Excessive Caloric Intake Research Articles

Сучасні аспекти діагностики, лікування та профілактики ожиріння в дітей

Ожиріння є однією з актуальних медико-соціальних проблем сучасності. Відзначається збільшення поширеності ожиріння серед дітей. Кількість дітей у світі віком до 5 років із надлишковою масою тіла та ожирінням становить 44 мільйони. Ожиріння в дитячому віці є фактором ризику для розвитку тяжкої супутньої патології. Дитяче ожиріння — тяжкий прогностичний фактор ожиріння в дорослих. Реєструється підвищений рівень передчасної смерті в дорослих, які страждали від ожиріння в дитинстві. Заходи профілактики та лікування дитячого ожиріння повинні бути спрямовані на всю родину, а не тільки на хвору дитину. З метою профілактики ожиріння слід обмежувати надлишкове вживання калорій. Для підвищення ефективності профілактики ожиріння в дітей вживання енергії потрібно поєднувати з підвищенням фізичної активності. Основним методом лікування ожиріння в дітей є модифікація способу життя, що включає корекцію харчування, призначення фізичних навантажень та поведінкову терапію. Впровадження шкільних програм, що передбачають збільшення фізичної активності та оптимізацію харчування школярів, підвищує ефективність боротьби з дитячим ожирінням. Фармакотерапія при ожирінні в дітей призначається при неефективності програм з модифікації способу життя. Для медикаментозного лікування ожиріння в дітей застосовується орлістат. Ефективність фармакотерапії підвищується при її поєднанні з комплексними програмами з модифікації способу життя. За кордоном при морбідному ожирінні в підлітків у разі неефективності нехірургічного лікування використовується баріатрична хірургія. У результаті оперативного втручання знижується індекс маси тіла, покращується перебіг супутніх захворювань, підвищується якість життя пацієнтів. Баріатрична хірургія пов’язана з ризиком розвитку побічних ефектів, що потребує проведення безперервного моніторингу ускладнень. Для лікування та профілактики ожиріння в дітей необхідним є мультидисциплінарний підхід із залученням спеціалістів різного профілю.

Sugars and Sweet Taste: Addictive or Rewarding?

The notion of food “addiction” often focuses on the overconsumption of sweet tasting foods or so-called sugar “addiction”. In the extreme, some have suggested that sugar and sweet tastes elicit neural and behavioral responses analogous to those observed with drugs of abuse. These concepts are complicated by the decades long uncertainty surrounding the validity and reproducibility of functional magnetic resonance imaging (fMRI) methodologies used to characterize neurobiological pathways related to sugar and sweet taste stimuli. There are also questions of whether sweet taste or post-ingestion metabolic consequences of sugar intake would lead to addiction or excessive caloric intake. Here, we present a focused narrative review of literature related to the reward value of sweet taste which suggests that reward value can be confounded with the construct of “addictive potential”. Our review seeks to clarify some key distinctions between these constructs and questions the applicability of the addiction construct to human over-eating behaviors. To adequately frame this broad discussion requires the flexibility offered by the narrative review paradigm. We present selected literature on: techniques used to link sugar and sweet tastes to addiction neurobiology and behaviors; sugar and sweet taste “addiction”; the relationship of low calorie sweetener (LCS) intake to addictive behaviors and total calorie intake. Finally, we examined the reward value of sweet tastes and contrasted that with the literature describing addiction. The lack of reproducibility of fMRI data remains problematic for attributing a common neurobiological pathway activation of drugs and foods as conclusive evidence for sugar or sweet taste “addiction”. Moreover, the complicated hedonics of sweet taste and reward value are suggested by validated population-level data which demonstrate that the consumption of sweet taste in the absence of calories does not increase total caloric intake. We believe the neurobiologies of reward value and addiction to be distinct and disagree with application of the addiction model to sweet food overconsumption. Most hypotheses of sugar “addiction” attribute the hedonics of sweet foods as the equivalent of “addiction”. Further, when addictive behaviors and biology are critically examined in totality, they contrast dramatically from those associated with the desire for sweet taste. Finally, the evidence is strong that responses to the palatability of sweets rather than their metabolic consequences are the salient features for reward value. Thus, given the complexity of the controls of food intake in humans, we question the usefulness of the “addiction” model in dissecting the causes and effects of sweet food over-consumption.

Approach to Obesity in Childhood

Childhood obesity prevalence is increasing worldwide. The most common cause of obesity in children is a positive energy balance due to excess caloric intake in contrast to caloric expenditure combined with a genetic predisposition for weight gain. Obesity causes type 2 diabetes mellitus, hypertension, cardiovascular diseases, osteoporosis and some cancers. There is limited information on the efficacy and safety of medications for weight loss in children. In this paper, definition, etiopathogenesis, differential diagnosis, co-morbidities, and treatment of obesity in children will be reviewed.

Effect of Advanced Glycation End-Products and Excessive Calorie Intake on Diet-Induced Chronic Low-Grade Inflammation Biomarkers in Murine Models.

Chronic Low-Grade Inflammation (CLGI) is a non-overt inflammatory state characterized by a continuous activation of inflammation mediators associated with metabolic diseases. It has been linked to the overconsumption of Advanced Glycation End-Products (AGEs), and/or macronutrients which lead to an increase in local and systemic pro-inflammatory biomarkers in humans and animal models. This review provides a summary of research into biomarkers of diet-induced CLGI in murine models, with a focus on AGEs and obesogenic diets, and presents the physiological effects described in the literature. Diet-induced CLGI is associated with metabolic endotoxemia, and/or gut microbiota remodeling in rodents. The mechanisms identified so far are centered on pro-inflammatory axes such as the interaction between AGEs and their main receptor AGEs (RAGE) or increased levels of lipopolysaccharide. The use of murine models has helped to elucidate the local and systemic expression of CLGI mediators. These models have enabled significant advances in identification of diet-induced CLGI biomarkers and resultant physiological effects. Some limitations on the translational (murine → humans) use of biomarkers may arise, but murine models have greatly facilitated the testing of specific dietary components. However, there remains a lack of information at the whole-organism level of organization, as well as a lack of consensus on the best biomarker for use in CLGI studies and recommendations as to future research conclude this review.

The role of ghrelin and serotonin in the control of eating behavior in patients with obesity and diabetes mellitus type 2

In recent years, the incidence of obesity and type 2 diabetes mellitus (DM) has been increasing steadily; therefore, the search for hormonal and metabolic substances the correction of which can normalize human eating behavior is required. The main system for controlling hunger and appetite — the melanocortin pathway — is located in the hypothalamus. Activation of this signa­ling system by melanocortins leads to appetite decrease and causes a feeling of satiety. Neuropeptide Y and agouti-related protein act antagonistically and enhance hunger. There are different types of eating disorders, such as binge eating and night ­eating syndrome, which are most common among obese patients and those with type 2 DM. They are characterized by excessive intake of food and, consequently, complication of the course of underlying disease due to its negative impact on carbohydrate and lipid metabolism. There are various hormonal and metabolic substances that are responsible for suppressing and stimulating the center of hunger in the hypothalamus. This article examines the effect of ghrelin and serotonin on the mechanism of eating habits formation and the control of eating behavior in patients with obesity and type 2 DM. This article highlights the role of ghrelin and serotonin in eating behavior. Ghrelin is an orexigenic hormone and is capable of activating the center of hunger. The concentration of this hormone in patients with obesity and/or type 2 DM is reduced compared to healthy individuals that indicates the adaptation of the body to positive energy balance and excess calorie intake by humans. In turn, serotonin, whose receptors are also present in the hypothalamus, upon bin­ding to 5-HT2C receptor causes inhibition of neuropeptide Y secretion that leads to feeling of satiety and normalization of appetite and weight, thus exhibiting anorexigenic properties. Lorcaserin is currently the only serotonin receptor agonist approved by the Food and Drug Administration for the treatment of obesity. That is why studies of hormonal and metabolic substances that are involved in the signaling pathways of the hypothalamus hunger center will help find effective ways to treat obesity and type 2 DM.

Black Community Conversations About Opposing Ethnically Targeted Marketing of Unhealthy Foods and Beverages.

Efforts to reduce disparities in obesity prevalence affecting Black Americans are having limited success. One reason for this may be the disproportionate, ethnically targeted marketing of foods and beverages high in fat and sugar (FBHFS) to Black consumers. Such marketing promotes high consumption of FBHFS, leading to excess caloric intake and unintentional weight gain. We convened focus groups with Black men and women (total n = 57) in collaboration with community groups in three localities to elicit their views, as consumers and parents/caregivers, about targeted FBHFS marketing and potential ways to combat it. At each location, trained community members facilitated two sets of focus groups: one for adults aged 18 to 25 years and another for adults aged 26 to 55 years who had a 3-to-17-year-old child at home. Each group met twice to discuss food and beverage marketing practices to Black communities and reviewed a booklet about ethnically targeted marketing tactics in between. A directed content analysis of participant comments identified and explored salient themes apparent from initial summarization of results. Results show how parents are concerned with and critical of pervasive FBHFS marketing. In particular, comments emphasize the involvement of Black celebrities in FBHFS marketing—how and why they engage in such marketing and whether this could be shifted towards healthier foods. These findings suggest a potential role for counter marketing efforts focused on Black celebrity endorsements of FBHFS, possibly with a youth focus. They also underscore the need for additional, qualitative exploration of Black consumer views of ethnically targeted FBHFS marketing more generally.

Calcium phosphate microcrystals in the renal tubular fluid accelerate chronic kidney disease progression.

The Western pattern diet is rich not only in fat and calories but also in phosphate. The negative effects of excessive fat and calorie intake on health are widely known, but the potential harms of excessive phosphate intake are poorly recognized. Here, we show the mechanism by which dietary phosphate damages the kidney. When phosphate intake was excessive relative to the number of functioning nephrons, circulating levels of FGF23, a hormone that increases the excretion of phosphate per nephron, were increased to maintain phosphate homeostasis. FGF23 suppressed phosphate reabsorption in renal tubules and thus raised the phosphate concentration in the tubule fluid. Once it exceeded a threshold, microscopic particles containing calcium phosphate crystals appeared in the tubule lumen, which damaged tubule cells through binding to the TLR4 expressed on them. Persistent tubule damage induced interstitial fibrosis, reduced the number of nephrons, and further boosted FGF23 to trigger a deterioration spiral leading to progressive nephron loss. In humans, the progression of chronic kidney disease (CKD) ensued when serum FGF23 levels exceeded 53 pg/mL. The present study identified calcium phosphate particles in the renal tubular fluid as an effective therapeutic target to decelerate nephron loss during the course of aging and CKD progression.

How obesity influence psoriasis severity in developing countries

Psoriasis is a common chronic inflammatory skin disease with a complex pathogenesis consisting of a genetic component, immune dysfunction, and environmental factors. It is associated with numerous comorbidities including psoriatic arthritis, cardiovascular disease, metabolic syndrome, and obesity. The dietary habits in industrialized nations promote high-fat, high-salt, and high-sugar diets with excess caloric intake resulting in an obesity epidemic. Meta-analyses have shown that (1) genetically higher BMI increased the odds of psoriasis occurrence; (2) obesity is associated with higher incidence and prevalence of psoriasis as well as psoriasis severity; (3) obesity is associated with lower efficacy to anti-TNF agents and may predict biologic treatment discontinuation; and (4) weight loss through diet and physical exercise may improve pre-existing psoriasis. Obesity is one of the major public health concerns due to its upward trend in both developing and developed countries. In developing countries, the consequence of obesity not only affects health but also creates a burden on individual and national healthcare budgets. The prevalence of overweight and obesity in developing countries is increasing faster than the world average. This fast-paced growth has been accompanied by notable increases in the burden of non-communicable diseases (NCDs). While obesity is gradually increasing in developing countries, where NCD is yet to implement. If proper NCD program is not implement in right time, severity of psoriasis will increase with increase prevalence of obesity.

Effect of Polyphenols Intake on Obesity-Induced Maternal Programming.

Excess caloric intake and body fat accumulation lead to obesity, a complex chronic disease that represents a significant public health problem due to the health-related risk factors. There is growing evidence showing that maternal obesity can program the offspring, which influences neonatal phenotype and predispose offspring to metabolic disorders such as obesity. This increased risk may also be epigenetically transmitted across generations. Thus, there is an imperative need to find effective reprogramming approaches in order to resume normal fetal development. Polyphenols are bioactive compounds found in vegetables and fruits that exert its anti-obesity effect through its powerful anti-oxidant and anti-inflammatory activities. Polyphenol supplementation has been proven to counteract the prejudicial effects of maternal obesity programming on progeny. Indeed, some polyphenols can cross the placenta and protect the fetal predisposition against obesity. The present review summarizes the effects of dietary polyphenols on obesity-induced maternal reprogramming as an offspring anti-obesity approach.

On the Role of Paraoxonase-1 and Chemokine Ligand 2 (C-C motif) in Metabolic Alterations Linked to Inflammation and Disease. A 2021 Update.

Infectious and many non-infectious diseases share common molecular mechanisms. Among them, oxidative stress and the subsequent inflammatory reaction are of particular note. Metabolic disorders induced by external agents, be they bacterial or viral pathogens, excessive calorie intake, poor-quality nutrients, or environmental factors produce an imbalance between the production of free radicals and endogenous antioxidant systems; the consequence being the oxidation of lipids, proteins, and nucleic acids. Oxidation and inflammation are closely related, and whether oxidative stress and inflammation represent the causes or consequences of cellular pathology, both produce metabolic alterations that influence the pathogenesis of the disease. In this review, we highlight two key molecules in the regulation of these processes: Paraoxonase-1 (PON1) and chemokine (C-C motif) ligand 2 (CCL2). PON1 is an enzyme bound to high-density lipoproteins. It breaks down lipid peroxides in lipoproteins and cells, participates in the protection conferred by HDL against different infectious agents, and is considered part of the innate immune system. With PON1 deficiency, CCL2 production increases, inducing migration and infiltration of immune cells in target tissues and disturbing normal metabolic function. This disruption involves pathways controlling cellular homeostasis as well as metabolically-driven chronic inflammatory states. Hence, an understanding of these relationships would help improve treatments and, as well, identify new therapeutic targets.

Role of Leptin in Non-Alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD), which affects about a quarter of the global population, poses a substantial health and economic burden in all countries, yet there is no approved pharmacotherapy to treat this entity, nor well-established strategies for its diagnosis. Its prevalence has been rapidly driven by increased physical inactivity, in addition to excessive calorie intake compared to energy expenditure, affecting both adults and children. The increase in the number of cases, together with the higher morbimortality that this disease entails with respect to the general population, makes NAFLD a serious public health problem. Closely related to the development of this disease, there is a hormone derived from adipocytes, leptin, which is involved in energy homeostasis and lipid metabolism. Numerous studies have verified the relationship between persistent hyperleptinemia and the development of steatosis, fibrinogenesis and liver carcinogenesis. Therefore, further studies of the role of leptin in the NAFLD spectrum could represent an advance in the management of this set of diseases.

Bioaccessibility and Bioavailability of Minerals in Relation to a Healthy Gut Microbiome

Adequate amounts of a wide range of micronutrients are needed by body tissues to maintain health. Dietary intake must be sufficient to meet these micronutrient requirements. Mineral deficiency does not seem to be the result of a physically active life or of athletic training but is more likely to arise from disturbances in the quality and quantity of ingested food. The lack of some minerals in the body appears to be symbolic of the modern era reflecting either the excessive intake of empty calories or a negative energy balance from drastic weight-loss diets. Several animal studies provide convincing evidence for an association between dietary micronutrient availability and microbial composition in the gut. However, the influence of human gut microbiota on the bioaccessibility and bioavailability of trace elements in human food has rarely been studied. Bacteria play a role by effecting mineral bioavailability and bioaccessibility, which are further increased through the fermentation of cereals and the soaking and germination of crops. Moreover, probiotics have a positive effect on iron, calcium, selenium, and zinc in relation to gut microbiome composition and metabolism. The current literature reveals the beneficial effects of bacteria on mineral bioaccessibility and bioavailability in supporting both the human gut microbiome and overall health. This review focuses on interactions between the gut microbiota and several minerals in sport nutrition, as related to a physically active lifestyle.

Nontraditional Risk Factors for Obesity in Modern Society.

Overweight and obesity, which have rapidly increased around the world in recent years, are significant health problems. They can lead to various morbidities, including cardiovascular diseases, cerebrovascular diseases, type 2 diabetes, some types of cancer, and even death. Obesity is caused by an energy imbalance due to excessive calorie intake and insufficient energy consumption, and genetic factors and individual behavioral problems are also known to be major contributing factors. However, these are insufficient to explain the surge in obesity that has occurred in recent decades. Recent studies have suggested that environmental factors arising from the process of socioeconomic development and modernization contribute to this phenomenon. These environmental factors include light pollution due to artificial lighting, air pollution, endocrine-disrupting chemicals, and reduced exposure to green spaces due to urbanization of residential areas. In this manuscript, the findings and mechanisms of these novel risk factors causing overweight and obesity are reviewed.

Mental health impact of covid on athletes

IntroductionThe coronavirus pandemic continues to impact all aspects of the daily life of the public worldwide. With decreased economic activity, the sports industry faces significant challenges of maintaining athletes’ mental health while seeking the best strategies for eventual return to sports competition.ObjectivesWe aim to evaluate COVID-19 related factors impacting on the mental health of athletes and provide appropriate management steps.MethodsWe examined MeSH terms “Athletes,” “Sports,” “COVID-19,” in the context of “Mental Health,” “Mental Disorders,” “Behavioral Medicine,” “Risk Factors.” We identified seven studies for the qualitative synthesis per the PRISMA guidelines, searching Medline, PubMed, PubMed Central, and PsychInfo databases until July 2020.ResultsThe pandemic has negatively impacted athletes’ mental wellbeing due to decreased physical activities, limited resources, fears, and delays or cancellations of the sporting event. The negative psychological impact on athletes is due to self-isolation measures leading to worries of less preparedness for the lockdown, reduced physical activity, loss of competitive advantages, fear of being infected, social isolation, and loneliness. During this period, athletes struggled to maintain baseline routine and engaged in excessive calorie intake, eating low-quality food, substance use, and sleep disruption. It has caused anxiety, depression, PTSD, and mood disorder at varying degrees of severity in athletes.ConclusionsLimited resources during a pandemic have caused adverse mental impact on athletes. We recommend improving physical activity through confined or virtual training programs with colleagues. A collaborative approach is required by clinicians, psychologists, coaches, sports organizations, government bodies to limit the pandemic’s mental health impact.

Region-specific nutritious, environmentally friendly, and affordable diets in India

Region-specific nutritious, environmentally friendly, and affordable diets in India

A Scoping Review on Lipocalin-2 and Its Role in Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma.

Excess calorie intake and a sedentary lifestyle have made non-alcoholic fatty liver disease (NAFLD) one of the fastest growing forms of liver disease of the modern world. It is characterized by abnormal accumulation of fat in the liver and can range from simple steatosis and non-alcoholic steatohepatitis (NASH) to cirrhosis as well as development of hepatocellular carcinoma (HCC). Biopsy is the golden standard for the diagnosis and differentiation of all NAFLD stages, but its invasiveness poses a risk for patients, which is why new, non-invasive ways of diagnostics ought to be discovered. Lipocalin-2 (LCN2), which is a part of the lipocalin transport protein family, is a protein formally known for its role in iron transport and in inflammatory response. However, in recent years, its implication in the pathogenesis of NAFLD has become apparent. LCN2 shows significant upregulation in several benign and malignant liver diseases, making it a good candidate for the NAFLD biomarker or even a therapeutic target. What makes LCN2 more interesting to study is the fact that it is overexpressed in HCC development induced by chronic NASH, which is one of the primary causes of cancer-related deaths. However, to this day, neither its role as a biomarker for NAFLD nor the molecular mechanisms of its implication in NAFLD pathogenesis have been completely elucidated. This review aims to gather and closely dissect the current knowledge about, sometimes conflicting, evidence on LCN2 as a biomarker for NAFLD, its involvement in NAFLD, and NAFLD-HCC related pathogenesis, while comparing it to the findings in similar pathologies.

Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial

Excessive fructose intake is associated with increased de novo lipogenesis, blood triglycerides, and hepatic insulin resistance. We aimed to determine whether fructose elicits specific effects on lipid metabolism independently of excessive caloric intake. A total of 94 healthy men were studied in this double-blind, randomized trial. They were assigned to daily consumption of sugar-sweetened beverages (SSBs) containing moderate amounts of fructose, sucrose (fructose-glucose disaccharide) or glucose (80g/day) in addition to their usual diet or SSB abstinence (control group) for 7 weeks. De novo fatty acid (FA) and triglyceride synthesis, lipolysis and plasma free FA (FFA) oxidation were assessed by tracer methodology. Daily intake of beverages sweetened with free fructose and fructose combined with glucose (sucrose) led to a 2-fold increase in basal hepatic fractional secretion rates (FSR) compared to control (median FSR %/day: sucrose 20.8 (p= 0.0015); fructose 19.7 (p= 0.013); control 9.1). Conversely, the same amounts of glucose did not change FSR (median of FSR %/day 11.0 (n.s.)). Fructose intake did not change basal secretion of newly synthesized VLDL-triglyceride, nor did it alter rates of peripheral lipolysis, nor total FA and plasma FFA oxidation. Total energy intake was similar across groups. Regular consumption of both fructose- and sucrose-sweetened beverages in moderate doses - associated with stable caloric intake - increases hepatic FA synthesis even in a basal state; this effect is not observed after glucose consumption. These findings provide evidence of an adaptative response to regular fructose exposure in the liver. This study investigated the metabolic effects of daily sugar-sweetened beverage consumption for several weeks in healthy lean men. It revealed that beverages sweetened with the sugars fructose and sucrose (glucose and fructose combined), but not glucose, increase the ability of the liver to produce lipids. This change may pave the way for further unfavorable effects on metabolic health. NCT01733563.

Pyruvate Dehydrogenase as a Therapeutic Target for Nonalcoholic Fatty Liver Disease.

Excess caloric intake combined with a sedentary lifestyle in the general population has greatly increased the prevalence of obesity and nonalcoholic fatty liver disease (NAFLD), which is defined as the accumulation of excess fat in the liver in the absence of alcohol abuse or other attributable causes such as infection with hepatitis C. Furthermore, NAFLD increases the risk for insulin resistance, type 2 diabetes (T2D), and cardiovascular disease, while currently having no approved therapy to counteract its pathology. Thus, increasing efforts to understand the mechanisms responsible for NAFLD have been pursued in preclinical studies, in the hopes of developing novel therapies that can prevent the progression of insulin resistance and/or T2D. The pathology of NAFLD is multifactorial, with proposed mechanisms including inflammation, oxidative stress, and mitochondrial dysfunction to name a few. The latter remains a subject of ongoing debate, but may be attributed to impaired hepatic fatty acid oxidation, thereby increasing the accumulation of triacylglycerol within hepatocytes. More recent studies have also demonstrated that the mitochondrial dysfunction in NAFLD may also encompass impairments in glucose oxidation, despite oxidative energy production having minimal contribution to overall glucose/pyruvate metabolism in the liver. Accordingly, strategies to reverse this defect in glucose oxidation can ameliorate hepatic steatosis and improve glucose homeostasis. We will review herein the evidence supporting impaired hepatic glucose oxidation as a mechanism of NAFLD, while discussing the validity of pyruvate dehydrogenase (PDH), the rate-limiting enzyme of glucose oxidation, as a potential target for NAFLD. In addition, we will discuss potential mechanisms of action by which increased hepatic PDH activity and subsequent glucose oxidation can reverse the pathology of obesity-induced NAFLD, as well as opportunities to target this pathway with clinical agents.

Psychological Resilience, Experimentally Manipulated Social Status, and Dietary Intake among Adolescents.

Relative to other racial/ethnic groups in the United States, Hispanic American (HA) youth have higher rates of overweight and obesity. Previous work suggests that low perceived social status (SS) promotes excess caloric intake and, thereby, development of obesity. Psychological resilience may play a role in reducing adverse eating behaviors and risk for obesity. The objective of this study was to investigate whether resilience (as measured by the Connor Davidson Resilience Scale) interacts with experimentally manipulated SS to affect dietary intake among HA adolescents (n = 132). Using a rigged game of Monopoly (Hasbro, Inc.), participants were randomized to a high or low SS condition. Following the Monopoly game, participants consumed an ad libitum lunch and their dietary intake was assessed. There was a significant interaction between resilience and experimentally manipulated SS for total energy intake (p = 0.006), percent energy needs consumed (p = 0.005), and sugar intake (p = 0.004). For the high SS condition, for each increase in resilience score, total energy intake decreased by 7.165 ± 2.866 kcal (p = 0.014) and percent energy needs consumed decreased by 0.394 ± 0.153 (p = 0.011). In the low SS condition, sugar intake increased by 0.621 ± 0.240 g for each increase in resilience score (p = 0.011). After correction for multiple comparisons, the aforementioned interactions, but not simple slopes, were statistically significant.

Changing trends in the disease burden of esophageal cancer in China from 1990 to 2017 and its predicted level in 25 years.

BackgroundNearly half of the cases of esophageal cancer in the world were in China, but the corresponding burden in China has not been estimated for the past decades or for the near future.MethodsData on the incidence, mortality, and disability‐adjusted life years (DALYs) rates owing to esophageal cancer in China from 1990 to 2017 were extracted from the Global Burden of Disease Study 2017. To reflect the trend in the disease burden, we calculated the estimated annual percentage change (EAPC) in the age‐standardized rates of these three outcomes in China from 1990 to 2017.ResultsThe age‐standardized incidence rate (ASIR) for esophageal cancer decreased from 19.38/100,000 in 1990 to 12.23/100,000 in 2017, with an EAPC of −2.53 (95%CI: −2.90, −2.16), but the number of cases of esophageal cancer increased from 164,473 to 234,624. The age‐standardized rates of esophageal cancer in females were always lower than they were in males during the study period, and there was a downward trend that was more pronounced among females than males. The most common risk factors for males were smoking and alcohol consumption, while the most common risk factors for females were a diet low in fruits and a high body mass index (BMI). New cases of, and deaths from esophageal cancer are predicted to increase by about 1.5 times in the coming 25 years.ConclusionAlthough the age‐standardized burden of esophageal cancer has been declining, the number of new cases of, and deaths from esophageal cancer have increased in China over the past 30 years, and they will continue to increase in the near future. Hence, national policies should be adopted to promote the prevention and management of known risk factors for it, especially smoking and excessive caloric intake.