The obesity epidemic has been widely publicized in the media worldwide. Investigators at all levels have been looking for factors that have contributed to the development of this epidemic. Two major ...theories have been proposed: (1) sedentary lifestyle and (2) variety and ease of inexpensive palatable foods. In the present review, we analyze how nutrients like sugar that are often used to make foods more appealing could also lead to habituation and even in some cases addiction thereby uniquely contributing to the obesity epidemic. We review the evolutionary aspects of feeding and how they have shaped the human brain to function in "survival mode" signaling to "eat as much as you can while you can." This leads to our present understanding of how the dopaminergic system is involved in reward and its functions in hedonistic rewards, like eating of highly palatable foods, and drug addiction. We also review how other neurotransmitters, like acetylcholine, interact in the satiation processes to counteract the dopamine system. Lastly, we analyze the important question of whether there is sufficient empirical evidence of sugar addiction, discussed within the broader context of food addiction.
The role of stress, trauma, and adversity particularly early in life has been identified as a contributing factor in both drug and food addictions. While links between traumatic stress and substance ...use disorders are well documented, the pathways to food addiction and obesity are less established. This review focuses on psychosocial and neurobiological factors that may increase risk for addiction-like behaviors and ultimately increase BMI over the lifespan. Early childhood and adolescent adversity can induce long-lasting alterations in the glucocorticoid and dopamine systems that lead to increased addiction vulnerability later in life. Allostatic load, the hypothalamic-pituitary-adrenal axis, and emerging data on epigenetics in the context of biological embedding are highlighted. A conceptual model for food addiction is proposed, which integrates data on the biological embedding of adversity as well as upstream psychological, social, and environmental factors. Dietary restraint as a feature of disordered eating is discussed as an important contextual factor related to food addiction. Discussion of various public health and policy considerations are based on the concept that improved knowledge of biopsychosocial mechanisms contributing to food addiction may decrease stigma associated with obesity and disordered eating behavior.
Ultra-processed foods (UPFs) like pastries, packaged snacks, fast foods, and sweetened beverages have become dominant in the modern food supply and are strongly associated with numerous public health ...concerns. While the physical health consequences of UPF intake have been well documented (e.g., increased risks of cardiometabolic conditions), less empirical discussion has emphasized the mental health consequences of chronic UPF consumption. Notably, the unique characteristics of UPFs (e.g., artificially high levels of reinforcing ingredients) influence biological processes (e.g., dopamine signaling) in a manner that may contribute to poorer psychological functioning for some individuals. Importantly, gold-standard behavioral lifestyle interventions and treatments specifically for disordered eating do not acknowledge the direct role that UPFs may play in sensitizing reward-related neural functioning, disrupting metabolic responses, and motivating subsequent UPF cravings and intake. The lack of consideration for the influences of UPFs on mental health is particularly problematic given the growing scientific support for the addictive properties of these foods and the utility of ultra-processed food addiction (UPFA) as a novel clinical phenotype endorsed by 14–20% of individuals across international samples. The overarching aim of the present review is to summarize the science of how UPFs may affect mental health, emphasizing contributing biological mechanisms. Specifically, the authors will (1) describe how corporate-sponsored research and financial agendas have contributed to contention and debate about the role of UPFs in health; (2) define UPFs and their nutritional characteristics; (3) review observed associations between UPF intake and mental health conditions, especially with depression; (4) outline the evidence for UPFA; and (5) describe nuanced treatment considerations for comorbid UPFA and eating disorders.
It is well established that obesity has reached pandemic proportions. Over the last four decades the prevalence of obesity and morbid obesity have risen substantially in both men and women worldwide. ...Although there are many causative factors leading to excessive weight gain including genetics and sedentary lifestyle, the transformation of the food environment has undoubtedly contributed to the dangerously high rates of obesity. The current food landscape is inundated with food engineered to contain artificially high levels of sugar and fat. Overconsumption of these types of food overrides the homeostatic mechanisms, which under normal circumstances regulate appetite and body mass, leading to hedonic eating. Evidence from the animal literature has illustrated nutrition-influenced perturbations that occur within the mesolimbic dopamine pathway, as well as maladaptive behavioral responses that result from chronic ingestion of highly palatable foods. These neurobehavioral adaptations are similar to what is observed in drugs of abuse. Recent evidence also supports that maternal exposure to these foods is capable of provoking neurobehavioral alterations in offspring. Therefore the purpose of this review is to summarize the current developments on the addictive potential of highly palatable foods, as well as illuminate the impact of maternal hyperphagia and obesity on the reward-related neurocircuitry and addiction-like behaviors in the offspring.
The opioid crisis has reached epidemic proportions in the United States with rising overdose death rates. Identifying the underlying factors that contribute to addiction vulnerability may lead to ...more effective prevention strategies. Supply side environmental factors are a major contributing component. Psychosocial factors such as stress, trauma, and adverse childhood experiences have been linked to emotional pain leading to self-medication. Genetic and epigenetic factors associated with brain reward pathways and impulsivity are known predictors of addiction vulnerability. This review attempts to present a biopsychosocial approach that connects various social and biological theories related to the addiction crisis. The emerging role of nutrition therapy with an emphasis on gastrointestinal health in the treatment of opioid use disorder is presented. The biopsychosocial model integrates concepts from several disciplines, emphasizing multicausality rather than a reductionist approach. Potential solutions at multiple levels are presented, considering individual as well as population health. This single cohesive framework is based on the interdependency of the entire system, identifying risk and protective factors that may influence substance-seeking behavior. Nutrition should be included as one facet of a multidisciplinary approach toward improved recovery outcomes. Cross-disciplinary collaborative efforts, new ideas, and fiscal resources will be critical to address the epidemic.
•Adverse childhood experiences (ACEs) have been associated with a wide range of unfavorable health conditions, including substance use disorders and obesity.•Meta-analysis of observational studies ...(n=118,691) linking ACEs to adult obesity found a pooled odds ratio of 1.46 (1.28, 1.64) with moderate heterogeneity (I2=70.8%).•Systematic review of population-based studies linking ACEs to adult obesity suggests that social disruption, changes in health behaviors, and the chronic stress response are the most frequently mentioned explanations for this association.•Other unmeasured confounders such as food addiction and eating disorders likely exist and should be considered in future research.
Adverse childhood experiences (ACEs) can become biologically embedded leaving a lasting signature on multiple body systems. ACE scores have been used to associate childhood adversity to a wide range of adverse health conditions over the life course, most notably substance-related disorders. Multiple studies have shown that the presence of elevated ACE scores predicts obesity in adulthood. However, a gap exists in the literature elucidating the pathways from childhood adversity to increased BMI in adulthood. We systematically reviewed these mechanisms as well as discuss novel plausible pathways. We searched PubMed, PsycInfo, Embase, and Web of Science and after applying exclusion criteria identified 18 articles for qualitative analysis. The most commonly cited mechanisms linking ACEs to obesity are social disruption, health behaviors, and chronic stress response. Ten observational studies (n=118,691) were quantitatively summarized and demonstrated a positive association between ACE and adult obesity with a pooled odds ratio of 1.46 (CI=1.28, 1.64) with moderate heterogeneity (I2=70.8%). Our results found a 46% increase in the odds of adult obesity following exposure to multiple ACEs. Based on our qualitative synthesis and review of the most recent relevant literature, we propose biologically plausible explanations for the significant positive relationship between ACEs and adult obesity. Reducing exposure to ACEs, improved screening and detection of trauma, better access to trauma-informed care, and improvements to the food environment are likely to improve downstream health outcomes related to eating behavior.
We call for a reevaluation of the long-standing dogmatic nutritional principle that "all foods fit" for all cases of eating disorders (EDs) and its corollary, "there are no bad foods" (for anyone ...ever) during ED treatment. Based on accumulated scientific research, we challenge these ideologies as outdated, confusing, and potentially harmful to many patients. We review the evidence that indicates the folly of these assumptions and show there are a variety of exceptions to these rules, including (1) food allergies, sensitivities, and intolerances, (2) religious and spiritual preferences or doctrines, and (3) the ubiquitous emergence and widespread availability of ultra-processed foods leading to the potential development of addiction-like eating and a higher prevalence of various medical and psychiatric comorbidities, as well as higher mortality. This evidence supports a nutritional psychiatry approach that should be integrated into (rather than dissociated from) ED treatment research and practice.
Food addiction, specifically ultra-processed food addiction, has been discussed in thousands of peer-reviewed publications. Although 20% of adults meet criteria for this condition, food addiction is ...not a recognized clinical diagnosis, leading to a dearth of tested treatment protocols and published outcome data. Growing numbers of clinicians are offering services to individuals on the basis that the food addiction construct has clinical utility. This audit reports on clinical teams across three locations offering a common approach to programs delivered online. Each team focused on a whole food low-carbohydrate approach along with delivering educational materials and psychosocial support relating to food addiction recovery. The programs involved weekly sessions for 10–14 weeks, followed by monthly support. The data comprised pre- and post- program outcomes relating to food addiction symptoms measured by the modified Yale Food Addiction Scale 2.0, ICD-10 symptoms of food related substance use disorder (CRAVED), mental wellbeing as measured by the short version of the Warwick Edinburgh Mental Wellbeing Scale, and body weight. Sample size across programs was 103 participants. Food addiction symptoms were significantly reduced across settings; mYFAS2 score −1.52 (95% CI: −2.22, −0.81), CRAVED score −1.53 (95% CI: −1.93, −1.13) and body weight was reduced −2.34 kg (95% CI: −4.02, −0.66). Mental wellbeing showed significant improvements across all settings; short version Warwick Edinburgh Mental Wellbeing Scale 2.37 (95% CI: 1.55, 3.19). Follow-up data will be published in due course. Further research is needed to evaluate and compare long-term interventions for this complex and increasingly burdensome biopsychosocial condition.
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