Emotional & Psychological IssuesAddressed by the Morbidly Obese

Notwithstanding the current zeitgeist of political correctness, people who are obese or seriously obese are people whom it’s still okay to despise. They are widely regarded as suffering from a character disorder, mental illness or moral weakness.

They are the subject of demeaning jokes, viz., “I am often unfairly accused of being insensitive to the issue of obesity in America, treating it as a joke instead of as the formidable, gigantic, mountainous, flibbity-flabbity, wiggly-jiggly problem that it is” (Weingarten, 2010, p.32). They are subject to unmitigated sarcasm such as Theodore Dalrymple’s, article oh-so-cleverly- titled “Our Big Problem; Obesity is Spreading – and Eating Away at America’s Economy and Health.” In the Wall Street Journal (online), New York, New York.: May 7, 2010, he snarked, “In the West, the march (or waddle) of obesity is in step with other social (or antisocial) developments. Obesity in Britain, for example, has increased pari passu with the splintering of families: and now it is never too early to teach children lack of self-control.” Pari passu!

Highly educated mental health professionals deem themselves capable of rendering diagnostic judgments, sight unseen! In a letter to the editor of the December 2, 2007 New York Times Magazine, a psychiatrist said “I have no doubt that a markedly obese patient without other medical cause for obesity (i.e., thyroid disease) already has a severe problem. Without treating the compulsion that underlies such behavior, it is no wonder that patients who have surgery but no psychiatric treatment may [italics mine] develop “new” [quotes Dr.Amanda Itzkoff’s] psychiatric symptoms like gambling, compulsive shopping and alcoholism.” Note, Dr. Itzkoff has no doubt that the patient has “a severe problem”. What it is exactly that requires her to put quotes around “new” requires clarification; but the one idea the doctor can’t seem to entertain is that without psychiatric treatment the patient may just get thinner!

In their comparative case study of the way American news media report on eating disorders as opposed to overweight/obesity, Saguy and Gruys (2010) note that, “While anorexia and overweight/obesity are both medical categories related to body weight and eating, they have strikingly different social and moral connotations. In the contemporary United States, being heavy is seen as the embodiment of gluttony, sloth and/or stupidity, while slenderness is taken as the embodiment of virtue” (232) In the same article, they note that anorexics are portrayed by the media as “victims of a terrible illness beyond their and their parents’ control, while obesity is caused by bad individual behavior, including, in the case of children, parental neglect” (232)

Women who are obese are less likely to marry and are more likely to be poor and to earn far less than women of normal weight. In a simulated employment interview, moderately obese individuals, especially women, face bias in hiring. A study cited in the September 28, 2010 issue of the New York Times (D6), shows that While a man “racks up $2646 annually in extra expenses if he is obese, a woman’s obesity costs her $4879, almost twice as much.” This is attributable to the fact that the wages of obese and non-obese men are not significantly different, but those of obese women are significantly lower than those of non-obese women.

Notwithstanding their excellent literature review, Friedman and Brownell (1995) advocated taking a more “skeptical attitude” toward their finding that obesity is unrelated to psychopathology. They did develop a well-considered, programmatic approach to investigating the relationship between psychopathology and obesity. (Note, the authors used “psychopathology” and “psychological disturbance” interchangeably.) They examined studies that did use appropriate statistics and found no differences between obese and nonobese girls with respect to psychological disturbance. They found similar results in studies of obese adults. They even found some studies that reported that obese individuals display less psychopathology than normal weight individuals. They conclude, “It is reasonable to conclude from this considerable literature that obesity is not associated with increased psychopathology.”

Yet, still skeptical and reluctant to believe this data, they went on to state that meta-analyses suggested that obese individuals presenting for treatment of obesity (as distinct from the obese people who do not present for treatment) do display a higher prevalence of psychopathology, though the authors do not spell out the nature of the pathology. Obscuring the validity of that finding, however, is the fact that among those comprising the group which presented for treatment of obesity were patients who were not, in fact, obese (p.9)! Further, the direction of the obesity-psychopathology relationship is implied, yet the absence of “psychopathology” in the obese who do not present for treatment suggests that the two variables may be unrelated. That is, it is not clear whether the “psychopathology” promoted the obesity or the obesity promoted the psychopathology or something else promoted both or whether successfully treating the obesity would reduce the psychopathology.

The authors proposed that the “third generation” research should compare obese individuals in treatment with a variety of control groups, including comparing the profiles between those presenting for surgical vs. psychological treatment. In that vein, they hypothesized that bariatric surgery patients may have high rates of psychopathology. Their study drew their sample of 1000 from a single surgical practice at a large, urban medical center. Of that 1000, 36% consented to participate in research. In the end, only 29% (288) of these people participated. They were mostly women, white and married and had no more than a high school education. Of that group, only 28.5% (82 in number) had any personality disorder, the most common being Avoidant Personality Disorder 17% (49). That is, 5% of the original sample of 1000 had Avoidant Personality Disorder! They conclude, “Existing studies have been useful in demonstrating an absence of clear and consistent differences between obese and nonobese populations in general. Hence, it is probably safe to say that not all obese people suffer psychological distress from their condition…We believe that attention should turn from whether obese persons suffer psychological distress to who will suffer and in what ways.” P16

Finally, in a later study, Friedman and Brownell (2002) suggest “We believe attention should turn from whether obese persons suffer psychological distress to who will suffer and in what ways. This philosophy suggests a risk-factor approach that will identify individuals in whom psychological problems may occur, conditions likely to promote suffering and their interaction. Elucidating the psychological consequences of obesity may be important in establishing the pathogenesis and treatment of obesity, and in understanding the lives of obese individuals” (p 397).

In view of the data indicating the contempt with which the obese and seriously obese are often treated, as well as the prevalence of comorbid physical disorders, it would be surprising to find no evidence of “psychological distress”. In fact, studies searching for evidence of lifetime prevalence of Axis I and Axis II psychiatric disorders (Kalarchian, et. Al. 2007) do link mood, eating and weight disorders, as is typical, call for further research. But, as Wonderlich, (2002) has observed regarding eating disorders, “Relationships between eating disorders and personality have been frequently discussed in the literature: 1. Personality predisposes to or increases the risk of developing eating disorders; 2) elevations in personality traits or disorders are a simple complication, consequence, or scar of the eating disorder, and 3) eating disorders and personality share no causal relationship and both are either influenced by a third variable, or, perhaps rest on the same spectrum of disturbance. Only rarely have empirical studies tested any of these models” (p. 205).

A concept that was prevalent in the obesity literature is the notion that body weight is self-regulated and obesity represents a deviation from the norm. (Drewnowski, 2002) A typical view in the 70’s was that obesity is a psychological problem. One example, was the now-discredited ‘externality” hypothesis which held that the obese were more responsive to external cures than to the internal cues signaling hunger. (Drewnowski, 2002; Stroebe, p.6)

Currently, the tide with respect to understanding obesity is returning to interactionism. One proponent of this view is Stroebe (2008) who asked, “Why is self-regulation of weight so difficult for so many people? Rather than considering this a purely psychological problem, the book takes the broader perspective that the self-regulation of weight is determined by interplay of biological, environmental and psychological factors.” (p. 5) With respect to genetic epidemiology of the obesity epidemic, Bouchard in Fairburn and Brownell (2002) uses a statistic called the lambda coefficient. The lambda coefficient is the ratio of the risk of being obese when a biological relative is obese compared to the risk in the population at large. Lambda values are accepted as evidence for a strong genetic effect for obesity, particularly severe obesity. However, they note that the risk is also markedly elevated in the spouse of the proband (p. 17) and raises the complication of assortative mating (p. 19). In a study to be published in an upcoming article in The Journal of Clinical Endocrinology and Metabolism and cited in the September, 2010 edition of “Endocrine News, Vol. 35, No.9, p. 8, Crujeiras, AB; Goyenechea, E; Abete I, et al. placed a group of 104 obese/overweight volunteers on an 8-week hypocaloric diet and measured plasma fasting ghrelin, leptin and insulin at baseline, 8 weeks and 32 weeks. They assumed these hormones would point to those who were more prone to weight gain. They found a drop in ghrelin following 8 weeks on a hypocaloric diet correlated with an increased risk for weight regain, whereas a greater reduction in leptin indicated weight-loss maintenance.”

According to DiLalla (2004) “…from the point of view of explaining the genesis of behavior, the very attempt to separate [genotype or traits vs. environment or situation] is a fools’ errand. Both sides of the old nature-nurture debate have been led to the conclusion that internal and external mechanisms of behavior necessarily interact etiologically and statistically in the determination of behavior. P.186. Blundell (2002) presents a list of biological dispositions that create vulnerability for weight gain (p46). He characterizes the interaction of genes and environment in the following way: “These risk factors alone would be unlikely to lead to a positive energy balance in a benign environment; that is one in which the food supply and the cultural habits work against excessive consumption. In most of today’s societies, however, the food environment exploits the biologically based disposition that promotes the intake of high energy dense foods” (p. 46). Exposure to an abundance of palatable, energy-dense foods gives rise to an overconsumption of energy. This is not biologically driven by need state and not consciously intended and it is referred to as “passive overconsumption.” Passive overconsumption, he notes, does not appear to generate a desire to undereat. When eating is curtailed voluntarily, regulatory mechanisms will oppose this undersupply and generate a drive to eat (p 44). Obese people do not appear to get any help from their adipose tissue to reduce their appetites. The operation of the regulatory system is” asymmetrical” (p 45). Collier (2002) also reports that findings from twin studies suggest that about half the vulnerability to develop eating disorders is inherited. But, unlike Mendelian genetic disorders such as Huntington’s disease which are caused by the effect of a single gene in each person, “complex” diseases are caused by the interaction of multiple genes with the environment…An accumulation of these genes, together with adverse environmental factors, increases risk until the disease develops in those carrying the greatest genetic and environmental loading. This is known as the liability-threshold model. He notes that risk factors for complex genetic disorders cannot be reliability used to predict who will become ill. (243)

According to Bulik (2002), “modern westernized environments promote obesity” (p.22). Consistent with this statement, a demographic analysis of the rise in the prevalence of the US Population Overweight and/or Obese demonstrates that the increases in body mass index are primarily due to period effects, not cohort or age effects. From the ordered logistical regression analyses, the authors find that the protective influence of factors such as education, income and age on an individual’s body mass index have decreased over time. The US adult population has increased its BMI every 5-year period between 1976 and 2001. “The big picture is that no group has been immune to the increases.”

References

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