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The American Journal of Managed Care Jun 2016Body mass index of 30 kg/m2 or higher is used to identify individuals with obesity. In the last 3 decades, the worldwide prevalence of obesity has increased 27.5% for... (Review)
Review
Body mass index of 30 kg/m2 or higher is used to identify individuals with obesity. In the last 3 decades, the worldwide prevalence of obesity has increased 27.5% for adults and 47.1% for children. Obesity is the result of complex relationships between genetic, socioeconomic, and cultural influences. Consumption patterns, urban development, and lifestyle habits influence the prevalence of obesity. The condition may be the result of disease or pharmacologic treatment. It may also be a risk factor for the development of comorbid conditions. Persons who are obese have less school attendance, reduced earning potential, and higher healthcare costs that may result in an economic burden on society. A review of the prevalence and economic consequences of obesity is provided. Potential causes and comorbidities associated with obesity are also discussed.
Topics: Body Mass Index; Comorbidity; Female; Health Care Costs; Humans; Life Style; Male; Obesity; Prevalence; Public Health; Quality of Life; Risk Assessment; Socioeconomic Factors; United States
PubMed: 27356115
DOI: No ID Found -
The Indian Journal of Medical Research Jan 2020Obesity is a serious medical condition worldwide, which needs new approaches and recognized international consensus in treating diseases leading to morbidity. The aim of... (Review)
Review
Obesity is a serious medical condition worldwide, which needs new approaches and recognized international consensus in treating diseases leading to morbidity. The aim of this review was to examine heterogeneous links among the various phenotypes of obesity in adults. Proteins and associated genes in each group were analysed to differentiate between biomarkers. A variety of terms for classification and characterization within this pathology are currently in use; however, there is no clear consensus in terminology. The most significant groups reviewed include metabolically healthy obese, metabolically abnormal obese, metabolically abnormal, normal weight and sarcopenic obese. These phenotypes do not define particular genotypes or epigenetic gene regulation, or proteins related to inflammation. There are many other genes linked to obesity, though the value of screening all of those for diagnosis has low predictive results, as there are no significant biomarkers. It is important to establish a consensus in the terminology used and the characteristics attributed to obesity subtypes. The identification of specific molecular biomarkers is also required for better diagnosis in subtypes of obesity.
Topics: Adult; Biomarkers; Genotype; Humans; Obesity; Phenotype; Proteins
PubMed: 32134010
DOI: 10.4103/ijmr.IJMR_1768_17 -
Advances in Nutrition (Bethesda, Md.) Jan 2019The global obesity epidemic continues its relentless advance, currently affecting >2 billion people. This paper explores alternative ways to assess the potential disease...
The global obesity epidemic continues its relentless advance, currently affecting >2 billion people. This paper explores alternative ways to assess the potential disease impact of the epidemic, which is currently based almost exclusively on body mass index (BMI) data. It also argues in favor of concerted efforts to modify the built ecosystem that is driving the obesity epidemic. Most of the epidemiologic data on obesity are based on BMI (in kg/m2) and use the ranges of 18.5-24.9 for normality, 25-29.9 for overweight, and ≥30 for obesity. But the gap between the median of the "normal" BMI distribution (∼22) and the current population BMI of, for example, the United States (27.7) has become so wide that it is unlikely that we will be able to close that gap in the near future. Furthermore, the correlation between BMI and disease risk is not linear. Over 60% of the global disease burden of obesity affects individuals with a BMI ≥30, who comprise only ∼10% of the global population of overweight/obese persons. Furthermore, BMI accounts for only ∼17% of the risk of insulin resistance and subsequent type 2 diabetes in the BMI ≥25 population. Epigenetics, specifically DNA methylation, appears to play a far more important role than BMI in determining the risk of obesity's comorbidities, such as diabetes. Similarly, socioeconomic status carries a higher risk than BMI level for the development of obesity-related noncommunicable diseases. Finally, the built environment that sustains our species' lifestyle is a major driver of the obesity epidemic. Modifying that ecosystem will require no less than a social movement, one able to promote and sustain the necessary coordinated action of virtually all sectors of society.
Topics: Body Mass Index; Comorbidity; Cost of Illness; DNA Methylation; Diabetes Mellitus, Type 2; Ecosystem; Environment Design; Epigenesis, Genetic; Global Health; Humans; Insulin Resistance; Life Style; Obesity; Social Class
PubMed: 30721956
DOI: 10.1093/advances/nmy055 -
Fertility and Sterility Apr 2017The worldwide upward trend in obesity has been dramatic, now affecting more than 20% of American women of reproductive age. Obesity is associated with many adverse... (Review)
Review
The worldwide upward trend in obesity has been dramatic, now affecting more than 20% of American women of reproductive age. Obesity is associated with many adverse maternal and fetal effects prenatally, but it also exerts a negative influence on female fertility. Obese women are more likely to have ovulatory dysfunction due to dysregulation of the hypothalamic-pituitary-ovarian axis. Women with polycystic ovarian syndrome who are also obese demonstrate a more severe metabolic and reproductive phenotype. Obese women have reduced fecundity even when eumenorrheic and demonstrate poorer outcomes with the use of in vitro fertilization. Obesity appears to affect the oocyte and the preimplantation embryo, with disrupted meiotic spindle formation and mitochondrial dynamics. Excess free fatty acids may have a toxic effect in reproductive tissues, leading to cellular damage and a chronic low-grade inflammatory state. Altered levels of adipokines, such as leptin, in the obese state can affect steroidogenesis and directly affect the developing embryo. The endometrium is also susceptible, with evidence of impaired stromal decidualization in obese women. This may explain subfecundity due to impaired receptivity, and may lead to placental abnormalities as manifested by higher rates of miscarriage, stillbirth, and preeclampsia in the obese population. Many interventions have been explored to mitigate the effect of obesity on infertility, including weight loss, physical activity, dietary factors, and bariatric surgery. These data are largely mixed, with few high quality studies to guide us. As we improve our understanding of the pathophysiology of obesity in human reproduction we hope to identify novel treatment strategies.
Topics: Adipose Tissue; Adiposity; Bariatric Surgery; Diet; Female; Fertility; Genetic Predisposition to Disease; Healthy Lifestyle; Humans; Hypothalamo-Hypophyseal System; Infertility, Female; Lipid Metabolism; Obesity; Oocytes; Ovary; Pregnancy; Pregnancy Complications; Risk Assessment; Risk Factors; Risk Reduction Behavior; Sedentary Behavior; Weight Loss
PubMed: 28292619
DOI: 10.1016/j.fertnstert.2017.01.017 -
Pediatric Nephrology (Berlin, Germany) Apr 2021Primary hypertension is the dominant form of arterial hypertension in adolescents. Disturbed body composition with, among other things, increased visceral fat...
Primary hypertension is the dominant form of arterial hypertension in adolescents. Disturbed body composition with, among other things, increased visceral fat deposition, accelerated biological maturation, metabolic abnormalities typical for metabolic syndrome, and increased adrenergic drive constitutes the intermediary phenotype of primary hypertension. Metabolic syndrome is observed in 15-20% of adolescents with primary hypertension. These features are also typical of obesity-related hypertension. Metabolic abnormalities and metabolic syndrome are closely associated with both the severity of hypertension and the risk of target organ damage. However, even though increased body mass index is the main determinant of blood pressure in the general population, not every hypertensive adolescent is obese and not every obese patient suffers from hypertension or metabolic abnormalities typical for metabolic syndrome. Thus, the concepts of metabolically healthy obesity, normal weight metabolically unhealthy, and metabolically unhealthy obese phenotypes have been developed. The risk of hypertension and hypertensive target organ damage increases with exposure to metabolic risk factors which are determined by disturbed body composition and visceral obesity. Due to the fact that both primary hypertension and obesity-related hypertension present similar pathogenesis, the principles of treatment are the same and are focused not only on lowering blood pressure, but also on normalizing body composition and metabolic abnormalities.
Topics: Adolescent; Body Mass Index; Essential Hypertension; Humans; Hypertension; Metabolic Syndrome; Obesity; Obesity, Metabolically Benign; Phenotype; Risk Factors
PubMed: 32388582
DOI: 10.1007/s00467-020-04579-3 -
European Journal of Haematology Mar 2021The prevalence of obesity is increasing and progressively influencing physician-patient interactions. While there is a sizable amount of data demonstrating that obesity... (Review)
Review
The prevalence of obesity is increasing and progressively influencing physician-patient interactions. While there is a sizable amount of data demonstrating that obesity is a state of low-grade inflammation, to our knowledge, there is no single review summarizing its effects on hematologic parameters and thrombotic risk. We performed a literature search which largely surfaced observational studies, with a few systematic reviews and meta-analyses of these studies. We took care to review the mechanisms driving an inflammatory state and obesity's effect on white blood cells, red blood cells, platelets, and thrombotic risk. There is an observed relative, and sometimes absolute leukocytosis driven by this inflammatory state. Obesity is also associated with increased platelet counts and an increased risk for venous thromboembolism (VTE). Lastly, the association between obesity, iron deficiency (ID), and red blood cell counts may be present but remains uncertain. Recognizing the above associations may provide clinicians with reassurance regarding otherwise unexplained hematologic abnormalities in obese individuals. We hope this review will prompt future studies to further understand the underlying mechanisms driving these abnormalities and identify modifiable risk factors and potential therapeutic targets to prevent the development of probable obesity-associated conditions with significant morbidity and mortality, such as ID and VTE.
Topics: Adipose Tissue; Animals; Biomarkers; Cytokines; Disease Susceptibility; Humans; Inflammation; Inflammation Mediators; Leukocyte Count; Leukocytosis; Obesity; Sex Factors
PubMed: 33270290
DOI: 10.1111/ejh.13560 -
BMJ (Clinical Research Ed.) Feb 2017Obesity is the most common medical condition in women of reproductive age. Obesity during pregnancy has short term and long term adverse consequences for both mother and... (Review)
Review
Obesity is the most common medical condition in women of reproductive age. Obesity during pregnancy has short term and long term adverse consequences for both mother and child. Obesity causes problems with infertility, and in early gestation it causes spontaneous pregnancy loss and congenital anomalies. Metabolically, obese women have increased insulin resistance in early pregnancy, which becomes manifest clinically in late gestation as glucose intolerance and fetal overgrowth. At term, the risk of cesarean delivery and wound complications is increased. Postpartum, obese women have an increased risk of venous thromboembolism, depression, and difficulty with breast feeding. Because 50-60% of overweight or obese women gain more than recommended by Institute of Medicine gestational weight guidelines, postpartum weight retention increases future cardiometabolic risks and prepregnancy obesity in subsequent pregnancies. Neonates of obese women have increased body fat at birth, which increases the risk of childhood obesity. Although there is no unifying mechanism responsible for the adverse perinatal outcomes associated with maternal obesity, on the basis of the available data, increased prepregnancy maternal insulin resistance and accompanying hyperinsulinemia, inflammation, and oxidative stress seem to contribute to early placental and fetal dysfunction. We will review the pathophysiology underlying these data and try to shed light on the specific underlying mechanisms.
Topics: Disease Management; Female; Humans; Infant, Newborn; Obesity; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Time
PubMed: 28179267
DOI: 10.1136/bmj.j1 -
Biomedicine & Pharmacotherapy =... May 2021Currently, obesity has become a global health issue and is referred to as an epidemic. Dysfunctional obese adipose tissue plays a pivotal role in the development of... (Review)
Review
Currently, obesity has become a global health issue and is referred to as an epidemic. Dysfunctional obese adipose tissue plays a pivotal role in the development of insulin resistance. However, the mechanism of how dysfunctional obese-adipose tissue develops insulin-resistant circumstances remains poorly understood. Therefore, this review attempts to highlight the potential mechanisms behind obesity-associated insulin resistance. Multiple risk factors are directly or indirectly associated with the increased risk of obesity; among them, environmental factors, genetics, aging, gut microbiota, and diets are prominent. Once an individual becomes obese, adipocytes increase in their size; therefore, adipose tissues become larger and dysfunctional, recruit macrophages, and then these polarize to pro-inflammatory states. Enlarged adipose tissues release excess free fatty acids (FFAs), reactive oxygen species (ROS), and pro-inflammatory cytokines. Excess systemic FFAs and dietary lipids enter inside the cells of non-adipose organs such as the liver, muscle, and pancreas, and are deposited as ectopic fat, generating lipotoxicity. Toxic lipids dysregulate cellular organelles, e.g., mitochondria, endoplasmic reticulum, and lysosomes. Dysregulated organelles release excess ROS and pro-inflammation, resulting in systemic inflammation. Long term low-grade systemic inflammation prevents insulin from its action in the insulin signaling pathway, disrupts glucose homeostasis, and results in systemic dysregulation. Overall, long-term obesity and overnutrition develop into insulin resistance and chronic low-grade systemic inflammation through lipotoxicity, creating the circumstances to develop clinical conditions. This review also shows that the liver is the most sensitive organ undergoing insulin impairment faster than other organs, and thus, hepatic insulin resistance is the primary event that leads to the subsequent development of peripheral tissue insulin resistance.
Topics: Adipose Tissue; Animals; Humans; Insulin Resistance; Obesity
PubMed: 33561645
DOI: 10.1016/j.biopha.2021.111315 -
The Journal of Allergy and Clinical... Apr 2018Obesity is a vast public health problem and both a major risk factor and disease modifier for asthma in children and adults. Obese subjects have increased asthma risk,... (Review)
Review
Obesity is a vast public health problem and both a major risk factor and disease modifier for asthma in children and adults. Obese subjects have increased asthma risk, and obese asthmatic patients have more symptoms, more frequent and severe exacerbations, reduced response to several asthma medications, and decreased quality of life. Obese asthma is a complex syndrome, including different phenotypes of disease that are just beginning to be understood. We examine the epidemiology and characteristics of this syndrome in children and adults, as well as the changes in lung function seen in each age group. We then discuss the better recognized factors and mechanisms involved in disease pathogenesis, focusing particularly on diet and nutrients, the microbiome, inflammatory and metabolic dysregulation, and the genetics/genomics of obese asthma. Finally, we describe current evidence on the effect of weight loss and mention some important future directions for research in the field.
Topics: Adult; Asthma; Child; Humans; Microbiota; Obesity; Quality of Life; Syndrome
PubMed: 29627041
DOI: 10.1016/j.jaci.2018.02.004 -
Current Diabetes Reports Aug 2014The incidence of overweight and obesity among children has increased dramatically in recent decades, with about one-third of children in the U.S. currently being either... (Review)
Review
The incidence of overweight and obesity among children has increased dramatically in recent decades, with about one-third of children in the U.S. currently being either overweight or obese. Being overweight in early childhood increases risk for later obesity. There is evidence for the efficacy of family-based behavioral treatment to control weight and improve health outcomes. Obesity-related health risks have been documented, including metabolic syndrome. There is also increasing incidence of type 2 diabetes (T2D) among youth in recent years, with obesity and family history of T2D generally present. Lower income and ethnic minority status are associated with both obesity and T2D in youth. Most youth with T2D do not achieve optimal glycemic control, and are at high risk for later health complications. Obesity and T2D represent significant public health issues with potentially great personal and societal cost. Research addressing the prevention of obesity and T2D among youth is urgently needed.
Topics: Adolescent; Child; Diabetes Mellitus, Type 2; Humans; Obesity
PubMed: 24919749
DOI: 10.1007/s11892-014-0508-y