Obesity Reviews

doi: 10.1111/obr.13473pmid: N/A

No abstract is available for this article.

Steele, Margaret; Finucane, Francis M.

doi: 10.1111/obr.13590pmid: 37279872

The question of whether obesity should be regarded as a disease remains controversial. One source of controversy can be addressed by distinguishing between two ways in which the word “obesity” is used. In medicine, the word “obesity” now typically refers to some or all of a set of interrelated dysfunctions of metabolism, adipose tissue, and dietary intake regulation. In other contexts, such as government‐funded public education programs, the word “obesity” refers to a body mass index (BMI) category taken to indicate excess body fat. The result is that when medical experts say, “Obesity is a disease,” the majority of outside medicine inevitably takes this to mean “being fat is a disease.” In order to address this ambiguity, we apply key philosophical accounts of disease to the two different senses of “obesity.” We draw two major conclusions: First, although obesity as understood in clinical medicine meets the criteria to be considered a disease, obesity as defined by BMI does not. Second, adequately addressing this disease requires us to distinguish it clearly and unambiguously from high BMI. Making this distinction would help both the public and policymakers to better understand the disease of obesity, facilitating advances in both prevention and treatment.

Skrypnik, Damian; Skrypnik, Katarzyna; Suliburska, Joanna; Bogdański, Paweł

doi: 10.1111/obr.13575pmid: 37230803

By 2030, it is expected that a billion people will have suffer from obesity. Adipose tissue synthesizes leptin, an adipokine that affects cardiovascular risk. Leptin intensifies the synthesis of vascular endothelial growth factor (VEGF). Our study reviews recent reports on leptin–VEGF crosstalk in obesity and related disorders. PubMed, Web of Science, Scopus, and Google Scholar were searched. One hundred and one articles involving human, animal, and in vitro research were included. In vitro studies show the crucial role of interaction between endothelial cells and adipocytes and hypoxia as a factor that intensifies leptin's effects on VEGF. Leptin–VEGF crosstalk promotes the progression of cancer. The animal research reveal that a high‐fat diet enhances leptin and VEGF crosstalk. Genetic and epigenetic mechanisms and procreator‐offspring programming may be involved in leptin–VEGF crosstalk. Some female‐specific characteristics of leptin–VEGF relation in obesity were observed. The human studies have shown that increased leptin and VEGF synthesis and leptin–VEGF crosstalk are factors linking obesity with elevated cardiovascular risk. The studies of the last 10 years documented a range of significant aspects of leptin–VEGF crosstalk specific for obesity and related disorders, shedding new light on the link between obesity and increased cardiovascular risk.

Watso, Joseph C.; Fancher, Ibra S.; Gomez, Dulce H.; Hutchison, Zachary J.; Gutiérrez, Orlando M.; Robinson, Austin T.

doi: 10.1111/obr.13589pmid: 37336641

Hypertension is a primary risk factor for cardiovascular disease. Cardiovascular disease is the leading cause of death among adults worldwide. In this review, we focus on two of the most critical public health challenges that contribute to hypertension—obesity and excess dietary sodium from salt (i.e., sodium chloride). While the independent effects of these factors have been studied extensively, the interplay of obesity and excess salt overconsumption is not well understood. Here, we discuss both the independent and combined effects of excess obesity and dietary salt given their contributions to vascular dysfunction, autonomic cardiovascular dysregulation, kidney dysfunction, and insulin resistance. We discuss the role of ultra‐processed foods—accounting for nearly 60% of energy intake in America—as a major contributor to both obesity and salt overconsumption. We highlight the influence of obesity on elevated blood pressure in the presence of a high‐salt diet (i.e., salt sensitivity). Throughout the review, we highlight critical gaps in knowledge that should be filled to inform us of the prevention, management, treatment, and mitigation strategies for addressing these public health challenges.

McLennan, Steffane; Verhoeff, Kevin; Purich, Kieran; Dang, Jerry; Kung, Janice Y.; Mocanu, Valentin

doi: 10.1111/obr.13572pmid: 37150954

This systematic review and meta‐analysis evaluates metabolic and anthropometric outcomes of duodenal–jejunal bypass liners (DJBLs) compared to optimal medical management for the treatment of obesity and its associated metabolic complications. A systematic search of MEDLINE, Embase, Scopus, and Web of Science databases was conducted. Studies were reviewed and data were extracted following the PRISMA guidelines. The primary outcome was glycated hemoglobin (HbA1c) change at device explant with secondary outcomes including body mass index (BMI), weight, fasting plasma glucose (FPG), and adverse events. Twenty‐eight studies met inclusion criteria evaluating a total of 1229 patients undergoing DJBL treatment. When compared to medical management, DJBLs provided superior reductions in HbA1c (mean difference, MD −0.96%; 95% CI −1.43, −0.49; p < 0.0001), FPG (MD −1.76 mmol/L; 95% CI −2.80, −0.72; p = 0.0009), BMI (MD −2.80 kg/m2; 95% CI −4.18, −1.41; p < 0.0001), and weight (MD −5.45 kg; 95% CI −9.80, −1.09, p = 0.01). Post‐explant data reveals a gradual return to baseline status. Incidence of early device explant was 20.2%. Complications were resolved conservatively or with device explant without long‐term morbidity or mortality. We conclude that DJBLs provide significant metabolic and anthropometric improvements for patients with obesity. Uncertainty about the extent to which improvements are maintained after device removal may limit the use of DJBLs as a standalone treatment for obesity and associated metabolic complications.

Jong, Maxim; Jansen, Núria; Middelkoop, Marienke

doi: 10.1111/obr.13571pmid: 37226636

Numerous barriers are experienced by people with overweight and obesity that play a role in the implementation of lifestyle interventions. This systematic review aims to investigate the barriers and facilitators for children and adults with overweight or obesity when implementing lifestyle interventions targeting weight loss in primary care. A systematic review was conducted by searching four databases to identify eligible studies (1969–2022). The Critical Appraisal Skills Program was used to assess the study quality. A total of 28 studies were included, of which 21 focused on adults and seven on children and their parents. Thematic synthesis of the 28 studies included identified nine key themes, of which support, role of the general practitioner, structure of the lifestyle intervention program, logistics, and psychological factors were the most common. This review shows that a strong support system and a personalized lifestyle intervention are essential components for successful implementation. Additional research is needed to identify whether future lifestyle interventions can take these barriers and facilitators into account and still be feasible for losing weight.

García‐García, Isabel; Fernández‐Andújar, Marina; Narváez, Manuel; García‐Casares, Natalia

doi: 10.1111/obr.13573pmid: 37165483

Midlife obesity and late‐life weight loss confer a greater risk for developing dementia and Alzheimer's disease (AD), but the exact mechanisms behind this phenomenon are currently unknown. The answer could lie on the involvement of gastrointestinal factors, such as adipokines (e.g., leptin, adiponectin, and resistin) and ghrelin. In this context, we conducted a pre‐registered systematic review and meta‐analysis of 42 cross‐sectional and 13 longitudinal studies targeting the associations between leptin, adiponectin, resistin, and ghrelin and the prevalence of general dementia, AD, and mild cognitive impairment (MCI). We also examined the relationship between the four gastrointestinal factors and neurocognitive outcomes and AD‐related cerebrospinal fluid biomarkers. Patients with AD had lower blood leptin and higher resistin levels than cognitively normal participants. Lower leptin and higher resistin were associated with higher degree of cognitive impairment. Additionally, lower late‐life leptin levels might be associated with higher prospective risk of dementia and AD, although more studies are needed to corroborate this. Results in ghrelin and adiponectin were not conclusive, with age, sex distribution, obesity, and severity of dementia seemingly acting as moderators across several analyses. Our work might contribute to the identification of new preclinical blood markers of MCI and AD.

Akoumianakis, Ioannis; Zagaliotis, Anastasios; Konstantaraki, Maria; Filippatos, Theodosios D.

doi: 10.1111/obr.13574pmid: 37191219