Do Globalization and Free Markets Drive Obesity among Children and Youth? An Empirical Analysis, 1990–2013

Scholars of public health identify globalization as a major cause of obesity. Free markets are blamed for spreading high calorie, nutrient-poor diets, and sedentary lifestyles across the globe. Global trade and investment agreements apparently curtail government action in the interest of public health. Globalization is also blamed for raising income inequality and social insecurities, which contribute to “obesogenic” environments. Contrary to recent empirical studies, this study demonstrates that globalization and several component parts, such as trade openness, FDI flows, and an index of economic freedom, reduce weight gain and obesity among children and youth, the most likely age cohort to be affected by the past three decades of globalization and attendant lifestyle changes. The results suggest strongly that local-level factors possibly matter much more than do global-level factors for explaining why some people remain thin and others put on weight. The proposition that globalization is homogenizing cultures across the globe in terms of diets and lifestyles is possibly exaggerated. The results support the proposition that globalized countries prioritize health because of the importance of labor productivity and human capital due to heightened market competition, ceteris paribus, even if rising incomes might drive high consumption

Do Globalization and Free Markets Drive Obesity among Children and Youth? An Empirical Analysis, 1990–2013

Scholars of public health identify globalization as a major cause of obesity. Free markets are blamed for spreading high calorie, nutrient-poor diets, and sedentary lifestyles across the globe. Global trade and investment agreements apparently curtail government action in the interest of public health. Globalization is also blamed for raising income inequality and social insecurities, which contribute to “obesogenic” environments. Contrary to recent empirical studies, this study demonstrates that globalization and several component parts, such as trade openness, FDI flows, and an index of economic freedom, reduce weight gain and obesity among children and youth, the most likely age cohort to be affected by the past three decades of globalization and attendant lifestyle changes. The results suggest strongly that local-level factors possibly matter much more than do global-level factors for explaining why some people remain thin and others put on weight. The proposition that globalization is homogenizing cultures across the globe in terms of diets and lifestyles is possibly exaggerated. The results support the proposition that globalized countries prioritize health because of the importance of labor productivity and human capital due to heightened market competition, ceteris paribus, even if rising incomes might drive high consumption

Impact of a FTO gene risk variant on variables of energy metabolism in adults with obesity class 2 and 3

Purpose The metabolic consequences of carrying a FTO obesity-promoting risk allele have not been fully elucidated and may be confounded by obesity per se. Against this background, we investigated the impact of FTO allele (SNP rs9939609) on fasting and postprandial energy expenditure and fasting substrate expenditure in a study population of uniformly and similarly obese individuals. Procedures We studied a similar number of participants with BMI classes 2–3 (median BMI 42.8 kg/m2) who were either homozygote for the non-risk allele TT (n = 33, numbers increased by enrichment), heterozygote (AT) (n = 32), or homozygote for the risk allele AA (n = 35). Major findings Basal metabolic rate and postprandial energy expenditure did not differ between FTO-groups. However, fasting respiratory quotient (RQ) was increased in those carrying ≥1 risk allele (p = 0.008), whereas postprandial RQ was not. Conclusion In this study population, the FTO-risk allele associates with fasting reduced fat and increased carbohydrate oxidation

Nutritional risk is associated with long term mortality in hospitalized patients with chronic heart failure

SummaryBackground & aimsMortality among patients with chronic heart failure (CHF) is still high despite progress in medical and surgical treatment. The patients' nutritional condition may play an important role, and needs further investigation. The aim of this study was to evaluate whether nutritional risk in hospitalized patients with CHF was associated with three-year mortality.MethodsA prospective study was conducted in 131 hospitalized Norwegian patients with CHF. Nutritional screening was performed using Nutritional Risk Screening (NRS-2002). The primary clinical outcome was death from any cause.ResultsThe prevalence of nutritional risk was 57% (NRS-2002 score ≥ 3). The overall mortality rate was 52.6% within three-year follow up. More patients at nutritional risk (N = 51) died compared to patients not at nutritional risk (N = 18) (P < 0.001). In adjusted analyses patients at nutritional risk had more than five-time higher odds (OR 5.85; 95% CI 2.10–16.24) to die before three-year follow-up than those not at nutritional risk. In adjusted Cox multivariate analysis, the nutritional risk was associated with increased mortality (HR 2.78; 95% CI 1.53–5.03). Furthermore, in adjusted analysis components in NRS-2002 were associated with mortality, i.e. nutritional status (HR 1.82; 95% CI 1.03–3.22), severity of disease (NYHA-class IV) (HR 1.78; 95% CI 1.00–3.16) and age (≥ 70 year) (HR 3.24; 95% CI 1.48–7.10).ConclusionNutritional risk as defined by NRS-2002 in hospitalized patients with CHF was significantly associated with long term mortality

Effect of a ketogenic diet on pain and quality of life in patients with lipedema: The LIPODIET pilot study

Background Lipedema is an underdiagnosed condition in women, characterized by a symmetrical increase in subcutaneous adipose tissue (SAT) in the lower extremities, sparing the trunk. The lipedema SAT has been found to be resistant to diet, exercise and bariatric surgery, in regard to both weight loss (WL) and symptom relief. Current experience indicates that a low carbohydrate and high fat (LCHF-diet) might have a beneficial effect on weight and symptom management in lipedema. Objective To assess the impact of an eucaloric low carbohydrate, high fat (LCHF)-diet on pain and quality of life (QoL) in patients with lipedema. Methods Women diagnosed with lipedema, including all types and stages affecting the legs, (age 18-75 years, BMI 30-45 kg/m2) underwent 7 weeks (wk) of LCHF-diet and, thereafter 6 wk of a diet following the Nordic nutrition recommendations. Pain (visual analog scale) and QoL (questionnaire for lymphedema of the limbs), weight and body composition were measured at baseline, wk 7 and 13. Results Nine women (BMI: 36.7±4.5kg/m2 and age: 46.9±7 years) were recruited. The LCHF diet induced a significant WL -4.6±0.7 kg (-4.5±2.4%), P<0.001 for both, and reduction in pain (-2.3±0.4 cm, P=0.020). No correlation was found between WL and changes in pain at wk 7 (r = 0.283, P = 0.460). WL was maintained between wk 7 and 13 (0.3±0.7 kg, P=0.430), but pain returned to baseline levels at wk 13 (4.2±0.7 cm ,P=0.690). A significant increase in general QoL was found between baseline and wk 7 (1.0 (95% CI (2.0, 0.001), P=0.050) and 13 (1.0 95% CI (2.0, 0.001) P=0.050), respectively. Conclusion A LCHF-diet is associated with reduction in perceived pain and improvement in QoL, in patients with lipedema. Larger randomized clinical trials are needed to confirm these findings

Effect of a ketogenic diet on pain and quality of life in patients with lipedema: The LIPODIET pilot study

Background Lipedema is an underdiagnosed condition in women, characterized by a symmetrical increase in subcutaneous adipose tissue (SAT) in the lower extremities, sparing the trunk. The lipedema SAT has been found to be resistant to diet, exercise and bariatric surgery, in regard to both weight loss (WL) and symptom relief. Current experience indicates that a low carbohydrate and high fat (LCHF-diet) might have a beneficial effect on weight and symptom management in lipedema. Objective To assess the impact of an eucaloric low carbohydrate, high fat (LCHF)-diet on pain and quality of life (QoL) in patients with lipedema. Methods Women diagnosed with lipedema, including all types and stages affecting the legs, (age 18-75 years, BMI 30-45 kg/m2) underwent 7 weeks (wk) of LCHF-diet and, thereafter 6 wk of a diet following the Nordic nutrition recommendations. Pain (visual analog scale) and QoL (questionnaire for lymphedema of the limbs), weight and body composition were measured at baseline, wk 7 and 13. Results Nine women (BMI: 36.7±4.5kg/m2 and age: 46.9±7 years) were recruited. The LCHF diet induced a significant WL -4.6±0.7 kg (-4.5±2.4%), P<0.001 for both, and reduction in pain (-2.3±0.4 cm, P=0.020). No correlation was found between WL and changes in pain at wk 7 (r = 0.283, P = 0.460). WL was maintained between wk 7 and 13 (0.3±0.7 kg, P=0.430), but pain returned to baseline levels at wk 13 (4.2±0.7 cm ,P=0.690). A significant increase in general QoL was found between baseline and wk 7 (1.0 (95% CI (2.0, 0.001), P=0.050) and 13 (1.0 95% CI (2.0, 0.001) P=0.050), respectively. Conclusion A LCHF-diet is associated with reduction in perceived pain and improvement in QoL, in patients with lipedema. Larger randomized clinical trials are needed to confirm these findings

The fat mass and obesity-associated (FTO) gene allele rs9939609 and glucose tolerance, hepatic and total insulin sensitivity, in adults with obesity.

The objective of the study was to assess associations of the rs9939609 FTO allele to glucose tolerance, hepatic and total insulin sensitivity (IS) in individuals with obesity. From a low-dose hyperinsulinemic euglycemic clamp with glucose-tracer, hepatic IS was assessed by rates of basal and suppressed glucose appearance (Ra), a measure of endogenous glucose production (EGP), and the hepatic insulin resistance index (HIR). Total IS was assessed by rates of glucose infusion (GIR), disappearance (Rd), and metabolic clearance (MCR). From a meal test we assessed IS by the Matsuda index and glucose tolerance by glucose and insulin measurements in the fasted state and postprandially for 2.5 h. The meal test was performed in 97 healthy individuals with BMI ≥35 in similar-sized risk-allele groups (n = 32 T/T, 31 A/T, and 34 A/A), and 79 of them performed the clamp. We analyzed outcomes separately for males and females, and adjusted glucose Ra, Rd, MCR, GIR, and HIR for fat mass. We did not find genotype effects on EGP. Among males, genotype A/A was associated with a significantly lower glucose Rd, MCR, and Matsuda index score relative to genotype T/T. Glucose tolerance was significantly lower in males with genotype A/T vs. T/T and A/A. For females, there were no genotype effects on hepatic or total IS, or on glucose tolerance. Independently of genotypes, females displayed a significantly better hepatic and total IS, and better glucose tolerance than males. We conclude that in subjects with similar obesity we did not register any FTO risk-allele effect on hepatic IS. A FTO risk-allele effect on total IS was registered in males only, findings which need to be reproduced in further studies. Results confirm marked differences in IS between the biological sexes and extend present knowledge by demonstrating a lower endogenous glucose production in females vs. males in uniformly obese individuals

The fat mass and obesity-associated (FTO) gene allele rs9939609 and glucose tolerance, hepatic and total insulin sensitivity, in adults with obesity

The objective of the study was to assess associations of the rs9939609 FTO allele to glucose tolerance, hepatic and total insulin sensitivity (IS) in individuals with obesity. From a low-dose hyperinsulinemic euglycemic clamp with glucose-tracer, hepatic IS was assessed by rates of basal and suppressed glucose appearance (Ra), a measure of endogenous glucose production (EGP), and the hepatic insulin resistance index (HIR). Total IS was assessed by rates of glucose infusion (GIR), disappearance (Rd), and metabolic clearance (MCR). From a meal test we assessed IS by the Matsuda index and glucose tolerance by glucose and insulin measurements in the fasted state and postprandially for 2.5 h. The meal test was performed in 97 healthy individuals with BMI ≥35 in similar-sized risk-allele groups (n = 32 T/T, 31 A/T, and 34 A/A), and 79 of them performed the clamp. We analyzed outcomes separately for males and females, and adjusted glucose Ra, Rd, MCR, GIR, and HIR for fat mass. We did not find genotype effects on EGP. Among males, genotype A/A was associated with a significantly lower glucose Rd, MCR, and Matsuda index score relative to genotype T/T. Glucose tolerance was significantly lower in males with genotype A/T vs. T/T and A/A. For females, there were no genotype effects on hepatic or total IS, or on glucose tolerance. Independently of genotypes, females displayed a significantly better hepatic and total IS, and better glucose tolerance than males. We conclude that in subjects with similar obesity we did not register any FTO risk-allele effect on hepatic IS. A FTO risk-allele effect on total IS was registered in males only, findings which need to be reproduced in further studies. Results confirm marked differences in IS between the biological sexes and extend present knowledge by demonstrating a lower endogenous glucose production in females vs. males in uniformly obese individuals