Peter R. Martin: Historical Vocabulary of Addiction, Vol. II

Obesity

According to the electronic version of the Oxford English Dictionary (OED), the noun obesity is partially a borrowing from French and Latin.  The noun obésité is from Middle French dating to 1550.  This French noun was derived from the classical Latin noun obēsitāt-, obēsitās meaning “fatness, stoutness.”  The derivative of this classical Latin noun is the adjective obēsus meaning “fat, stout, plump” formed from combination of the prefix ob- (meaning “in the direction of, towards, against, in the way of, in front of, in view of, on account of…”) plus ēsus, past participle of edere (meaning “to eat”).  A word with this meaning and similar derivation is also found in other Romance languages: “Italian obeso (1588), Spanish obeso (1606), French obèse (1825).” 

Highly relevant to this discussion is the verb overeat (defined in OED as “To eat too much”) because overeating (the action of the verb overeat, defined as “excessive eating”) is typically necessary for an individual to gain the body weight that characterizes obesity.  Identifying an action or behavior that is implicated in development of obesity renders the condition amenable to analysis as an addictive disorder, or behavioral addiction (Martin 2016).  The verb overeat is formed within English by derivation from prefix over- (“Forming participial adjectives”) and the verb eat (“To take into the mouth piecemeal and masticate and swallow as food; to consume as food.”).  

There is only one definition of obesity in OED: “The condition of being extremely fat or overweight; stoutness, corpulence.”  The first appearance of obesityin the English language is as an entry in A dictionarie of the French and English tongues, a historically important bilingual dictionary that represented a breakthrough at the time, compiled and published by Randle Cotgrave (fl. 1587– c. 1634) an English lexicographer (Cotgrave, Hollyband and Sherwood 1632): “Obesité, obesitie.” 

An early example of the use of the word obesity is from the English physician and medical writer Tobias Venner (1577–1660) in his book Via Recta ad Vitam Longam (Venner 1623): “Those that feare obesity, that is, would not waxe grosse.”  As implied by the title of the book, the author advised readers about how to live a long and physically healthy life — obesity was not deemed consistent with what was understood as “living well,” or Via Recta.  It is believed that Venner may have been one of the first to refer to obesity as a disease caused by societal and individual factors (Gilman 2004). 

An early example of the use of the word overeat in the English language is from Benjamin Franklin (1706–1790), the American natural philosopher, writer and revolutionary politician (Franklin and Bartlett 1925): “In hot [weather]; beware of Over-Eating and Over-Heating.”  This quotation identifies an important principle of physics by linking the calories consumed in overeating with producing body heat in addition to weight gain.  

The notion of relating body habitus to health and clinical state is apparent from the following quotation in The physician's pulse-watch: or, An essay to explain the old art of feeling the pulse and to improve it by the help of a pulse-watch by the English physician Sir John Floyer (1649–1734), best known for introducing the practice of pulse rate measurement into medicine (Floyer 1707): “By the dryness we describe the gracility or hardness; and by the humidity the plumpness or obesity of the habit of the Body.”

The high prevalence of overeating has been recognized for some time as suggested by a quotation from the Scottish novelist, essayist, poet and travel writer Robert Louis Stevenson (1850 –1894) in his novel Travels with a Donkey in the Cevennes (Stevenson 1879): “Without doubt, the most of mankind grossly overeat themselves.”  The causal association of obesity with various medical illnesses is specifically suggested by a quote from an article in the Journal of the Royal Statistical Society (Benjamin, Grebenik, Logan et al. 1955): “Apart from suspicions that diet, obesity and lack of physical exercise have something to do with the disease, no great progress is being made towards prevention or cure.” This statement predicts the now recognized involvement of obesity in a plethora of human diseases which recent research has attributed to shared fundamental mechanisms of low-grade chronic inflammation and dysfunctional metabolism (Yuan, Chen, Xia et al. 2019; Yuan, Xu, Yang et al. 2025; Drucker and Holst 2023; Drucker 2024; Cifuentes, Verdejo, Castro et al. 2024).

The idea of obesity as a disease with defined pathophysiology and complications dates to the late 19^th century (Eknoyan 2006).  Early understanding of the diagnosis and treatment of obesity greatly preceded true scientific insights about its pathogenesis and tended to be intuitive rather than specific or evidence-based (Anonymous 1889).  At first, obesity was considered little more than a bad habit with adverse consequences for health, except for the occasional cases in which metabolic abnormalities could be identified (Means 1915).  Nevertheless, the clinical presentation of obesity was insightfully portrayed quite early in the literature (Anonymous 1891):

“The undue accumulation of fat in the subcutaneous tissues and around the internal organs is not only an inconvenience, but a diseased process.  In perfect health, with proper diet and a reasonable amount of' work, the percentage of fat ought not to exceed about five per cent, of the body weight (Burdach) — [the German physiologist Karl Friedrich Burdach (1776 –1847) who first used the word “biology”] — and more than this indicates a departure from the healthy metabolism of the organism.  It shows that the constructive forces are working in a wrong direction, and the energy which is used in the useless storing up of fat leaves the other tissues and organs in want.  Consequently, the adult man or woman who is “putting on flesh,” is not generally to be congratulated.  Fat people are less able to resist the attacks of disease or the shock of injuries and operations than the moderately thin.  In ordinary every-day life they are at a decided disadvantage; their respiratory muscles cannot so easily act; their heart is often handicapped by the deposit on it; and the least exertion throws them into a perspiration…  A person whose limbs and body are covered with adipose tissue is in the position of a man carrying a heavy burden and too warmly clothed…  In endeavouring to ascertain the reason why some people are corpulent and others not, we must realise at once that the condition is markedly hereditary.  As one breed of pigs is noted for the ease with which it fattens, so with men.

“The amount of food and the proportions of its constituents have, doubtless, something to do with obesity.  As to the actual quantity, it has often been observed that fat people eat less than thin ones; but when the process of fattening begins, it is almost always found that the subject is a great eater.” 

Obesity was eventually recognized to be a condition with generally two clinical presentations, each associated with distinct pathological features (Albrink and Meigs 1964): adult-onset obesity is characterized by a central distribution of fat tissue in the body with enlargement of the dimensions of individual fat cells (hypertrophy of adipocytes); and lifelong obesity in which there is both central and peripheral distributions of body fat tissue with a higher than normal number of fat cells in the tissue (hyperplasia of adipocytes).  Interestingly, a similar approach based on the age of onset of the disorder has been found useful for typing alcoholism with distinct implications for inheritance, pathogenesis and treatment of the disorder (Cloninger 1987). 

Like all addictive disorders, obesity is a complex, multifactorial condition with various contributing factors, including genetic predisposition (Loos and Yeo 2022), sedentary lifestyle, overconsumption of high-calorie and processed foods, psychological and emotional factors (stress, depression, anxiety and other mental health conditions), metabolic and hormonal imbalances (hypothyroidism, insulin resistance and hormonal dysregulation) and environmental and societal influences (access to healthy foods, food marketing and socioeconomic status).  Therefore, it cannot be casually assumed that obesity is simply the result of overeating beyond the metabolic needs of the individual (Williams 1981); but it has long been recognized that the majority of individuals with obesity, do indeed, ingest excessive amounts of food for a variety of reasons (Anonymous 1891; Newburgh and Johnston 1930; Dodd, Birky and Stalling 1976).  Of course, the role of overeating beyond one’s metabolic requirements in the etiology of obesity nicely parallels the pathogenesis of addictive disorders which are characterized by out-of-control and self-destructive involvement with substance use or other behaviors (Scott 1983; Martin, Weinberg and Bealer 2007). 

Around the turn of the 21^st century, research on dysfunctional regulation of the ingestion of food and/or of body weight came to the fore as mechanistically linked to obesity(Zhang, Proenca, Maffei et al. 1994; Shell 2003).  These related mechanisms have both been found to contribute not only to obesity, but also to eating disorders and other theoretically related conditions such as addictive disorders and certain mental and medical illnesses, e.g. anxiety/depression and type 2 diabetes mellitus (Simansky 2005).  

Moreover, non-homeostatic ingestion of food has been demonstrated to be related to changes in neurotransmitter metabolism and gene expression in brain regions relevant to the reward pathways and learning mechanisms both fundamental to addictive disorders (Martin 2019, 2023).  Additionally, behavioral findings, hormonal changes and neuroimaging data in animals and humans have also shown parallels between craving for drugs of abuse and appetite for highly rewarding foods (Martin 2020a).

Overlapping brain alterations demonstrated at the levels of genes/molecules/receptors, neurons and neural circuits as well as behavioral and neuroeconomic perspectives associated with craving and non-homeostatic consumption of food and of drugs of abuse have been translated to development of strategies for treating these disorders in the clinic.  The fact that several of the same medications may benefit both overeating and substance use disorders further supports the parallelism between these conditions (Chiu, Lee and Shen 2007; Takahashi 2010; Drucker 2024; Gudzune and Kushner 2024).  

Moreover, there is a long history of using surgical strategies to reduce body weight, from simple anatomical removal of unsightly fat depositions (Peters 1901) to more physiologically based bariatric surgery involving the surgical removal of absorptive surfaces of the bowel.  The most recent findings have shown that intensive medical therapy plus bariatric surgery resulted in glycemic control in significantly more patients than did medical therapy alone with enhanced quality of life (Schauer, Bhatt, Kirwan et al. 2014). 

However, the consequences of bariatric surgery are not all positive—for as yet unknown reasons (reward signaling, genetically mediated mechanisms and pharmacokinetics), certain bariatric procedures elevate the risk of alcohol use disorder post-operatively, again supporting the fascinating relationships between food ingestion and substance use disorders (King, Chen, Mitchell et al. 2012).  

Of course, the most exciting recent development in association of obesity and substance use disorders has been revealed by research showing that medications such as the glucagon-like peptide-1 (GLP-1) receptor agonists designated for treatment of obesity may potentially be effective in management of alcohol and drug use disorders (Jerlhag 2019).  (It would be even more interesting if such medications were found beneficial in management of other behavioral addictions such as gambling or sexual activity [Martin 2021, 2022], although no such research has yet been attempted.)

Some of the neurobiological effects of pharmacotherapy of obesity and addictive disorders may complement the beneficial effects of behavioral and psychosocial treatment strategies (Grilo, Ivezaj, Tek et al. 2024).  Therefore, an integrated pharmacopsychosocial approach, whereby psychosocial approaches are combined with medications, are thought to offer synergistic benefits and improved outcomes for care of patients with both nonhomeostatic eating and various addictive disorders (Martin, Weinberg and Bealer 2007).  Integrated treatment plans, including behavioral therapy, nutritional counseling, healthy lifestyle changes such as regular physical activity, balanced diet and stress management techniques and medical management, can benefit individuals struggling with both obesity and substance use disorders. 

In the same vein, behavioral interventions that have been demonstrated to be effective for prevention of childhood obesity (Heerman, Rothman, Sanders et al. 2024) very much resemble approaches that have been successfully employed for prevention of addictive disorders (Martin 2020b). 

Investigations of the parallels between the pathophysiological underpinnings of obesity and addictive disorders have received impetus from recent interest and advances in the neuroscience of brain reward circuits (Wang, Volkow, Thanos et al. 2004; Volkow, Michaelides and, Baler. 2019).  These studies initially focused on reward mechanisms underpinning substance use disorders but are now addressing behavioral addictions including obesity/overeating.  The neurotransmitter dopamine was originally related to alerting and motoric activity (Hornykiewicz 1966) and was not considered as particularly relevant to feeding behaviors (Hoebel 1971).

Subsequently, dopamine neurotransmission came to be viewed as fundamental to experience of pleasure and reward (Ungerstedt 1971; Smith and Schneider 1988; Everitt and Robbins 2005) and a neurobiologically important link has been shaped between addiction to substances and eating behaviors (Wang, , Shokri Kojori, Yuan et al. 2020).  Emerging research suggests that the overconsumption of highly palatable, processed foods can trigger similar neurological responses in brain reward and pleasure centers as substance addictions.  

Individuals susceptible to addictive behaviors may have a harder time moderating their intake of rewarding foods, leading to a cycle of craving, non-homeostatic ingestion of food or binge eating and weight gain.  This relationship between food and alcohol ingestion has been alluded to in the Big Book of Alcoholics Anonymous for almost a century (Alcoholics Anonymous 2020).

Our understanding of the phenotypic expression of obesity has also expanded much beyond the simple “disease concept” of non-homeostatic ingestion of food.  Accordingly, the high prevalence of obesity in the population (Ng, Dai, Cogen et al. 2024) has a synergistic impact on health through disease processes in which the consequences of overeating and substance use disorders interact (Matarazzo, Hennekens, Dunn et al. 2024). 

Obesity is now recognized to be inexorably intertwined with various chronic medical and psychiatric conditions in its clinical manifestations, acting as precursors or complications of the disorder.  The ever-expanding concept of co-occurring illnesses that comprise the phenotypic expression of obesity remains an area of active research for physicians and scientists from multiple specialties affected by overeating (Jebeile, Gow, Baur et al. 2019; Drucker and Holst 2023; Watanabe, Wilmanski, Diener et al. 2023; Drucker 2024).   

Medical conditions that are currently recognized to have a causal association with obesity include the following disorders: cardiovascular (hypertension, atherosclerosis), metabolic (type 2 diabetes mellitus, dyslipidemia, metabolic syndrome), respiratory (obstructive sleep apnea), gastrointestinal (gastroesophageal reflux disease [GERD], non-alcoholic fatty liver disease [NAFLD], non-alcoholic steatohepatitis [NASH], gallbladder disease), musculoskeletal (osteoarthritis, especially in weight-bearing joints like the knees and hips, gout), reproductive (polycystic ovary syndrome [PCOS], infertility, gestational diabetes and preeclampsia), increased risk of certain cancers and dermatological (Acanthosis nigricans).   

The connection between the many psychiatric disorders associated with obesity is strongly bidirectional in nature.  This means that obesity can contribute to the development of the psychiatric conditions which, in turn, can play an important role in causing obesity.  Individuals may use substances or food as a way to cope with stress, anxiety, depression or other emotional issues (Christensen 1993; Patel and Schlundt 2001).  This can lead to a cycle whereby mental disorders contribute to substance use or overeating, which in turn exacerbates mental health issues.

For example, obesity can lead to poor self-esteem, social isolation and body image concerns, which can contribute to depression (Jebeile, Gow, Baur et al. 2019).  Conversely, depression or the medications used for its treatment can lead to changes in eating and activity patterns that contribute to weight gain.   Analogously, some studies suggest that individuals with bipolar disorder may have higher rates of obesity, in part because of the use of certain mood-stabilizing medications, lifestyle factors, and the mood swings associated with bipolar disorder can contribute to weight gain (McElroy, Kotwal, Malhotra et al. 2004). 

Individuals with obesity may also experience higher levels of anxiety, potentially due to concerns about health, social stigma or body image and anxiety disorders have been linked with obesity.  Moreover, a specific relationship exists between trauma exposure and development of obesity and resulting post-traumatic stress disorder (PTSD) due to emotional eating (self-soothing), unhealthy food choices (Marquez, Risica, Mathis et al. 2021) and changes in metabolism and stress hormones which seems to implicate the shared role of allostatic load (McEwen 2000; Fischer, Na, Nagamatsu et al. 2024). 

Attention-deficit/hyperactivity disorder (ADHD) has been linked to obesity, possibly due to impulsive eating behaviors, difficulties with self-regulation, and the use of certain medications (Altfas 2002).  Finally, binge eating disorder is characterized by recurrent episodes of eating large quantities of food, often rapidly and to the point of discomfort and is significantly more common in individuals with obesity than is bulimia nervosa (ZelitchYanovski 1993).

In summary, obesity is the outcome of overeating, a behavior characterized by non-homeostatic ingestion of food.  Obesity has widespread effects on the mental and physical health of the population which parallels and interdigitates with some of the consequences of substance use disorders.  Overeating can result from dysfunctional regulation of appetite and/or body weight.  In particular, activation of appetite has been conceptualized as paralleling stimulation of reward circuits that underpin substance use disorders and allows us to consider overeating as a behavioral addiction. 

This construct is now receiving much support from recent advances in research on the possible benefits of newly developed medications such as incretins and other neuropharmacological agents for treatment of obesity, which seem also to have beneficial effects in treatment of substance use disorders but have yet to be studied in other behavioral addictions (gambling or sexual addiction).

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