well as associated signals such as sweetness or saltiness, which anticipates sodium, essential for organisms. This is compatible with evolutionary logic. Organisms evolved in an aquatic environment rich in salts, and animal physiology has depended from very early on on ionic gradients, especially of sodium, potassium, and chloride. Therefore, when organisms colonized terrestrial environments, obtaining sodium became a significant problem.
Certain combinations of macronutrients produce a stronger reward signal (refined carbohydrates and fat, salt, even a touch of sugar, and additives such as flavor enhancers and others to improve mouthfeel, etc.). However, this alone does not produce "food addiction."
WHAT IS AN ADDICTION?
The concept of addiction, which is often perceived as a biochemical effect of a substance on the brain, must first be analyzed. However, to speak of addiction, it is not enough for a stimulus to activate dopaminergic circuits or be highly pleasurable. We are not dealing with a simply biochemical effect; it is a complex construct defined more by a clinical consensus that usually includes criteria such as a loss of control over behavior, craving, difficulty inhibiting the response, conditioned learning to environmental cues, or persistence over time despite negative consequences. Determining an addiction does not necessarily require typical biological criteria of tolerance or withdrawal. These are two possible criteria, but a person can be addicted without clear withdrawal, and tolerance/withdrawal from prolonged use can also exist without addictive behavior. Therefore, one of the problems is taking for granted a concept as complex as addiction without fully understanding it.One difference is that some substances have a pharmacological component that could be considered sufficient to produce addictive behavior, for example, through the simple passive administration of the substance, without any additional behavioral or contextual factors. In other words, some substances can create neuroadaptations that result in addictive behavior, produced at a "purely pharmacological" level. However, in most addictions considered "pharmacological," there is a behavioral and contextual component: a ritual of administration, operant learning, conditioning to environmental cues, etc., including "hard drugs" (Escohotado comes to mind, of course). That is to say, many classically addictive substances are not addictive solely due to their pharmacological and passive effects. Some studies show that the active administration of a substance, compared to the passive administration of the same substance, can be more reinforcing, depending on the model, contingencies, and context. This implies that there is more than just the substance: a behavioral and contextual component also participates in reinforcement, producing learning in response to stimuli, reinforced operant responses, etc. Ultimately, biological addiction requires a pharmacological administration model that eliminates other causes of reinforcement and contingencies, something that doesn't happen directly with food in the nervous system. Intragastric infusions of glucose or nutrients can condition taste preferences or increase intake, showing that glucose can have reinforcing value beyond the cephalic phase (without enjoying its taste, etc.), but this differs from inducing sufficiently reinforcing behavior through passive administration to be considered addictive.
It has been claimed that sweets are more addictive than cocaine, generally referring to a well-known study (Lenoir et al., 2007). However, there is actually an experimental preference task in which rats more often chose the sweet stimulus than cocaine, a finding that also occurred with saccharin-sweetened water. The study does not suggest neuroadaptations, neurotoxicity, or more severe sugar withdrawal compared to cocaine; rather, it simply shows that sweetness won the behavioral choice over cocaine. This demonstrates that sweetness is a significant incentive for the nervous system, but addictive patterns related to saccharin intake are not typically observed. In other words, the reward associated with ingestion mechanisms is not systematically negated by the consumption of drugs like cocaine when other relevant sensory stimuli are available. Cocaine, however, produces higher presynaptic dopamine levels than sweetness, and despite this, even rats previously conditioned to cocaine showed a preference for accessing saccharin water, leading to an interesting conclusion regarding the neurobiological inevitability of addiction. Cocaine clearly produces a stronger increase in presynaptic dopamine than food; however, striatal opioid signaling may influence this preference despite the dopamine-related presynaptic dopamine.
Nevertheless, other studies show that animals prefer different rewards for different substances, not only saccharin water or various drugs, but also other rewards, such as social ones, like simply the opportunity to spend time with other rats. Although biological models of addiction produce a purely "chemical-centric" view, the evidence in animals and humans is much more nuanced. A central problem is the tendency toward a largely biological model of addiction, heavily focused on very specific signals like dopamine. Experimental models of addiction in animals often present the problem of forced choices. That is, in many cases, the animals spend 24 hours a day alone and isolated, with practically only one behavioral element available in their environment: pulling a lever that automatically administers a substance. The very act of pulling that lever depends, first and foremost, on creating a behavioral and vital amputation in the animal, forcing it into that experimental choice. Therefore, various researchers began conducting studies in less constrained environments, where animals have a variety of stimuli and rewards, allowing them to develop more flexible behavior and greater freedom of choice in their responses. In these models, the choice of drugs over other alternative behavioral options tends to decrease.
Without denying the existence of biological aspects, addiction also involves contextual and behavioral factors. This is applicable to research in humans. In real-life situations, a person is not faced with an experimental choice of "cocaine or nothing," but rather with a choice within a broader context: cocaine and work, relationships, play, food, romantic relationships, family, exploration, and so on. Many animal models of addiction begin by conditioning a rat, which has nothing to do for 24 hours a day except pull a lever that dispenses a substance-something far removed from an ecological framework compatible with the various rewards and choices available in real life. This leads to viewing addiction as a problem of choice, conditioned by two fundamental levels: neurocognitive (the individual's capacity to make decisions, evaluate consequences, alternatives, etc., a highly executive function) and environmental (the possibilities offered by an environment). The increase not only in screen time, but also in the rise of compulsive behaviors such as self-harm in children and adolescents, is largely due to the artificial life offered by computers and the lack of free time and physical play.
THE DIAGNOSIS OF FOOD ADDICTION
Tools such as the Yale Food Addiction Scale (YFAS) and extensive literature suggest that ultra-processed foods can produce a pattern that shares characteristics with the patterns that define classic addictions. However, not all frequent, impulsive, or excessive consumption constitutes a formal addiction, an eating disorder, or even something that should be diagnosed. Thus, the DSM, for example, does not offer a diagnosis of food addiction for a person who simply eats ultra-processed foods very frequently.The concept of food addiction would be problematic and would have more contextual and behavioral components, making it more accurately described as an "addiction to the behavior of consuming calorie-dense and/or highly palatable foods." Despite this, the term addiction would still be too strong. Food is reinforcing, as well as a reward signal; it generates a certain procedural learning that we could call habit (self-gratification can become somewhat automatic). Some people may be more sensitive to reward, have certain difficulties with inhibitory control, or simply have a tendency towards hyperphagia and find a high availability of calorie-dense food. All these people cannot be lumped under the same category of "food addiction." Another difference between food and other substances is that biological aspects such as reinforcement, but also craving or dependence, are integrated and depend on other physiological processes: hunger, satiety, energy reserves, hormonal and neuroendocrine signals, food incentives, etc., making it a physiology more integrated into energy homeostasis. A pharmacological substance is an exogenous agent, so its neurobiological action, unlike food, is more independent of human metabolism in a homeostatic-nutritional sense.
The concept of food addiction is also problematic as a nosological entity, presenting all the usual psychometric problems in mental health, in addition to concerns about overdiagnosis. That is, we cannot create diagnostic categories for every specific behavior: food addiction, electric scooter addiction, Pac-Man addiction, etc. Creating a diagnosis for every behavior we consider peculiar, perseverative, excessive, etc., is highly problematic. The various manifestations of behavior do not constitute "illnesses" in themselves, but rather are ways in which behavior is expressed. Even when excessive, this "excessiveness" alone is not enough to imply "mental health problems" or to produce diagnostic categories. A distinction must be made between the fact that a construct is measurable and that, by virtue of being measurable, it implies the need to create a diagnostic entity assuming an etiological logic, or that it is clinically or socially useful enough to become a formal diagnosis. Moreover, it distorts the human experience of oneself, one's health, morally acceptable behavior, etc. On the other hand, the construct of food addiction overlaps with traits such as impulsivity, affective dysregulation, obesity, and even eating disorders, so its lack of unidimensionality is also problematic for justifying it as a concrete category at a strictly psychometric level.
CONCLUSION
In short, it is true that certain palatable foods can produce a strong reward signal, induce learning by conditioning stimuli, and produce the consequent relevant neuroadaptations that connect them with responses that can be reinforced. The problem is turning this reinforcing capacity into a simple diagnostic entity called "food addiction." On the other hand, there must be certain characteristics of the person that predispose them to be vulnerable to certain types of stimuli and the reinforcement they receive in response to them. In eating, reinforcement does not depend on a passively administered substance, but on the interaction between incentives, environmental cues, reward, learning, individual traits, etc. Therefore, in many cases it would be more accurate to speak of patterns of impulsive or compulsive eating, or of a certain type of conditioning, than of food addiction in the "strong" sense. Where reinforcement ends and dependence begins, and where dependence ends and addiction begins, many language games have been played out with motivations more political and for social control than anything else.We have briefly discussed pop psychology concepts such as "emotional hunger" and similar terms elsewhere.
Pop psychology concepts like "emotional hunger" and similar ones we have briefly discussed them elsewhere
#addiction #ultra-processedfoods #sugar #drugs
References:
Lenoir, M., Serre, F., Cantin, L., & Ahmed, S. H. (2007). Intense sweetness surpasses cocaine reward. PLoS ONE, 2(8), e698. https://doi.org/10.1371/journal.pone.0000698
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