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Eating Speed, Eating Frequency, and Their Relationships with Diet Quality, Adiposity, and Metabolic Syndrome, or Its Components.
Garcidueñas-Fimbres, TE, Paz-Graniel, I, Nishi, SK, Salas-Salvadó, J, Babio, N
Nutrients. 2021;(5)
Abstract
Excess body weight is a major global health concern, particularly due to its associated increased health risks. Several strategies have been proposed to prevent overweight and obesity onset. In the past decade, it has been suggested that eating speed/rate and eating frequency might be related to obesity. The main aim of this narrative review was to summarize existing evidence regarding the impact of eating speed/rate and eating frequency on adiposity, metabolic syndrome (MetS), or diet quality (DQ). For this purpose, a literature search of observational and interventional trials was conducted between June and September 2020 in PubMed and Web of Sciences databases, without any data filters and no limitations for publication date. Results suggest that children and adults with a faster eating speed/rate may be associated with a higher risk of developing adiposity, MetS or its components. Furthermore, a higher eating frequency could be associated with diet quality improvement, lower adiposity, and lower risk of developing MetS or its components. Further interventional trials are warranted to clarify the mechanism by which these eating behaviors might have a potential impact on health.
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High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation.
Lechner, K, McKenzie, AL, Kränkel, N, Von Schacky, C, Worm, N, Nixdorff, U, Lechner, B, Scherr, J, Weingärtner, O, Krauss, RM
Metabolic syndrome and related disorders. 2020;(4):176-185
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Abstract
Current algorithms for assessing risk of atherosclerotic cardiovascular disease (ASCVD) and, in particular, the reliance on low-density lipoprotein (LDL) cholesterol in conditions where this measurement is discordant with apoB and LDL-particle concentrations fail to identify a sizeable part of the population at high risk for adverse cardiovascular events. This results in missed opportunities for ASCVD prevention, most notably in those with metabolic syndrome, prediabetes, and diabetes. There is substantial evidence that accumulation of ectopic fat and associated metabolic traits are markers for and pathogenic components of high-risk atherosclerosis. Conceptually, the subset of advanced lesions in high-risk atherosclerosis that triggers vascular complications is closely related to a set of coordinated high-risk traits clustering around a distinct metabolic phenotype. A key feature of this phenotype is accumulation of ectopic fat, which, coupled with age-related muscle loss, creates a milieu conducive for the development of ASCVD atherogenic dyslipidemia, nonresolving inflammation, endothelial dysfunction, hyperinsulinemia, and impaired fibrinolysis. Sustained vascular inflammation, a hallmark of high-risk atherosclerosis, impairs plaque stabilization in this phenotype. This review describes how metabolic and inflammatory processes that are promoted in large measure by ectopic adiposity, as opposed to subcutaneous adipose tissue, relate to the pathogenesis of high-risk atherosclerosis. Clinical biomarkers indicative of these processes provide incremental information to standard risk factor algorithms and advanced lipid testing identifies atherogenic lipoprotein patterns that are below the discrimination level of standard lipid testing. This has the potential to enable improved identification of high-risk patients who are candidates for therapeutic interventions aimed at prevention of ASCVD.
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Effects of Diets on Adipose Tissue.
Ezquerro, S, Rodríguez, A, Portincasa, P, Frühbeck, G
Current medicinal chemistry. 2019;(19):3593-3612
Abstract
BACKGROUND Obesity is a major health problem that has become a global epidemic. Overweight and obesity are commonly associated with the development of several pathologies, such as insulin resistance, cardiovascular diseases, sleep apnea and several types of cancer, which can lead to further morbidity and mortality. An increased abdominal adiposity renders overweight and obese individuals more prone to metabolic and cardiovascular problems. OBJECTIVE This Review aims to describe the dietary strategies to deal with excess adiposity given the medical, social and economic consequences of obesity. METHODS One hundred and eighty-five papers were included in the present Review. RESULTS Excess adiposity leads to several changes in the biology, morphology and function of the adipose tissue, such as adipocyte hypertrophy and hyperplasia, adipose tissue inflammation and fibrosis and an impaired secretion of adipokines, contributing to the onset of obesity- related comorbidities. The first approach for obesity management and prevention is the implementation of a diet combined with physical activity. The present review summarizes the compelling evidence showing body composition changes, impact on cardiometabolism and potential adverse effects of very-low calorie, low- and high-carbohydrate, high-protein or low-fat diets. The use of macronutrients during the preprandial and postprandial state has been also reviewed to better understand the metabolic changes induced by different dietary interventions. CONCLUSION Dietary changes should be individualised, tailored to food preferences and allow for flexible approaches to reducing calorie intake in order to increase the motivation and compliance of overweight and obese patients.
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The Effect of Low Glycemic Index and Glycemic Load Diets on Hepatic Fat Mass, Insulin Resistance, and Blood Lipid Panels in Individuals with Nonalcoholic Fatty Liver Disease.
Parker, A, Kim, Y
Metabolic syndrome and related disorders. 2019;(8):389-396
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease that is associated with insulin resistance and hepatic triglyceride accumulation. There is evidence to suggest that a low glycemic index (GI) diet can reduce glucose absorption, hepatic influx of glucose, and de novo lipogenesis. This review investigates the effect of low GI and glycemic load (GL) diets on hepatic fat mass, hepatic enzymes, insulin resistance, fasting blood glucose levels, and blood lipid panels in individuals with NAFLD. PubMed, Cumulative Index to Nursing and Allied Health Literature, and Web of Science were used in literature search. Search keywords included "glycemic index," "glycaemic index," "glycemic load," "glycaemic load," "nonalcoholic fatty liver disease," "NAFLD," "nonalcoholic steatohepatitis," and "NASH." Outcome measurements included hepatic fat mass, hepatic enzyme alanine transaminase (ALT), insulin resistance [homeostasis model assessment of insulin resistance (HOMA-IR)], fasting blood glucose levels, and/or blood lipid panels. Four eligible studies enrolling 281 individuals with NAFLD were included. Both hepatic fat mass and ALT showed significant reductions from baseline in both low GI and GL diets. One study showed no change, and another study showed significant reductions in HOMA-IR. No significant reduction in fasting blood glucose level, triglycerides, high-density lipoprotein-cholesterol, or low-density lipoprotein-cholesterol was observed from baseline in both low GI and GL diets. Findings from the review suggest that low GI and GL diets may reduce hepatic fat mass and ALT in individuals with NAFLD. Future research of large-scale, randomized controlled studies using isoenergetic, low GI and GL diets for long term is needed to draw conclusionary results.
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Effect of pasta in the context of low-glycaemic index dietary patterns on body weight and markers of adiposity: a systematic review and meta-analysis of randomised controlled trials in adults.
Chiavaroli, L, Kendall, CWC, Braunstein, CR, Blanco Mejia, S, Leiter, LA, Jenkins, DJA, Sievenpiper, JL
BMJ open. 2018;(3):e019438
Abstract
OBJECTIVE Carbohydrate staples such as pasta have been implicated in the obesity epidemic. It is unclear whether pasta contributes to weight gain or like other low-glycaemic index (GI) foods contributes to weight loss. We synthesised the evidence of the effect of pasta on measures of adiposity. DESIGN Systematic review and meta-analysis using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. DATA SOURCES MEDLINE, Embase, CINAHL and the Cochrane Library were searched through 7 February 2017. ELIGIBILITY CRITERIA FOR SELECTING STUDIES We included randomised controlled trials ≥3 weeks assessing the effect of pasta alone or in the context of low-GI dietary patterns on measures of global (body weight, body mass index (BMI), body fat) and regional (waist circumference (WC), waist-to-hip ratio (WHR), sagittal abdominal diameter (SAD)) adiposity in adults. DATA EXTRACTION AND SYNTHESIS Two independent reviewers extracted data and assessed risk of bias. Data were pooled using the generic inverse-variance method and expressed as mean differences (MDs) with 95% CIs. Heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic). GRADE assessed the certainty of the evidence. RESULTS We identified no trial comparisons of the effect of pasta alone and 32 trial comparisons (n=2448 participants) of the effect of pasta in the context of low-GI dietary patterns. Pasta in the context of low-GI dietary patterns significantly reduced body weight (MD=-0.63 kg; 95% CI -0.84 to -0.42 kg) and BMI (MD=-0.26 kg/m2; 95% CI -0.36 to -0.16 kg/m2) compared with higher-GI dietary patterns. There was no effect on other measures of adiposity. The certainty of the evidence was graded as moderate for body weight, BMI, WHR and SAD and low for WC and body fat. CONCLUSIONS Pasta in the context of low-GI dietary patterns does not adversely affect adiposity and even reduces body weight and BMI compared with higher-GI dietary patterns. Future trials should assess the effect of pasta in the context of other 'healthy' dietary patterns. TRIAL REGISTRATION NUMBER NCT02961088; Results.
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Sleep, Health, and Metabolism in Midlife Women and Menopause: Food for Thought.
Kravitz, HM, Kazlauskaite, R, Joffe, H
Obstetrics and gynecology clinics of North America. 2018;(4):679-694
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Abstract
Sleep and metabolism are essential components of health. Metabolic health depends largely on individual's lifestyle. Disturbances in sleep health, such as changes in sleep patterns that are associated with menopause/reproductive aging and chronologic aging, may have metabolic health consequences. Sleep restriction and age-related changes in sleep and circadian rhythms may influence changes in appetite and reproductive hormones, energy expenditure, and body adiposity. In this article, the authors describe how menopause-related sleep disturbance may affect eating behavior patterns, immunometabolism, immunometabolic dysfunction, and associations between sleep and metabolic outcomes.
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Adipokines, adiposity, and bone marrow adipocytes: Dangerous accomplices in multiple myeloma.
Morris, EV, Edwards, CM
Journal of cellular physiology. 2018;(12):9159-9166
Abstract
Obesity has become a global epidemic influencing the establishment and progression of a wide range of diseases, such as diabetes, cardiovascular disease, and cancer. In 2016, International Agency for Research on Cancer reported that obesity is now associated with 13 different cancers, one of which is multiple myeloma (MM), a destructive cancer of plasma cells that predominantly reside in the bone marrow. Obesity is the accumulation of excess body fat, which causes metabolic, endocrine, immunologic, and inflammatory-like changes. Obesity is usually associated with an increase in visceral and/or subcutaneous fat; however, an additional fat depot that also responds to diet-induced changes is bone marrow adipose tissue (BMAT). There have been several studies over the past few decades that have identified BMAT as a key driver in MM progression. Adipocytes secrete numerous adipokines, such as leptin, adiponectin, resistin, adipsin, and visfatin, which when secreted at normal controlled levels have protective properties. However, in obesity these levels of secretion change, coupled with an increase in adipocyte number and size causing a profound and lasting effect on the bone microenvironment, contributing to MM cell growth, survival, and migration as well as potentially fueling bone destruction. Obesity is a modifiable risk factor making it an attractive option for targeted therapy. This review discusses the link between obesity, monoclonal gammopathy of undetermined significance (a benign condition that precedes MM), and myeloma, and the contribution of key adipokines to disease establishment and progression.
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From inflammation to sexual dysfunctions: a journey through diabetes, obesity, and metabolic syndrome.
Maiorino, MI, Bellastella, G, Giugliano, D, Esposito, K
Journal of endocrinological investigation. 2018;(11):1249-1258
Abstract
Metabolic diseases are associated with chronic low-grade inflammation, which has been indicated as a potential mediator of endothelial dysfunction and cardiovascular disease. Visceral adiposity is thought to be the starting condition of the inflammatory state through the release of inflammatory cytokines, including TNF-alpha, CRP, and IL-6, which in turn promote endothelial dysfunction, endothelial expression of chemokines (IL-1) and adhesion molecules (ICAM-1, VCAM-1, and P-selectin), and the inhibition of anti-atherogenic factors (adiponectin). Obesity, metabolic diseases, and diabetes, all conditions characterized by abdominal fat, are well-recognized risk factors for sexual dysfunction in both sexes. Evidence from randomized-controlled trials supports the association between inflammatory milieau and erectile dysfunction in men suffering from metabolic diseases, whereas, in women, this has to be confirmed in further studies. A healthy lifestyle based on dietary pattern with high content of whole grain, fruit, nuts and seeds, and vegetables and low in sodium and saturated fatty acids plus regular physical activity may help to modulate the pro-inflammatory state associated with metabolic diseases and the related burden of sexual dysfunctions.
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Adiposity and gastrointestinal cancers: epidemiology, mechanisms and future directions.
Murphy, N, Jenab, M, Gunter, MJ
Nature reviews. Gastroenterology & hepatology. 2018;(11):659-670
Abstract
Excess adiposity is a risk factor for several cancers of the gastrointestinal system, specifically oesophageal adenocarcinoma and colorectal, small intestine, pancreatic, liver, gallbladder and stomach cancers. With the increasing prevalence of obesity in nearly all regions of the world, this relationship could represent a growing source of cancers of the digestive system. Experimental and molecular epidemiological studies indicate important roles for alterations in insulin signalling, adipose tissue-derived inflammation and sex hormone pathways in mediating the association between adiposity and gastrointestinal cancer. The intestinal microbiome, gut hormones and non alcoholic fatty liver disease (NAFLD) also have possible roles. However, important gaps remain in our knowledge. For instance, our understanding of how adiposity throughout the life course is related to the risk of gastrointestinal cancer development and of how obesity influences gastrointestinal cancer prognosis and survival is limited. Nonetheless, the increasing use of state-of-the-art analytical methods (such as omics technologies, Mendelian randomization and MRI) in large-scale epidemiological studies offers exciting opportunities to advance our understanding of the complex relationship between adiposity and gastrointestinal cancers. Here, we examine the epidemiology of associations between obesity and gastrointestinal cancer, explore potential mechanisms underlying these relationships and highlight important unanswered research questions.
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Adiposity, vitamin D requirements, and clinical implications for obesity-related metabolic abnormalities.
Hyppönen, E, Boucher, BJ
Nutrition reviews. 2018;(9):678-692
Abstract
This review was conducted to clarify both the complex interrelationship between adiposity and vitamin D and the clinical implications of vitamin D status on metabolic abnormalities associated with obesity. Obesity increases the risk of vitamin D deficiency, a finding consistently reported across all ages and in different population groups. According to genetic studies, this is driven by the effect of higher adiposity, which causes a reduction in circulating concentrations of 25-hydroxyvitamin D [25(OH)D, used as an indicator of vitamin D status]. Conversely, higher concentrations of 25(OH)D do not appear to affect the risk of obesity. Evidence from clinical trials using vitamin D supplementation to achieve weight reduction is limited. Some trials, however, have suggested that concomitant supplementation with vitamin D and calcium potentially reduces central fat deposits, especially in individuals with low dietary calcium intakes. Adiposity has important implications for the efficacy of vitamin D supplementation, and increases in 25(OH)D concentrations are generally lower in obese than in normal-weight individuals. Active hormonal vitamin D has many mechanistic effects, both physiologically and biochemically, that could counteract the harmful effects of obesity on metabolism and reduce the risks of metabolic abnormalities and tissue damage consequent to adiposity. Whether improvements in the overall obesogenic metabolic profile can be achieved by vitamin D supplementation, however, is still unknown.