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Rethinking Obesity
... There have been a number of articles published in the last few years bemoaning the "obesity paradox," as it has been called-namely, that individuals who fall prey to diabetes or a number of other conditions live longer and have fewer complications than those who are slimmer when diagnosed [28,29]. Additionally, individuals who are "normal weight" have lower death rates than those who are merely 20% under "normal weight;" those who are above the "ideal weight" have lower death rates still [30]. ...
... It is important to note that throughout this paper, we use the term 'fatness' interchangeably with the term, 'obesity', although the first may be preferred, as being more precise. As Ernsberger and Haskew [30] point out, 'obesity' is defined by the mathematical derivation of body mass index (BMI), rather than actual body mass composition, whereas 'fatness' refers to the adipose content of the body. In deference to widespread convention, however, we have generally used the term 'obesity'. ...
This review offers an overview of the relationship between diabetes, obstructive sleep apnea (OSA), obesity, and heart disease. It then addresses evidence that the traditional understanding of this relationship is incomplete or misleading. In the process, there is a brief discussion of the evolutionary rationale for the development and retention of OSA in light of blood sugar dysregulation, as an adaptive mechanism in response to environmental stressors, followed by a brief overview of the general concepts of epigenetics. Finally, this paper presents the results of a literature search on the epigenetic marks and changes in gene expression found in OSA and diabetes. (While some of these marks will also correlate with obesity and heart disease, that is beyond the scope of this project). We conclude with an exploration of alternative explanations for the etiology of these interlinking diseases.
... An important way to temper or qualify alarmist reporting is to air scientific debates over risk. In the area of obesity, there is debate over whether obesity per se is a serious health problem or whether current weight guidelines are appropriate (Andres et al., 1985;Campos, 2004;Campos et al., 2006;Ernsberger and Haskew, 1987;Flegal et al., 2005;Gaesser, 1996; see Saguy and Riley, 2005 for an analysis of these debates). A large body of research also documents that people who are physically fit, as measured by a treadmill test, have excellent health profiles, even if they fall into the overweight or obese categories (Blair et al., 1995(Blair et al., , 1996Blair and Church, 2004;Katzmarzyk et al., 2005;Wei et al., 1999). ...
In recent years, the “obesity epidemic” has emerged as a putative public health crisis. This article examines the interconnected role of medical science and news reporting in shaping the way obesity is framed as a social problem. Drawing on a sample of scientific publications on weight and health, and press releases and news reporting on these publications, we compare and contrast social problem frames in medical science and news reporting. We find substantial overlap in science and news reporting, but the news media do dramatize more than the studies on which they are reporting and are more likely than the original science to highlight individual blame for weight. This is partly due to the news media’s tendency to report more heavily on the most alarmist and individual-blaming scientific studies. We find some evidence that press releases also shape which articles receive media coverage and how they are framed.
... OBESITY IS one of the most prevalent diseases in the United States, affecting an estimated 25-35% of the population (9,17). However, factors that contribute to the susceptibility of the disease are only recently coming to light. ...
Sprague-Dawley rats, which become obese (obesity prone) when fed a moderately high-fat (MHF; 32.5% of kcal as fat) diet, have decreased growth hormone (GH) concentrations compared with obesity-resistant rats fed the same diet. To determine whether plasma GH concentrations are different in obesity-prone rats compared with obesity-resistant rats before diet-induced obesity occurs, total integrated GH concentrations were determined in male Sprague-Dawley rats before exposure to the MHF diet. After initial blood sampling, rats were fed an MHF diet for 15 wk, over which time the animals were separated into two discrete populations based on body weight gain. Analysis of GH in episodic blood samples showed that the obesity-prone group had a GH secretion deficit before the onset of obesity (115.2 +/- 12.9 ng . ml-1 . 200 min-1) compared with obesity-resistant rats (237.2 +/- 47.1 ng . ml-1 . 200 min-1). The GH concentration difference was due to a decrease in mean GH peak height in rats that later became obese (34.8 ng/ml) compared with rats that remained lean (74.2 ng/ml). The results suggest that GH secretion impairment exists before dietary challenge or onset of obesity and may contribute to the susceptibility to obesity observed in these animals.
Chronic and acute protein-energy malnutrition impairs immune function but little is known of the effects of energy deprivation alone. Indexes of cell-mediated immunity (CMI) were therefore studied during a 6-wk very-low-energy diet (VLED) (1.7 MJ/d, weight loss 13 +/- 1 kg, means +/- SEM) in 12 nondiabetic obese [body mass index 33 +/- 1 (in kg/m2)] subjects. Significant decreases (P less than 0.05) were observed in the numbers of total leukocytes, neutrophils, lymphocytes, and monocytes from 1 to 2 wk of the VLED and onward. Only lymphocyte counts returned to baseline levels with refeeding. The proportions of other monoclonal-antibody-defined mononuclear cell populations (except a small decrease in CD4+) did not change during dieting. [3H]Thymidine uptake by mononuclear cells cultured for 96 h decreased significantly (P less than 0.05) at wk 6 in response to concanavalin A, phytohemagglutinin, and pokeweed mitogen and after only 1 wk to phorbol myristate acetate + ionomycin. Delayed-type-hypersensitivity skin-test responses did not decrease at wk 5 vs those at baseline. The VLED produced nonspecific decreases in circulating leukocyte numbers and in vitro responses to several mitogens (of different cell-subset specificity), suggesting that in susceptible individuals or if there is longer exposure to such diets, such responses could assume clinical significance.
Type 2 diabetes, cardiovascular disease, and hypertension are comorbities associated with obesity. Treatment and prevention strategies for these comorbidities of obesity are often assumed to be the same-weight loss. Although many persons may lose weight initially, recidivism is a major concern. Therefore, medical nutrition therapy for obese persons with comorbidities should be refocused from weight loss to attaining and maintaining metabolic parameters--normal blood glucose levels, optimal lipid levels, and blood pressure levels within normal limits. Moderate weight loss is only one lifestyle strategy that can be recommended. Research has also supported other lifestyle strategies, including becoming more physically fit. In type 2 diabetes, a restricted energy diet even without weight loss, spacing of meals throughout the day, and fat intake modifications have been shown to improve glycemia. Dyslipidemia can be improved by reducing or changing the fat content of the diet. Blood pressure levels can be reduced by a diet high in fruits and vegetables and low in fat. Research is underway to determine if weight loss can prevent chronic disease; however, once comorbidities are present, lifestyle strategies should be directed toward the improvement of metabolic parameters associated with the comorbidity.
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