Thirty Obesity Myths, Misunderstandings, and/or Oversimplifications: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022

Abstract

Background: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) is intended to provide clinicians an overview of 30 common obesity myths, misunderstandings, and/or oversimplifications.

Methods: The scientific support for this CPS is based upon published citations, clinical perspectives of OMA authors, and peer review by the Obesity Medicine Association leadership.

Results: This CPS discusses 30 common obesity myths, misunderstandings, and/or oversimplifications, utilizing referenced scientific publications such as the integrative use of other published OMA CPSs to help explain the applicable physiology/pathophysiology.

Conclusions: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) on 30 common obesity myths, misunderstandings, and/or oversimplifications is one of a series of OMA CPSs designed to assist clinicians in the care of patients with the disease of obesity. Knowledge of the underlying science may assist the obesity medicine clinician improve the care of patients with obesity.

Keywords: Adiposopathy; Clinical practice statement; Myths; Obesity; Pre-obesity.

Fig. 1

Bodyweight “Setpoint.” Some patients with obesity are said to be “set in their ways,” with established habits, behaviors, and environmental factors (e.g., social/familial culture) contributing to a bodyweight setpoint. Physical and metabolic health (e.g., mobility, insulin sensitivity/resistance) and various hormones can also contribute to bodyweight setpoint. Weight reduction maintenance may be achieved by establishing a new setpoint via altering these factors. Gravitation back towards prior habits, behaviors, environmental factors, and ill-health may result in weight regain and return to a setpoint closer to before weight reduction. The effects of weight reduction on satiety/hunger hormones are variable, with a potential long-term (1 - 2 years) hormonal changes that may favor weight regain compared to before weight reduction. Body weight reduction reduces resting metabolic rate, which contributes to a multifactorial “new setpoint” compared to before weight reduction. The net result of weight reduction is often a new setpoint with increased hunger, reduced metabolic rate, and increased potential for weight regain [33,40,41].

Fig. 2

Bodyweight “Setpoint”: Hormone Adaptations. Hormones impact body weight and alter a person's “setpoint,” often by impacting satiety and hunger [33,40,41]. An increase in body weight is generally due to an increase in caloric balance, with increased fat and muscle mass and increase in resting metabolic rate. While often ineffectual in preventing an increase in body fat, satiety hormones are typically increased, and hunger hormones are typically decreased. Once all these factors are stabilized, then this helps to establish a new “setpoint.”

Fig. 3

Illustrative Ways to Alter Bodyweight “Setpoint.”The body's “setpoint” is not fixed and may be altered through factors such as nutrition, physical activity, behavior, environmental factors, and hormones [33,40,41].

Fig. 4

Genetic, epigenetic, and familial/cultural/societal factors potentially contribute to obesity [7]. For the purposes of this figure, “Mother” is intended to identify the female origin of the egg. “Father” is intended to identify the male origin of the sperm. The terms Mother and Father are also intended to metaphorically represent caregivers of offspring – which may not necessarily by the patient's biologic Mother or Father. Epigenetic modifications involve alterations in genetic expression (e.g., deoxynucleic acid methylation and demethylation and histone modification), and not alterations in the gene sequencing. Alterations in epigenetic gene expression influences the predisposition of individuals to common metabolic diseases such as obesity, diabetes, cardiovascular disease and cancer [5,57,58].

Fig. 5

Body Weight Homeostasis. Variance exists among individuals regarding resting metabolic rate (RMR). RMR is increased among younger individuals and genetic factors such as male sex, increased height, and increased muscle. Obesity may also increase RMR, largely due to increased energy required to maintain the increased body tissues (i.e., increased adipose tissue and if applicable, increased muscle mass). Beyond RMR, other common contributors to variances in energy expenditure include non-exercise activity thermogenesis (NEAT), physical activity, and diet-induced thermogenesis (DIT). Finally, RMR can be affected by climate. Hotter environments increase RMR to cool the body; colder environments increase RMR through non-shivering thermogenesis to warm the body [8].

Fig. 6

Energy density of foods. The caloric intake of foods is not only dependent on the amount of food, but also the caloric density of food. Shown examples of the variance in kcal or Calories of foods per 100 grams of each food.

Fig. 7

Food energetics involve food choice, thermic effect of food (i.e., energy required to digest, absorb, and metabolize the macronutrient), and the storage of food macronutrients. After food is processed, marketed, and chosen (all which affect “calories in”), the energetics of food consumption includes: (a) the thermic effect of food reflecting the energy required to digest, absorb, and metabolize the macronutrient, (b) utilization of absorbed and metabolized macronutrients to perform work and other body metabolic processes, (c) and the storage of remaining excess energy – mostly as body fat. The thermic effect of food can be quantified by the percent of the macronutrient energy consumed with its digestion, absorption, and storage metabolism [95].

Fig. 8

Body heat origins. Body heat is generated by the digestion and absorption of food, generation of adenosine triphosphate or ATP (i.e., the fuel that drives cellular processes), and when ATP is used to perform cellular work. The heat generated by the cellular work of enzymatic processes can be influenced by hormones (e.g., thyroid hormone), and total body heat is regulated by the brain (i.e., hypothalamus). ∗Depending on how and when measured, the thermic effect of food may include heat generated by cellular respiration and cellular work.

Fig. 9

Factors involved in “Calories in Equals Calories Out.” Beyond the physics, clinical application of “Calories In and Calories Out” requires consideration of the complexities of multiple factors applicable to management of obesity [8,9,11,27]. ∗ Gastrointestinal hormones that may increase hunger include ghrelin and neuropeptide Y; gastrointestinal hormones that may decrease hunger/increase satiety include somatostatin, cholecystokinin, motilin, insulin, glucagon, pancreatic polypeptide, glucagon like peptide-1, oxyntomodulin, fibroblast growth factor 19, peptide YY, and amylin [9].

Fig. 10

Inaccurate perpetual energy deficit model versus physiologic adaptation and new “setpoint” model. This figure describes an adult human male weighing 66 kg (145 pounds) and who has total body energy stores of 125,822 kcal [235]. Assuming this adult human male is consuming 2000 kcal per day, then if this individual were to consume 500 kcal less per day, then the perpetual energy deficit model would predict the absurd notion this adult male would consume his entire body caloric body mass at 251 days (125,822/500) or about 8 months, despite a dietary intake of 1500 kcal per day. Conversely, the physiologic adaptation and new setpoint model might predict that a new daily caloric intake of 1500 kcal per day would result in about 5% non-water weight reduction (and thus a 5% reduction in total body energy stores), followed by a plateau and new setpoint at around 6 months determined by the patient's new energy balance [236]. This figure has acknowledged limitations in its calculations for the purpose of simplicity. Its intent is not precision in number figures, but rather to highlight the fallacy of the perpetual energy deficit model.

Fig. 11

Obesity, diabetes mellitus, hypertension, and dyslipidemia are all chronic diseases that require chronic treatment. In each case, treatment typically includes healthful nutrition, routine physical activity, behavior modification, medications, and possibly bariatric surgery. If these chronic metabolic diseases are well-controlled on medication, then stopping the medication will likely cause the chronic disease to be less well-controlled.

Fig. 12

US percent comparison of patients eligible for antiobesity medication and bariatric surgery versus those receiving antiobesity medication and bariatric procedures such as surgical treatment. The total eligible to receive anti-obesity medication is shown as 100%. The percent of eligible patients treated with anti-obesity medication is 2% [256]. The total eligible to receive bariatric surgery is shown as 100%. The percent of eligible patients treated with bariatric surgery is 1% [257].