Being overweight or obese is a medical disease like diabetes or hypertension. It is important for everyone to understand this.
Like diabetes and hypertension, overweight/obesity requires medical treatment. None of the three diseases is simply a matter of will power. All three diseases require medical treatment.
And, fortunately, our medical treatments for overweight/obesity are getting better.
And that’s why I’ve excerpted from today’s article.
Here are excerpts:
The widespread, but unproven, assumption that body weight is entirely controllable by lifestyle choices and that self-directed efforts can reverse even severe forms of obesity or type 2 diabetes44 could explain the low level of public support for coverage of anti-obesity interventions beyond diet and exercise45, regardless of their evidence base. For example, many public and private health insurers either do not provide coverage or have substantive limitations in the coverage of metabolic surgery, including fulfilment of a number of criteria for which there is limited or no clinical evidence46,47. These attitudes are in stark contrast with coverage of treatment for other chronic diseases (for example, cancer, heart disease, and osteoarthritis) that are not conditional to similar restrictions, and for which use of similarly arbitrary coverage criteria would be socially indefensible and ethically objectionable.
Stigmatization of surgical treatment for obesity
Metabolic surgery (also known as bariatric surgery) provides a compelling example of how weight stigma can also extend to treatments for obesity. Compared with individuals who lose weight using diet and exercise alone, those who lose weight through metabolic surgery can be at risk of stronger stigma because they are stereotyped as being lazy and being less responsible for their weight loss48,49. It is not surprising that many hide their surgical status49.
Despite evidence of efficacy and cost-effectiveness50,51 of surgical interventions for obesity, only 0.1–2% of surgical candidates who qualify worldwide currently undergo such surgery52. A research survey in the United States showed that only 19.2% of responders supported insurance coverage of metabolic operations45.
Discrimination in employment
Workplace discrimination against individuals with overweight and obesity is common in high-income countries58. Individuals with obesity have reported receiving lower starting salaries, can be ranked as less qualified, and can work longer hours than do thinner employees59. Persons with obesity can be perceived to be less suitable for employment and are less likely to be invited for an interview60, or, if employed, are perceived to be less successful compared with thinner peers61. Women with obesity are the especially unlikely to be hired62.
For the vast majority of individuals with obesity who experience discrimination in recruitment or the workplace, there is generally no protection under current legislations62. Although some US states have recently introduced a legislation that protects against height and weight discrimination65, the Civil Rights Act of 1964 does not identify weight as a protected characteristic, and only in some instances a condition of very high BMI can meet the definition of disability under a 2008 amendment of the Americans with Disabilities Act legislation66. This amendment, however, does not cover individuals who are not disabled, even though they can also be victims of weight discrimination.
Weight bias and research
Research into obesity and diabetes is underfunded compared with other diseases, relative to their burden and costs on society. For example, the US National Institutes of Health’s projected budgets for cancer, HIV/AIDS, and digestive diseases are 5–10 times greater than the budget for obesity, despite that the latter affecting substantially more Americans.
Causes and contributors for weight stigma
Evidence from several countries68,69,70,71 shows that when individuals attribute the causes of obesity primarily to internal, controllable factors or personal choices, they exhibit higher weight bias, whereas acknowledging the complex causes of obesity (including elements such as genetics, biology, and environmental factors) is associated with lower levels of weight bias and less blame. These findings suggest that the prevailing narrative of obesity in news coverage, public health campaigns, and political discourse—centered heavily on notions of personal responsibility72,73—can play an important part in the expression of weight stigma and reinforce weight-based stereotypes74.
The gap between scientific evidence and misconceptions in the public narrative
The notion that the causes of overweight and obesity depend on individuals’ faults, such as laziness and gluttony, stems from the assumption that body weight is entirely under volitional control. This assumption and many of its corollaries are now at odds with a definitive body of biological and clinical evidence developed over the last few decades.
Here are five falsehoods debunked in the above article:
1. Body weight = calories in – calories out [False]
This equation is often oversimplified in the public narrative of obesity, and even by HCPs, as if the two variables (calories in and calories out) were dependent only on two factors, amount of food consumed and exercise performed, therefore implying that body weight is completely controllable by voluntary decisions to eat less and exercise more.
However, both variables of the equation depend on factors additional to just eating and exercising. For instance, energy intake depends on the amount of food consumed, but also on the amount of food-derived energy absorbed through the gastrointestinal tract, which in turn is influenced by multiple factors, such as digestive enzymes, bile acids, microbiota, gut hormones, and neural signals, none of which are under voluntary control. Similarly, energy output is not entirely accounted for by physical activity, which only contributes to ~30% of total daily energy expenditure. Metabolic rate accounts for 60–80% of total daily energy expenditure, with the thermic effect of feeding constituting approximately 10%77. Thus, even when individuals expend energy via exercise, except for elite athletes the overall contribution to energy expenditure is relatively small78.
The existence of a powerful, precise homeostatic system that maintains body weight within a relatively narrow, individualized range is supported by scientific evidence. This regulatory system can counteract voluntary efforts to reduce body weight by activating potent compensatory biologic responses (for example, increased appetite and decreased metabolic rate) that promote weight regain. Clinical evidence shows that a 10% weight loss elicits compensatory changes in energy expenditure79, and modifications of appetite signals that increase hunger and reduce satiety. These metabolic and biologic adaptations can persist long-term after losing weight and continue even after partial weight regain80.
2. Obesity is primarily caused by voluntary overeating and a sedentary lifestyle [False]
Although this concept might appear to be a straightforward conclusion, given common personal experiences of the fluctuations of body weight during periods of excess energy intake or sedentary lifestyle, the evidence supports a more nuanced situation. For example, in a Canadian study that used accelerometers to measure physical activity, girls with obesity took more steps per day than girls within the normal weight range81. Similar findings have been observed for adults82. Despite substantially higher levels of physical activity, total daily energy expenditure among hunter-gatherers in Africa’s savannahs today is largely similar to that of adults living in modern European or US cities, where obesity prevalence is high83. These findings contrast with conventional views that primarily attribute the cause of obesity to sedentary lifestyles and suggest that compensatory metabolic adaptations maintain total energy expenditure relatively constant among human populations and across various levels of physical activities.
Additional evidence is now also available indicating other possible causes and contributors to obesity, including genetic84 and epigenetic factors85, foodborne factors86, sleep deprivation and circadian dysrhythmia87, psychological stress, endocrine disruptors, medications, and intrauterine and intergenerational effects. These factors do not require overeating or physical inactivity to explain excess weight88,89,90. A dominant role of genetic factors in obesity pathogenesis has also been demonstrated in studies comparing the concordance of body weight among fraternal versus identical twins91, for example, as well as studies of adults adopted as infants compared with their biological and adoptive parents77,92. Hence, overeating and reduced physical activity, when present, might be symptoms rather than the root causes of obesity93. Finally, the frequent failure of therapeutic and public-health strategies focused on the recommendation to ‘eat less and move more’ should call into question a causal role of voluntary overeating and sedentary lifestyle as primary causes of obesity.
3. Obesity is a lifestyle choice [False]
Persons with obesity typically recognize obesity as a serious health problem, rather than a conscious choice. More than two thirds of 3,008 individuals with obesity surveyed in the ACTION Study considered obesity to be as or more serious than other health conditions, including high blood pressure, diabetes, and depression94. Given the negative effects of obesity on quality of life, the well-known risks of serious complications and reduced life expectancy associated with it, it is a misconception to define obesity as a choice.
4. Obesity is a condition, not a disease [False]
Labeling obesity as a disease, risk factor, or condition has implications for treatment and policy development and can contribute to promoting or mitigating stigmatizing views toward affected individuals. An argument often used against labeling obesity a disease is that doing so communicates a societal message that individual responsibility is not relevant in obesity, thus reducing adherence to healthier lifestyles. Defining obesity as a disease, or not, however, should be based on objective medical and biological evidence, not sociologic implications.
The criteria generally used for recognition of disease status are clearly fulfilled in many individuals with obesity as commonly defined, albeit not all. These criteria include specific signs or symptoms (such as increased adiposity), reduced quality of life, and/or increased risk of further illness, complications, and deviation from normal physiology—or well-characterized pathophysiology (for example, inflammation, insulin resistance, and alterations of hormonal signals regulating satiety and appetite).
As reviewed in a statement from the World Obesity Federation95, many medical societies as well as the World Health Organization, the US Food and Drug Association, the US National Institutes of Health, and the Nagoya Declaration have now defined obesity as a disease or disease process.
Admittedly, however, defining obesity as a disease, but measuring it only by BMI thresholds (as in contemporary medical practice), risks labeling as ill some individuals who, despite possibly being at risk of future illness, have no current evidence of disease—for example, in cases where high BMI results from being particularly muscular or having short stature. This potential risk of misdiagnosis underscores the inadequacy of current diagnostic criteria for obesity, and the need to identify more meaningful clinical and biological criteria than just BMI to diagnose the disease.
5. Severe obesity is usually reversible by voluntarily eating less and exercising more [False]
This assumption is also not supported by evidence. First, body weight and fat mass are known to be regulated by numerous physiological mechanisms, beyond voluntary food intake and physical exercise. A large body of clinical evidence has shown that voluntary attempts to eat less and exercise more render only modest effects on body weight in most individuals with severe obesity96,97. When fat mass decreases, the body responds with reduced resting energy expenditure79,80 and changes in signals that increase hunger and reduce satiety93 (for example, leptin, ghrelin)98. These compensatory metabolic and biologic adaptations promote weight regain and persist for as long as persons are in the reduced-energy state, even if they gain some weight back98.
Metabolic surgery is often referred to as an easy way out, based on assumptions that these interventions mechanically restrict food intake in a manner that individuals are not sufficiently disciplined to achieve on their own. However, evidence demonstrates that surgical interventions elicit numerous metabolic effects opposite to the compensatory physiologic responses normally triggered by diet-induced weight reduction, thereby promoting major, long-term weight loss99. Such mechanisms include a paradoxical decrease in appetite and increase in metabolic rate, which change adaptively in the opposite directions to those following most non-surgical weight loss77. There are also favorable post-operative alterations in gastrointestinal hormones, bile-acid signaling, gut microbiota, absorption and utilization of glucose by the gut, modulations of gastrointestinal nutrient signaling that influence insulin sensitivity, and others100.