The Socioeconomic Burden of Obesity

Kjellberg, Jakob; Larsen, Arendse Tange; Ibsen, Rikke; Højgaard, Betina

doi:10.1159/000480404

Cited by 58 publications

(45 citation statements)

References 43 publications

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“…However, despite socioeconomic deprivation, we have nowadays more than sufficient food for most, and therefore little need to have an expanded energy reservoir. Hence, obesity is no longer considered a survival advantage but a source of obesity-associated comorbidities, which www.wjmh.org chronically orchestrate unhealthy consequences as a function of lifetime expanding [18,19]. There is no doubt that secondary, functional HG is one of these unhealthy consequences.…”

Section: Obesity Metabolic Syndrome and Functional Hypogonadismmentioning

confidence: 99%

Treatment of Functional Hypogonadism Besides Pharmacological Substitution

Corona

Rastrelli

Morelli

et al. 2020

World J Mens Health

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Section: Obesity Metabolic Syndrome and Functional Hypogonadismmentioning

confidence: 99%

Treatment of Functional Hypogonadism Besides Pharmacological Substitution

Corona

Rastrelli

Morelli

et al. 2020

World J Mens Health

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“…Because of these serious consequences, 1 in 5 deaths in the United States is associated with obesity. Furthermore, cost and socioeconomic burden of overweight and obesity to individuals and to the nations are huge (8)(9)(10). In view of these, in June 2013, the American Medical Association recognized obesity as a disease (11).…”

Section: Introductionmentioning

confidence: 99%

P2Y2 Receptor Promotes High-Fat Diet-Induced Obesity

et al. 2020

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P2Y 2 , a G protein-coupled receptor (R), is expressed in all organs involved in the development of obesity and insulin resistance. To explore the role of it in diet-induced obesity, we fed male P2Y 2-R whole body knockout (KO) and wild type (WT) mice (B6D2 genetic background) with regular diet (CNT; 10% calories as fat) or high-fat diet (HFD; 60% calories as fat) with free access to food and water for 16 weeks, and euthanized them. Adjusted for body weights (BW), KO mice consumed modestly, but significantly more HFD vs. WT mice, and excreted well-formed feces with no taint of fat or oil. Starting from the 2nd week, HFD-WT mice displayed significantly higher BW with terminal mean difference of 22% vs. HFD-KO mice. Terminal weights of white adipose tissue (WAT) were significantly lower in the HFD-KO vs. HFD-WT mice. The expression of P2Y 2-R mRNA in WAT was increased by 2-fold in HFD-fed WT mice. Serum insulin, leptin and adiponectin levels were significantly elevated in the HFD-WT mice, but not in the HFD-KO mice. When induced in vitro, preadipocytes derived from KO mice fed regular diet did not differentiate and mature as robustly as those from the WT mice, as assessed by cellular expansion and accumulation of lipid droplets. Blockade of P2Y 2-R by AR-C118925 in preadipocytes derived from WT mice prevented differentiation and maturation. Under basal conditions, KO mice had significantly higher serum triglycerides and showed slightly impaired lipid tolerance as compared to the WT mice. HFD-fed KO mice had significantly better glucose tolerance (GTT) as compared to HFD-fed WT mice. Whole body insulin sensitivity and mRNA expression of insulin receptor, IRS-1 and GLUT4 in WAT was significantly higher in HFD-fed KO mice vs. HFD-fed WT mice. On the contrary, the expression of pro-inflammatory molecules MCP-1, CCR2, CD68, and F4/80 were significantly higher in the WAT of HFD-fed WT vs. HFD-fed KO mice. These data suggest that P2Y 2-R plays a significant role in the development of diet-induced obesity by promoting adipogenesis and inflammation, and altering the production of adipokines and lipids and their metabolism in adipose tissue, and thereby facilitates HFD-induced insulin resistance.

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“…A recent study showed that the health care costs to society of having a Body Mass Index (BMI) between 30 and 40 are app. € 1400 higher per year than the costs of the average person [ 70 ]. The study was based on data in various registries.…”

Section: Discussionmentioning

confidence: 99%

In Defence of informed consent for health record research - why arguments from ‘easy rescue’, ‘no harm’ and ‘consent bias’ fail

Ploug

2020

BMC Med Ethics

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Background Health data holds great potential for improved treatments. Big data research and machine learning models have been shown to hold great promise for improved diagnostics and treatment planning. The potential is tied, however, to the availability of personal health data. In recent years, it has been argued that data from health records should be available for health research, and that individuals have a duty to make the data available for such research. A central point of debate is whether such secondary use of health data requires informed consent. Main body In response to recent writings this paper argues that a requirement of informed consent for health record research must be upheld. It does so by exploring different contrasting notions of the duty of easy rescue and arguing that none of them entail a perfect duty to participate in health record research. In part because the costs of participation cannot be limited to 1) the threat of privacy breaches, but includes 2) the risk of reduced trust and 3) suboptimal treatment, 4) stigmatization and 5) medicalisation, 6) further stratification of solidarity and 7) increased inequality in access to treatment and medicine. And finally, it defends the requirement of informed consent by arguing that the mere possibility of consent bias provides a rather weak reason for making research participation mandatory, and that there are strong, independent reasons for making. Conclusion Arguments from the duty of easy rescue in combination with claims about little risk of harm and potential consent bias fail to establish not only a perfect duty to participate in health record research, but also that participation in such research should be mandatory. On the contrary, an analysis of these arguments indicates that the duty to participate in research is most adequately construed as an imperfect duty, and reveals a number of strong reasons for insisting that participation in health records research is based on informed consent.

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The Socioeconomic Burden of Obesity

Cited by 58 publications

References 43 publications

Treatment of Functional Hypogonadism Besides Pharmacological Substitution

Treatment of Functional Hypogonadism Besides Pharmacological Substitution

P2Y2 Receptor Promotes High-Fat Diet-Induced Obesity

In Defence of informed consent for health record research - why arguments from ‘easy rescue’, ‘no harm’ and ‘consent bias’ fail

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