The Canadian Obesity Epidemic: An Historical Perspective

Objective: To examine temporal trends in stature, body mass, body mass index (BMI), and the prevalence of overweight and obesity in Canada. Research Methods and Procedures: Data for adults 20 to 64 years of age were compared across eight Canadian surveys conducted between 1953 and 1998. Temporal trends in stature and body mass were examined using regression, and changes in weight‐for‐height were expressed as changes from 1953. BMI data were available from 1970 to 1972 to examine changes in overweight and obesity. Qualitative changes in the BMI distribution were examined using Tukey mean‐difference plots. Results: Significant temporal trends in stature and body mass have occurred since 1953 in Canada. Median stature increased 1.4 cm/decade in men and 1.1 cm/decade in women, whereas median body mass increased 1.9 kg/decade in men and 0.8 kg/decade in women. Increases in the 75th percentile of body mass were larger than the median. The average weight‐for‐height increased 5.1% in men and 4.9% in women from 1953. Furthermore, the prevalences of overweight and obesity have increased from 40.0% and 9.7% in 1970–1972 to 50.7% and 14.9% in 1998, respectively. The entire BMI distribution has shifted to the right since 1970–1972 and has become more skewed to the right for men than for women. Discussion: There have been significant increases in stature and body mass in Canada over the last 45 years. Body mass has increased more than stature, particularly in the upper percentiles, which has resulted in the currently observed high prevalences of overweight and obesity.     

Self‐Selected Macronutrient Diet Affects Energy and Glucose Metabolism in Brown Fat‐Ablated Mice

Objective: Obese transgenic UCP‐DTA mice have largely ablated brown adipose tissue and develop obesity and diabetes, which are highly susceptible to a high‐fat diet. We investigated macronutrient self‐selection and its effect on development of obesity, diabetes, and energy homeostasis in UCP‐DTA mice. Research Methods and Procedures: UCP‐DTA and wild‐type littermates were fed a semisynthetic macronutrient choice diet (CD) ad libitum from weaning until 17 weeks. Energy homeostasis was assessed by measurement of food intake, food digestibility, body composition, and energy expenditure. Diabetes was assessed by blood glucose measurements and insulin tolerance test. Results: Wild‐type and UCP‐DTA mice showed a high fat preference and increased energy digestion on CD compared with a low‐fat standard diet. On CD, wild‐type mice accumulated less body fat (16.9%) than UCP‐DTA (32.6%) mice, although they had a higher overall energy intake. Compared with wild‐type mice, resting metabolic rate was reduced in UCP‐DTA mice irrespective of diet. UCP‐DTA mice progressively decreased their carbohydrate intake, resulting in an almost complete avoidance of carbohydrate. UCP‐DTA mice developed severe insulin resistance but showed decreased fed and fasted blood glucose on CD. Discussion: In contrast to wild‐type mice, UCP‐DTA mice were not able to reduce their weight gain efficiency on CD. This suggests that, because of the high fat preference of the background strain and the increased metabolic efficiency, brown adipose tissue‐deficient mice still develop obesity and insulin resistance on a macronutrient CD even when decreasing overall energy intake. Through the avoidance of carbohydrates, however, they are able to maintain normoglycemia.     

Neural regulation of bone remodeling: Identifying novel neural molecules and pathways between brain and bone

The metabolism and homeostasis of the skeletal system have historically been considered to be associated with the endocrine system. However, this view has been expanded with the recognition of several neural pathways playing important roles in the regulation of bone metabolism via central relays. In particular, bone metabolism and homeostasis have been reported to be precisely modulated by the central neural signaling. Initiated by the finding of leptin, the axis of neural regulation on bone expands rapidly. The semaphorin–plexin system plays an important role in the cross-talk between osteoclasts and osteoblasts; a complex system has also been identified and includes neuropeptide Y and cannabinoids. These findings facilitate our understanding of the central neuropeptides and neural factors in the modulation of bone metabolism and homeostasis, and these neuronal pathways also represent an area of research scenario that identifies the novel regulation between brain and bone. These regulatory mechanisms correlate with other homeostatic networks and demonstrate a more intricate and synergetic bone biology than previously envisioned. As such, this review summarizes the current knowledge of the neural regulation of bone metabolism and homeostasis, as well as its role in skeletal diseases and discusses the emerging challenges presented in this field.     

Norepinephrine‐ and Epinephrine‐deficient Mice Gain Weight Normally on a High‐fat Diet

Objective: Signaling through adrenergic receptors (ARs) by norepinephrine (NE) and epinephrine (Epi) regulates weight gain when mice are fed a high‐fat diet (HFD) by controlling diet‐induced thermogenesis. Thus, one would predict that mice unable to make NE/Epi because of inactivation of the dopamine β‐hydroxylase gene (Dbh‐null mice) would have a propensity to become obese. We characterized the response of Dbh‐null and control mice to a HFD. Research Methods and Procedures: Dbh‐null and control mice were fed an HFD or a regular diet (RD) for 2 months. Body weight, adiposity, muscle triglyceride levels, and adipocyte size were measured, as were circulating leptin, adiponectin, triglyceride, glucose, and insulin levels. A glucose tolerance test was also preformed. Results: Dbh‐null mice gain weight normally on an HFD and have the same adiposity. Their serum triglyceride and leptin levels are normal, but adipocytes are ～30% smaller than controls. Dbh‐null mice maintain low blood glucose levels and glucose tolerance when exposed to the HFD in contrast to controls. Discussion: Complete lack of NE/Epi does not predispose to obesity. Because mice lacking all three βARs become obese on an HFD, an imbalance of signaling through α‐ and βARs seems to be responsible for obesity. Surprisingly, Dbh‐null mice maintain glucose tolerance.     

Effects of Obesity Phenotype on Coronary Heart Disease Risk Factors in Response to Weight Loss

Objective: To determine whether there is a difference in risk‐factor improvement for coronary heart disease (CHD) between the intra‐abdominal fat (IF) and subcutaneous fat (SF) obesity phenotypes after weight loss. Research Methods and Procedures: Subjects included 55 mildly obese women (body mass index, 25 to 36 kg/m²; age range, 34 to 63 years) who had at least two of three CHD risk factors [systolic blood pressure (SBP), >140 mm Hg; total cholesterol (TC), >220 mg/dL; fasting plasma glucose, >110 mg/dL). Using computed tomography, IF obesity was classified as ≥110 cm² of the IF area measured; subjects with <110 cm² were classified as having SF obesity. The IF and SF obesity groups were divided into diet‐only and diet‐plus‐exercise groups. Assays and measurements were performed before and after a 14‐week (98‐day) intervention. Results: Weight was reduced by 7 to 10 kg in each group. The IF and SF areas, SBP, diastolic blood pressure, TC, and low‐density lipoprotein‐cholesterol were significantly reduced in all groups (p < 0.01). Reduction in IF area was greater in IF obesity than in SF obesity, whereas no differences were observed in the improvement of CHD risk factors. Sample sizes needed for observing a significant difference for SBP, TC, triglycerides, and fasting plasma glucose were greater than the number of subjects in this study. Discussion: Our results suggest that the influence of the obesity phenotype on improving CHD risk factors is not apparent. A larger study is needed to prove the validity of this finding.     

The Quantitative Relationship Between “The Metabolic Syndrome” and Abdominal Obesity in Women

Abdominal obesity is closely associated with the presence of metabolic risk factors and elevated blood pressure in selected materials. This has, however, never been analyzed quantitatively in a non-selected cohort. Therefore, in a population-based study of 1462 Swedish women, four selected risk factors for non-insulin dependent diabetes mellitus (NIDDM) and cardiovascular disease (CVD), serum triglycerides, blood glucose and systolic blood pressure and also serum insulin in a subsample, were examined in relation to regional and overall obesity. This was performed by subdividing the age adjusted sample into quintiles of waist to hip circumference ratio (WHR) or body mass index (BMI) as indicators of abdominal distribution of body fat and overall obesity, respectively. The risk factors serum triglycerides, blood glucose, blood pressure and serum insulin were defined as being elevated when the value of the risk factor was higher than the mean plus one or two standard deviations of the total age-adjusted cohort. The percentage of women with elevated risk factors according to this definition was then calculated in each of these quintiles. Having a risk factor which was elevated according to the definition was significantly correlated to WHR and BMI (p<0.0001) independent of age. The presence of one or several of these elevated risk factors was clearly higher than expected in the fifth quintile of WHR, and to a lesser extent in the fifth quintile of BMI while this was not the case in the lower quintiles of WHR and BMI. When studying the combination of the WHR and BMI, the presence of risk factors higher than the mean plus two standard deviations increased gradually with WHR in all five quintiles of BMI. A significant association was observed between WHR and presence of risk factors independent of BMI (p<0.0001) but BMI did not remain significantly correlated to presence of risk factors when controlling for WHR (p=0.09). These results indicate that abdominal distribution of body fat in women independently of general obesity is closely associated with metabolic risk factors including elevated blood pressure, a metabolic syndrome with increased risk for cardiovascular disease and non-insulin dependent diabetes mellitus.     

Establishing Meal Patterns by Lickometry in the Marmoset Monkey (Callithrix jacchus): Translational Applications From the Bench to the Field and the Clinic

The ability to measure and interpret variables associated with feeding behavior and food intake is essential to a variety of nonhuman primate study modalities. The development of a technique to accurately and efficiently measure food intake and meal patterning in captivity will enhance both the interpretation of foraging behavior in the wild as well as our ability to model clinically relevant human feeding pathologies. In this study, we successfully developed the use of a rodent lickometer system to monitor meal patterning in captive common marmosets. We describe the modifications necessary for this type of instrumentation to be used successfully with marmosets. We define variables of interest that relate to both previous rodent literature and human clinical measures. Finally, we relate our findings to potential translational value for both primate field research and biomedical applications. Am. J. Primatol. 74:901‐914, 2012. © 2012 Wiley Periodicals, Inc.     

The Thermic Effect of Food and Obesity: A Critical Review

DE JONGE, LILIAN, GEORGE BRAY. The thermic effect of food and obesity: A critical review. This review has examined the factors that influence the thermic effect of food (TEF) by evaluating 49 studies that have compared subjects who are obese with those who are lean. Meal size, meal composition, the nature of the previous diet, insulin resistance, physical activity, and ageing influence TEF. In the studies of individuals who are obese or lean, of those who used intravenous glucose infusions, all but one found an impaired thermic response. A total of 29 out of 49 studies of individuals of normal weight or with obesity were identified where there was no difference in age between the groups, and where the subjects who were “overweight” were clearly obese. Of these 29, 22 reported a statistically significant reduction in TEF, 3 studies were not designed to look primarily at the effect of obesity on TEF, and the other 4 may not have had sufficiently palatable meals. From this review, we conclude that the reduction of TEF in obesity is related to the degree of insulin resistance, which may be influenced by a low level of sympathetic activity.     

Stimulatory Effect of Leptin on Nitric Oxide Production Is Impaired in Dietary‐Induced Obesity

Objective: We investigated the effect of leptin on nitric oxide production in lean and rats made obese by a high‐calorie diet. Research Methods and Procedures: The animals were placed in metabolic cages, and urine was collected in 2‐hour periods after leptin (1 mg/kg intraperintoneally) or vehicle administration. Blood was obtained 0.5, 1, 2, 4, or 6 hours after injection. Results: Leptin had no effect on systolic blood pressure in either lean or obese animals. Plasma concentration of NO metabolites (nitrites + nitrates, NO_x) increased in lean rats by 31.5%, 58.0%, and 27.9% at 1, 2, and 4 hours after leptin injection, respectively. In the obese group, plasma NO_x increased only at 2 hours (+36.5%). Leptin increased urinary NO_x excretion by 31.8% in the first 2‐hour period after injection in lean but not in obese rats. In lean animals, leptin elevated plasma cyclic 3′, 5′‐guanosine monophosphate (cGMP) at 1, 2, and 4 hours by 35.3%, 96.3%, and 57.3%, respectively. In the obese group, plasma cGMP was higher only at 2 and 4 hours (+44.6% and +32.1%, respectively). Urinary excretion of cGMP increased in lean animals by 67.1% in the first period and by 50.4% in the second period. In the obese group, leptin induced a 53.9% increase in urinary cGMP excretion only in the first 2‐hour period. Discussion: The stimulatory effect of leptin on NO production is impaired in dietary‐induced obesity; however, leptin does not increase blood pressure in obese animals, suggesting that other NO—independent depressor mechanisms are stimulated.     

Leptin Responses to Weight Loss in Postmenopausal Women: Relationship to Sex‐Hormone Binding Globulin and Visceral Obesity

Objective: Leptin concentrations increase with obesity and tend to decrease with weight loss. However, there is large variation in the response of serum leptin levels to decreases in body weight. This study examines which endocrine and body composition factors are related to changes in leptin concentrations following weight loss in obese, postmenopausal women. Research Methods and Procedures: Body composition (DXA), visceral obesity (computed tomography), leptin, cortisol, insulin, and sex hormone‐binding globulin (SHBG) concentrations were measured in 54 obese (body mass index [BMI] = 32.0 ± 4.5 kg/m²; mean ± SD), women (60 ± 6 years) before and after a 6‐month hypocaloric diet (250 to 350 kcal/day deficit). Results: Body weight decreased by 5.8 ± 3.4 kg (7.1%) and leptin levels decreased by 6.6 ± 11.9 ng/mL (14.5%) after the 6‐month treatment. Insulin levels decreased 10% (p < 0.05), but mean SHBG and cortisol levels did not change significantly. Relative changes in leptin with weight loss correlated positively with relative changes in body weight (r = 0.50, p < 0.0001), fat mass (r = 0.38, p < 0.01), subcutaneous fat area (r = 0.52, p < 0.0001), and with baseline values of SHBG (r = 0.38, p < 0.01) and baseline intra‐abdominal fat area (r = ?0.27, p < 0.06). Stepwise multiple regression analysis showed that baseline SHBG levels (r² = 0.24, p < 0.01), relative changes in body weight (cumulative r² = 0.40, p < 0.05), and baseline intra‐abdominal fat area (cumulative r² = 0.48, p < 0.05) were the only independent predictors of the relative change in leptin, accounting for 48% of the variance. Discussion: These results suggest that obese, postmenopausal women with a lower initial SHBG and more visceral obesity have a greater decrease in leptin with weight loss, independent of the amount of weight lost.     

Influence of dietary saturated fat content on adiposity,macrophage behavior,inflammation, and metabolism: composition matters

We examined the effects of three high-fat diets (HFD), differing in the percentage of total calories from saturated fat (SF) (6%, 12%, and 24%) but identical in total fat (40%), on body composition, macrophage behavior, inflammation, and metabolic dysfunction in mice. Diets were administered for 16 weeks. Body composition and metabolism [glucose, insulin, triglycerides, LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), total cholesterol (TC)] were examined monthly. Adipose tissue (AT) expression of marker genes for M1 and M2 macrophages and inflammatory mediators [Toll-like receptor (TLR)-2, TLR-4, MCP-1, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, suppressor of cytokine signaling (SOCS)1, IFN-γ] was measured along with activation of nuclear factor kappa-B (NFκB), c-Jun N-terminal kinase (JNK), and p38- mitogen-activated protein kinase (MAPK). AT macrophage infiltration was examined using immunohistochemistry. Circulating MCP-1, IL-6, adiponectin, and leptin were also measured. SF content, independent of total fat, can profoundly affect adiposity, macrophage behavior, inflammation, and metabolic dysfunction. In general, the 12%-SF diet, most closely mimicking the standard American diet, led to the greatest adiposity, macrophage infiltration, and insulin resistance (IR), whereas the 6%-SF and 24%-SF diets produced lower levels of these variables, with the 24%-SF diet resulting in the least degree of IR and the highest TC/HDL-C ratio. Macrophage behavior, inflammation, and IR following HFD are heavily influenced by dietary SF content; however, these responses are not necessarily proportional to the SF percentage.     

Recent insights into body weight control: from physiology to pathology.

Over the past several years, new modulators of feeding and body weight have been discovered, and our knowledge of the mechanisms and neurohumoral interactions between anorexigenic and orexigenic compounds has increased dramatically. This review aims to summarize the present knowledge of the role of leptin and several hypothalamic neuropeptides, such as neuropeptide Y (NPY), corticotropin-releasing hormone (CRH) and melanocortins, in the regulation of appetite and body weight. It also presents the progress made in the design of interactions between leptin and hypothalamic peptides in the regulation of feeding. The role of these compounds in the pathogenesis of obesity in animals and humans, and their potential usefulness in the treatment of this disorder, are discussed.     

肥胖成因的新视角：代谢性炎症诱导食物奖赏异常

近年来,肥胖已成为全球亟待解决的重要公共卫生问题。越来越多的研究发现,食物奖赏在肥胖的形成与发展过程中发挥重要作用。最近的研究表明,由于能量过剩引发的代谢性炎症可能通过多种生理途径干扰正常的奖赏信号传递,从而促进肥胖的发展。基于这一观点,推测产生肥胖的原因可能与代谢性炎症诱导食物奖赏异常有关。因此,深入探讨肥胖、食物奖赏和代谢性炎症之间的关系,总结代谢性炎症诱导食物奖赏异常的可能机制,可为预防和治疗肥胖提供新的思路和理论支持。     

Obesity in Older Adults: Technical Review and Position Statement of the American Society for Nutrition and NAASO,The Obesity Society

Obesity causes serious medical complications and impairs quality of life. Moreover, in older persons, obesity can exacerbate the age‐related decline in physical function and lead to frailty. However, appropriate treatment for obesity in older persons is controversial because of the reduction in relative health risks associated with increasing body mass index and the concern that weight loss could have potential harmful effects in the older population. This joint position statement from the American Society for Nutrition and NAASO, The Obesity Society reviews the clinical issues related to obesity in older persons and provides health professionals with appropriate weight‐management guidelines for obese older patients. The current data show that weight‐loss therapy improves physical function, quality of life, and the medical complications associated with obesity in older persons. Therefore, weight‐loss therapy that minimizes muscle and bone losses is recommended for older persons who are obese and who have functional impairments or medical complications that can benefit from weight loss.     

The Effects of Drugs Used to Treat Obesity on the Autonomic Nervous System

Objective: Body fatness is partly under hypothalamic control with effector limbs, which include the endocrine system and the autonomic nervous system (ANS). In previous studies we have shown, in both obese and never‐obese subjects, that weight increase leads to increased sympathetic and decreased parasympathetic activity, whereas weight decrease leads to decreased sympathetic and increased parasympathetic activity. We now report on the involvement of such ANS mechanisms in the action of anti‐obesity drugs, independent of change in weight. Research Methods and Procedures: Normal weight males (ages 22 to 38 years) were fed a solid food diet, carefully measured to maintain body weight, for at least 2 weeks, as inpatients at the Rockefeller University General Clinical Research Center. In a single‐blind, placebo/drug/placebo design, eight subjects received dexfenfluramine, seven phentermine (PHE), and seven sibutramine (SIB). ANS measures of parasympathetic and sympathetic activity included: determination of amount of parasympathetic control (PC) and sympathetic control (SC) of heart period (interbeat interval), using sequential pharmacological blockade by intravenous administration of atropine and esmolol. These autonomic controls of heart period are used to estimate the overall level of parasympathetic and sympathetic activities. Norepinephrine, dopamine, and epinephrine levels in 24‐hour urine collections were measured and also resting metabolic rate (RMR). Results: Sufficient food intake maintained constant body weight in all groups. PHE and SIB produced significant increases in SC but no change in PC or in RMR. In contrast, dexfenfluramine produced marked decreases in SC, PC, and RMR. For all three drugs, the effects on urine catecholamines directly paralleled changes in cardiac measures of SC. Discussion: ANS responses to PHE and SIB were anticipated. The large, and unanticipated, response to dexfenfluramine suggests further study to determine whether there could be any relation of these ANS changes to the adverse cardiovascular effects of treatment with dexfenfluramine.     

食源性肥胖对SD大鼠卵泡发育相关激素及瘦素水平的影响

目的:通过建立大鼠肥胖模型,检测其血脂水平与一系列卵泡发育相关激素指标,试探讨肥胖对大鼠卵泡发育相关激素的影响及可能机制。方法:从30只6-7周龄的SD雌性大鼠中随机选取10只采用普通饲料饲养8周作为对照组(con组);其余20只采用高脂饲料饲养2周,再从中选取体质量增长较快的10只大鼠,继续高脂饮食饲养6周,作为肥胖组(orl组)。第8周末,称量两组大鼠体质量后,禁食水24小时,次日用断尾法采血,离心分离血清,应用化学发光法检测血清雌激素(Eestrogen,E2)、卵泡刺激素(Follicle-Stimulating Hormone,FSH)、黄体生成素(Luteinizing Hormone,LH)、睾酮(Testosterone,T)、瘦素(Leptin)及血脂水平。结果:1.肥胖组大鼠的血清血脂Leptin水平较对照组明显升高;2.肥胖组大鼠血清T水平较对照组明显升高3.肥胖组大鼠血清Leptin水平较对照组明显升高,差异无显著性;4.肥胖组大鼠血清LH水平较对照组稍降低,差异无显著性;5.肥胖组大鼠血清E2、FSH水平与对照组水平相当,无显著变化。结论:高脂饮食诱导的肥胖可能会引起大鼠一系列激素水平的变化,进而影响卵泡发育,这可能与瘦素水平升高有关。     

持续高频刺激改变短刺激产生的神经网络效应

不同时长的电脉冲高频刺激(high frequency stimulation,HFS)对于脑神经系统具有不同的作用.其中,数秒时长的短促HFS可通过"点燃"效应制作动物癫痫模型,也可以产生长时间保持的突触可塑性变化,而数分钟以上的长时HFS却可以安全地用于临床的深部脑刺激,治疗多种脑疾病.因此推测,持续的HFS可以改变短促刺激产生的效应.为了验证此推测,在大鼠海马CA1区的输入轴突纤维Schaffer侧支上,分别施加5 s和2 min两种时长的100 Hz HFS,并监测刺激结束后下游神经元群体对于单脉冲测试的响应电位,即群峰电位(population spike,PS).结果显示,5 s短HFS结束时会紧跟后放电痫样活动,并且,从测试脉冲诱发的PS幅值和潜伏期可见,短HFS诱导的兴奋性增强可以维持数十分钟.反之,2 min的长HFS结束时紧随之后的是数十秒无发放活动的静息期,而且,PS在数分钟内即恢复到HFS前的基线水平.这些结果表明,长时HFS的后期刺激可以改变前期短促刺激对于下游神经网络的作用,即消除短刺激可能产生的长时程兴奋效应.此发现对于深入了解高频刺激的作用机制、促进深部脑刺激的临床应用具有重要意义.     

The interaction between predation risk and food ration on behavior and morphology of Eurasian perch

The risk of both predation and food level has been shown to affect phenotypic development of organisms. However, these two factors also influence animal behavior that in turn may influence phenotypic development. Hence, it might be difficult to disentangle the behavioral effect from the predator or resource‐level effects. This is because the presence of predators and high resource levels usually results in a lower activity, which in turn affects energy expenditure that is used for development and growth. It is therefore necessary to study how behavior interacts with changes in body shape with regard to resource density and predators. Here, we use the classic predator‐induced morphological defense in fish to study the interaction between predator cues, resource availability, and behavioral activity with the aim to determine their relative contribution to changes in body shape. We show that all three variables, the presence of a predator, food level, and activity, both additively and interactively, affected the body shape of perch. In general, the presence of predators, lower swimming activity, and higher food levels induced a deep body shape, with predation and behavior having similar effect and food treatment the smallest effect. The shape changes seemed to be mediated by changes in growth rate as body condition showed a similar effect as shape with regard to food‐level and predator treatments. Our results suggests that shape changes in animals to one environmental factor, for example, predation risk, can be context dependent, and depend on food levels or behavioral responses. Theoretical and empirical studies should further explore how this context dependence affects fitness components such as resource gain and mortality and their implications for population dynamics.     

The Harm of Bioethics: A Critique of Singer and Callahan on Obesity

Debate concerning the social impact of obesity has been ongoing since at least the 1980s. Bioethicists, however, have been relatively silent. If obesity is addressed it tends to be in the context of resource allocation or clinical procedures such as bariatric surgery. However, prominent bioethicists Peter Singer and Dan Callahan have recently entered the obesity debate to argue that obesity is not simply a clinical or personal issue but an ethical issue with social and political consequences. This article critically examines two problematic aspects of Singer and Callahan's respective approaches. First, there is an uncritical assumption that individuals are autonomous agents responsible for health‐related effects associated with food choices. In their view, individuals are obese because they choose certain foods or refrain from physical activity. However, this view alone does not justify intervention. Both Singer and Callahan recognize that individuals are free to make foolish choices so long as they do not harm others. It is at this point that the second problematic aspect arises. To interfere legitimately in the liberty of individuals, they invoke the harm principle. I contend, however, that in making this move both Singer and Callahan rely on superficial readings of public health research to amplify the harm caused by obese individuals and ignore pertinent epidemiological research on the social determinants of obesity. I argue that the mobilization of the harm principle and corresponding focus on individual behaviours without careful consideration of the empirical research is itself a form of harm that needs to be taken seriously.