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Background: Whether physical activity could mitigate the adverse impacts of sugar-sweetened beverages (SSBs) or artificially sweetened beverages (ASBs) on incident cardiovascular disease (CVD) remains uncertain. Objectives: This study aimed to examine the independent and joint associations between SSB or ASB consumption and physical activity and risk of CVD, defined as fatal and nonfatal coronary artery disease and stroke, in adults from 2 United States-based prospective cohort studies. Methods: Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% CIs between SSB or ASB intake and physical activity with incident CVD among 65,730 females in the Nurses’ Health Study (1980–2016) and 39,418 males in the Health Professional's Follow-up Study (1986–2016), who were free from chronic diseases at baseline. SSBs and ASBs were assessed every 4-y and physical activity biannually. Results: A total of 13,269 CVD events were ascertained during 3,001,213 person-years of follow-up. Compared with those who never/rarely consumed SSBs or ASBs, the HR for CVD for participants consuming ≥2 servings/d was 1.21 (95% CI: 1.12, 1.32; P-trend < 0.001) for SSBs and 1.03 (95% CI: 0.97, 1.09; P-trend = 0.06) for those consuming ≥2 servings/d of ASBs. The HR for CVD per 1 serving increment of SSB per day was 1.18 (95% CI: 1.10, 1.26) and 1.12 (95% CI: 1.04, 1.20) for participants meeting and not meeting physical activity guidelines (≥7.5 compared with <7.5 MET h/wk), respectively. Compared with participants who met physical activity guidelines and never/rarely consumed SSBs, the HR for CVD was 1.47 (95% CI: 1.37, 1.57) for participants not meeting physical activity guidelines and consuming ≥2 servings/wk of SSBs. No significant associations were observed for ASB when stratified by physical activity. Conclusions: Higher SSB intake was associated with CVD risk regardless of physical activity levels. These results support current recommendations to limit the in

The obesity pandemic continues unabated despite a persistent public health campaign to decrease energy intake ("eat less") and increase energy expenditure ("move more"). One explanation for this failure is that the current approach, based on the notion of energy balance, has not been adequately embraced by the public. Another possibility is that this approach rests on an erroneous paradigm. A new formulation of the energy balance model (EBM), like prior versions, considers overeating (energy intake > expenditure) the primary cause of obesity, incorporating an emphasis on "complex endocrine, metabolic, and nervous system signals" that control food intake below conscious level. This model attributes rising obesity prevalence to inexpensive, convenient, energy-dense, "ultra-processed" foods high in fat and sugar. An alternative view, the carbohydrate-insulin model (CIM), proposes that hormonal responses to highly processed carbohydrates shift energy partitioning toward deposition in adipose tissue, leaving fewer calories available for the body's metabolic needs. Thus, increasing adiposity causes overeating to compensate for the sequestered calories. Here, we highlight robust contrasts in how the EBM and CIM view obesity pathophysiology and consider deficiencies in the EBM that impede paradigm testing and refinement. Rectifying these deficiencies should assume priority, as a constructive paradigm clash is needed to resolve long-standing scientific controversies and inform the design of new models to guide prevention and treatment. Nevertheless, public health action need not await resolution of this debate, as both models target processed carbohydrates as major drivers of obesity.

BACKGROUND: The extent to which physical activity attenuates the detrimental effects of sugar (SSBs)- or artificially-sweetened beverages (ASBs) on the risk of cardiovascular disease is unknown.METHODS: We used Cox proportional-hazards models to calculate hazard ratios and 95% confidence interval [HR (CI)] between SSB or ASB intake and physical activity with cardiovascular disease risk among 65,730 women in the Nurses' Health Study (1980-2016) and 39,418 men in the Health Professional's Follow-up Study (1986-2016), who were free from chronic diseases at baseline. SSBs and ASBs were assessed every 4-years and physical activity biannually.RESULTS: A total of 13,269 cardiovascular events were ascertained during 3,001,213 person-years of follow-up. Compared with those that never/rarely consumed SSBs or ASBs, HR and 95% CI for cardiovascular disease for participants consuming ≥2 servings/day were 1.21 (95% CI,1.12 to 1.32; P -trend<0.001) and 1.03 (95% CI, 0.97 to 1.09; P -trend=0.06), respectively. In the joint analyses, for participants meeting and not meeting physical activity guidelines (<7.5 vs ≥7.5 MET-h/week) as well as consuming ≥2 servings/day of SSBs or ASBs, the HRs for cardiovascular disease were 1.15 (95% CI, 1.08 to 1.23) and 0.96 (95% CI, 0.91 to 1.02), and 1.47 (95% CI, 1.37 to 1.57) and 1.29 (95% CI, 1.22 to 1.37) respectively, compared with participants who met physical activity guidelines and never/rarely consumed these beverages. Similar patterns were observed when coronary heart disease and stroke were analyzed. CONCLUSIONS: Our findings suggest that among physically active participants, higher SSB intake, but not ASBs, is associated with a higher cardiovascular risk. Our results support current recommendations to limit the intake of SSB and maintain adequate physical activity levels.CLINICAL PERSPECTIVE: What is new?: Consumption of sugar- or artificially-sweetened beverages and physical activity are independentl

BACKGROUND: The extent to which physical activity attenuates the detrimental effects of sugar (SSBs)- or artificially-sweetened beverages (ASBs) on the risk of cardiovascular disease is unknown.METHODS: We used Cox proportional-hazards models to calculate hazard ratios and 95% confidence interval [HR (CI)] between SSB or ASB intake and physical activity with cardiovascular disease risk among 65,730 women in the Nurses' Health Study (1980-2016) and 39,418 men in the Health Professional's Follow-up Study (1986-2016), who were free from chronic diseases at baseline. SSBs and ASBs were assessed every 4-years and physical activity biannually.RESULTS: A total of 13,269 cardiovascular events were ascertained during 3,001,213 person-years of follow-up. Compared with those that never/rarely consumed SSBs or ASBs, HR and 95% CI for cardiovascular disease for participants consuming ≥2 servings/day were 1.21 (95% CI,1.12 to 1.32; P -trend<0.001) and 1.03 (95% CI, 0.97 to 1.09; P -trend=0.06), respectively. In the joint analyses, for participants meeting and not meeting physical activity guidelines (<7.5 vs ≥7.5 MET-h/week) as well as consuming ≥2 servings/day of SSBs or ASBs, the HRs for cardiovascular disease were 1.15 (95% CI, 1.08 to 1.23) and 0.96 (95% CI, 0.91 to 1.02), and 1.47 (95% CI, 1.37 to 1.57) and 1.29 (95% CI, 1.22 to 1.37) respectively, compared with participants who met physical activity guidelines and never/rarely consumed these beverages. Similar patterns were observed when coronary heart disease and stroke were analyzed. CONCLUSIONS: Our findings suggest that among physically active participants, higher SSB intake, but not ASBs, is associated with a higher cardiovascular risk. Our results support current recommendations to limit the intake of SSB and maintain adequate physical activity levels.CLINICAL PERSPECTIVE: What is new?: Consumption of sugar- or artificially-sweetened beverages and physical activity are independentl

Worldwide dietary guidelines in the late 20th century promoted a low-fat diet, based, in part, on the notion that dietary fat, the most energy dense macronutrient, causes excess weight gain. However, high-quality evidence accumulating since then refute a direct association between dietary fat and adiposity. Moreover, substitution of carbohydrates for unsaturated fat can increase insulin resistance and cardiometabolic disease, especially among populations with highly prevalent insulin resistance. In this context, the recent WHO conditional recommendation to carry forward the guidance to limit dietary fat to ≤30% seems ill advised and should be reconsidered.

According to a commonly held view, the obesity pandemic is caused by overconsumption of modern, highly palatable, energy-dense processed foods, exacerbated by a sedentary lifestyle. However, obesity rates remain at historic highs, despite a persistent focus on eating less and moving more, as guided by the energy balance model (EBM). This public health failure may arise from a fundamental limitation of the EBM itself. Conceptualizing obesity as a disorder of energy balance restates a principle of physics without considering the biological mechanisms that promote weight gain. An alternative paradigm, the carbohydrate-insulin model (CIM), proposes a reversal of causal direction. According to the CIM, increasing fat deposition in the body-resulting from the hormonal responses to a high-glycemic-load diet-drives positive energy balance. The CIM provides a conceptual framework with testable hypotheses for how various modifiable factors influence energy balance and fat storage. Rigorous research is needed to compare the validity of these 2 models, which have substantially different implications for obesity management, and to generate new models that best encompass the evidence.

According to a commonly held view, the obesity pandemic is caused by overconsumption of modern, highly palatable, energy-dense processed foods, exacerbated by a sedentary lifestyle. However, obesity rates remain at historic highs, despite a persistent focus on eating less and moving more, as guided by the energy balance model (EBM). This public health failure may arise from a fundamental limitation of the EBM itself. Conceptualizing obesity as a disorder of energy balance restates a principle of physics without considering the biological mechanisms that promote weight gain. An alternative paradigm, the carbohydrate-insulin model (CIM), proposes a reversal of causal direction. According to the CIM, increasing fat deposition in the body-resulting from the hormonal responses to a high-glycemic-load diet-drives positive energy balance. The CIM provides a conceptual framework with testable hypotheses for how various modifiable factors influence energy balance and fat storage. Rigorous research is needed to compare the validity of these 2 models, which have substantially different implications for obesity management, and to generate new models that best encompass the evidence.

When lean people adopt carbohydrate-restricted diets (CRDs), they may develop a lipid profile consisting of elevated LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) with low triglycerides (TGs). The magnitude of this lipid profile correlates with BMI such that those with lower BMI exhibit larger increases in both LDL-C and HDL-C. The inverse association between BMI and LDL-C and HDL-C change on CRD contributed to the discovery of a subset of individuals-termed Lean Mass Hyper-Responders (LMHR)-who, despite normal pre-diet LDL-C, as compared to non-LMHR (mean levels of 148 and 145 mg/dL, respectively), exhibited a pronounced hyperlipidemic response to a CRD, with mean LDL-C and HDL-C levels increasing to 320 and 99 mg/dL, respectively, in the context of mean TG of 47 mg/dL. In some LMHR, LDL-C levels may be in excess of 500 mg/dL, again, with relatively normal pre-diet LDL-C and absent of genetic findings indicative of familial hypercholesterolemia in those who have been tested. The Lipid Energy Model (LEM) attempts to explain this metabolic phenomenon by positing that, with carbohydrate restriction in lean persons, the increased dependence on fat as a metabolic substrate drives increased hepatic secretion and peripheral uptake of TG contained within very low-density lipoproteins (VLDL) by lipoprotein lipase, resulting in marked elevations of LDL-C and HDL-C, and low TG. Herein, we review the core features of the LEM. We review several existing lines of evidence supporting the model and suggest ways to test the model's predictions.

When lean people adopt carbohydrate-restricted diets (CRDs), they may develop a lipid profile consisting of elevated LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) with low triglycerides (TGs). The magnitude of this lipid profile correlates with BMI such that those with lower BMI exhibit larger increases in both LDL-C and HDL-C. The inverse association between BMI and LDL-C and HDL-C change on CRD contributed to the discovery of a subset of individuals-termed Lean Mass Hyper-Responders (LMHR)-who, despite normal pre-diet LDL-C, as compared to non-LMHR (mean levels of 148 and 145 mg/dL, respectively), exhibited a pronounced hyperlipidemic response to a CRD, with mean LDL-C and HDL-C levels increasing to 320 and 99 mg/dL, respectively, in the context of mean TG of 47 mg/dL. In some LMHR, LDL-C levels may be in excess of 500 mg/dL, again, with relatively normal pre-diet LDL-C and absent of genetic findings indicative of familial hypercholesterolemia in those who have been tested. The Lipid Energy Model (LEM) attempts to explain this metabolic phenomenon by positing that, with carbohydrate restriction in lean persons, the increased dependence on fat as a metabolic substrate drives increased hepatic secretion and peripheral uptake of TG contained within very low-density lipoproteins (VLDL) by lipoprotein lipase, resulting in marked elevations of LDL-C and HDL-C, and low TG. Herein, we review the core features of the LEM. We review several existing lines of evidence supporting the model and suggest ways to test the model's predictions.

Advanced age, followed by male sex, by far poses the greatest risk for severe COVID-19. An unresolved question is the extent to which modifiable comorbidities increase the risk of COVID-19-related mortality among younger patients, in whom COVID-19-related hospitalization strongly increased in 2021. A total of 3,163 patients with SARS-COV-2 diagnosis in the Lean European Open Survey on SARS-CoV-2-Infected Patients (LEOSS) cohort were studied. LEOSS is a European non-interventional multi-center cohort study established in March 2020 to investigate the epidemiology and clinical course of SARS-CoV-2 infection. Data from hospitalized patients and those who received ambulatory care, with a positive SARS-CoV-2 test, were included in the study. An additive effect of obesity, diabetes and hypertension on the risk of mortality was observed, which was particularly strong in young and middle-aged patients. Compared to young and middle-aged (18-55 years) patients without obesity, diabetes and hypertension (non-obese and metabolically healthy; n = 593), young and middle-aged adult patients with all three risk parameters (obese and metabolically unhealthy; n = 31) had a similar adjusted increased risk of mortality [OR 7.42 (95% CI 1.55-27.3)] as older (56-75 years) non-obese and metabolically healthy patients [n = 339; OR 8.21 (95% CI 4.10-18.3)]. Furthermore, increased CRP levels explained part of the elevated risk of COVID-19-related mortality with age, specifically in the absence of obesity and impaired metabolic health. In conclusion, the modifiable risk factors obesity, diabetes and hypertension increase the risk of COVID-19-related mortality in young and middle-aged patients to the level of risk observed in advanced age.

Weight gain indicates a positive energy balance, with calorie intake exceeding expenditure. However, this fact of physics cannot inform causality. Potential pathways to obesity include a positive energy balance that drives weight gain or weight gain that drives the positive energy balance. Here, we propose an integrated model of obesity pathogenesis that incorporates both pathways.

The doubly labeled water (DLW) method measures total energy expenditure (TEE) in free-living subjects. Several equations are used to convert isotopic data into TEE. Using the International Atomic Energy Agency (IAEA) DLW database (5,756 measurements of adults and children), we show considerable variability is introduced by different equations. The estimated rCO2 is sensitive to the dilution space ratio (DSR) of the two isotopes. Based on performance in validation studies, we propose a new equation based on a new estimate of the mean DSR. The DSR is lower at low body masses (<10 kg). Using data for 1,021 babies and infants, we show that the DSR varies non-linearly with body mass between 0 and 10 kg. Using this relationship to predict DSR from weight provides an equation for rCO2 over this size range that agrees well with indirect calorimetry (average difference 0.64%; SD = 12.2%). We propose adoption of these equations in future studies.

The doubly labeled water (DLW) method measures total energy expenditure (TEE) in free-living subjects. Several equations are used to convert isotopic data into TEE. Using the International Atomic Energy Agency (IAEA) DLW database (5,756 measurements of adults and children), we show considerable variability is introduced by different equations. The estimated rCO2 is sensitive to the dilution space ratio (DSR) of the two isotopes. Based on performance in validation studies, we propose a new equation based on a new estimate of the mean DSR. The DSR is lower at low body masses (<10 kg). Using data for 1,021 babies and infants, we show that the DSR varies non-linearly with body mass between 0 and 10 kg. Using this relationship to predict DSR from weight provides an equation for rCO2 over this size range that agrees well with indirect calorimetry (average difference 0.64%; SD = 12.2%). We propose adoption of these equations in future studies.

According to a commonly held view, the obesity pandemic is caused by overconsumption of modern, highly palatable, energy-dense processed foods, exacerbated by a sedentary lifestyle. However, obesity rates remain at historic highs, despite a persistent focus on eating less and moving more, as guided by the energy balance model (EBM). This public health failure may arise from a fundamental limitation of the EBM itself. Conceptualizing obesity as a disorder of energy balance restates a principle of physics without considering the biological mechanisms that promote weight gain. An alternative paradigm, the carbohydrate-insulin model (CIM), proposes a reversal of causal direction. According to the CIM, increasing fat deposition in the body-resulting from the hormonal responses to a high-glycemic-load diet-drives positive energy balance. The CIM provides a conceptual framework with testable hypotheses for how various modifiable factors influence energy balance and fat storage. Rigorous research is needed to compare the validity of these 2 models, which have substantially different implications for obesity management, and to generate new models that best encompass the evidence.

According to a commonly held view, the obesity pandemic is caused by overconsumption of modern, highly palatable, energy-dense processed foods, exacerbated by a sedentary lifestyle. However, obesity rates remain at historic highs, despite a persistent focus on eating less and moving more, as guided by the energy balance model (EBM). This public health failure may arise from a fundamental limitation of the EBM itself. Conceptualizing obesity as a disorder of energy balance restates a principle of physics without considering the biological mechanisms that promote weight gain. An alternative paradigm, the carbohydrate-insulin model (CIM), proposes a reversal of causal direction. According to the CIM, increasing fat deposition in the body-resulting from the hormonal responses to a high-glycemic-load diet-drives positive energy balance. The CIM provides a conceptual framework with testable hypotheses for how various modifiable factors influence energy balance and fat storage. Rigorous research is needed to compare the validity of these 2 models, which have substantially different implications for obesity management, and to generate new models that best encompass the evidence.

The doubly labeled water (DLW) method measures total energy expenditure (TEE) in free-living subjects. Several equations are used to convert isotopic data into TEE. Using the International Atomic Energy Agency (IAEA) DLW database (5,756 measurements of adults and children), we show considerable variability is introduced by different equations. The estimated rCO2 is sensitive to the dilution space ratio (DSR) of the two isotopes. Based on performance in validation studies, we propose a new equation based on a new estimate of the mean DSR. The DSR is lower at low body masses (<10 kg). Using data for 1,021 babies and infants, we show that the DSR varies non-linearly with body mass between 0 and 10 kg. Using this relationship to predict DSR from weight provides an equation for rCO2 over this size range that agrees well with indirect calorimetry (average difference 0.64%; SD = 12.2%). We propose adoption of these equations in future studies.

Ouvrage fascinant, best-seller du New York Times ! Pour en finir avec les fringales! Et perdre du poids pour de bon. Les recherches du Dr Ludwig sur le contrôle du poids le prouvent: ce n'est pas parce qu'on mange trop que l'on grossit, mais que c'est parce que l'on grossit que l'on mange trop. Pourquoi? Parce que les cellules adipeuses affamées par une alimentation déséquilibrée stockent tout ce qu'elles peuvent. Et déclenchent des envies de grignoter. Le Dr Ludwig propose un programme en trois étapes qui permet de réapprendre à vous alimenter afin de remettre de l'ordre dans votre organisme et de briser le cercle infernal de la prise de poids. Étape 1 Un «camp d'entraînement alimentaire» de deux semaines pour faire disparaître les envies de grignoter compulsives. Étape 2 Quelques semaines de remise à niveau pour reprogrammer vos cellules adipeuses. Étape 3 Un régime personnalisé pour ne plus jamais reprendre les kilos perdus et plus de 100 recettes adaptées. Résultat? Des cellules adipeuses rééduquées qui libèrent efficacement les calories stockées, et un cerveau reprogrammé qui cesse d'envoyer à votre corps des signaux de faim à tort et à travers. Oubliez les calories. Oubliez les envies de grignoter. Oubliez les régimes. L'approche du Dr Ludwig vous permettra de dompter votre faim une fois pour toutes et de perdre du poids... pour de bon!

Ouvrage fascinant, best-seller du New York Times ! Pour en finir avec les fringales! Et perdre du poids pour de bon. Les recherches du Dr Ludwig sur le contrôle du poids le prouvent: ce n'est pas parce qu'on mange trop que l'on grossit, mais que c'est parce que l'on grossit que l'on mange trop. Pourquoi? Parce que les cellules adipeuses affamées par une alimentation déséquilibrée stockent tout ce qu'elles peuvent. Et déclenchent des envies de grignoter. Le Dr Ludwig propose un programme en trois étapes qui permet de réapprendre à vous alimenter afin de remettre de l'ordre dans votre organisme et de briser le cercle infernal de la prise de poids. Étape 1 Un «camp d'entraînement alimentaire» de deux semaines pour faire disparaître les envies de grignoter compulsives. Étape 2 Quelques semaines de remise à niveau pour reprogrammer vos cellules adipeuses. Étape 3 Un régime personnalisé pour ne plus jamais reprendre les kilos perdus et plus de 100 recettes adaptées. Résultat? Des cellules adipeuses rééduquées qui libèrent efficacement les calories stockées, et un cerveau reprogrammé qui cesse d'envoyer à votre corps des signaux de faim à tort et à travers. Oubliez les calories. Oubliez les envies de grignoter. Oubliez les régimes. L'approche du Dr Ludwig vous permettra de dompter votre faim une fois pour toutes et de perdre du poids... pour de bon!

Ouvrage fascinant, best-seller du New York Times ! Pour en finir avec les fringales! Et perdre du poids pour de bon. Les recherches du Dr Ludwig sur le contrôle du poids le prouvent: ce n'est pas parce qu'on mange trop que l'on grossit, mais que c'est parce que l'on grossit que l'on mange trop. Pourquoi? Parce que les cellules adipeuses affamées par une alimentation déséquilibrée stockent tout ce qu'elles peuvent. Et déclenchent des envies de grignoter. Le Dr Ludwig propose un programme en trois étapes qui permet de réapprendre à vous alimenter afin de remettre de l'ordre dans votre organisme et de briser le cercle infernal de la prise de poids. Étape 1 Un «camp d'entraînement alimentaire» de deux semaines pour faire disparaître les envies de grignoter compulsives. Étape 2 Quelques semaines de remise à niveau pour reprogrammer vos cellules adipeuses. Étape 3 Un régime personnalisé pour ne plus jamais reprendre les kilos perdus et plus de 100 recettes adaptées. Résultat? Des cellules adipeuses rééduquées qui libèrent efficacement les calories stockées, et un cerveau reprogrammé qui cesse d'envoyer à votre corps des signaux de faim à tort et à travers. Oubliez les calories. Oubliez les envies de grignoter. Oubliez les régimes. L'approche du Dr Ludwig vous permettra de dompter votre faim une fois pour toutes et de perdre du poids... pour de bon!

Ouvrage fascinant, best-seller du New York Times ! Pour en finir avec les fringales! Et perdre du poids pour de bon. Les recherches du Dr Ludwig sur le contrôle du poids le prouvent: ce n'est pas parce qu'on mange trop que l'on grossit, mais que c'est parce que l'on grossit que l'on mange trop. Pourquoi? Parce que les cellules adipeuses affamées par une alimentation déséquilibrée stockent tout ce qu'elles peuvent. Et déclenchent des envies de grignoter. Le Dr Ludwig propose un programme en trois étapes qui permet de réapprendre à vous alimenter afin de remettre de l'ordre dans votre organisme et de briser le cercle infernal de la prise de poids. Étape 1 Un «camp d'entraînement alimentaire» de deux semaines pour faire disparaître les envies de grignoter compulsives. Étape 2 Quelques semaines de remise à niveau pour reprogrammer vos cellules adipeuses. Étape 3 Un régime personnalisé pour ne plus jamais reprendre les kilos perdus et plus de 100 recettes adaptées. Résultat? Des cellules adipeuses rééduquées qui libèrent efficacement les calories stockées, et un cerveau reprogrammé qui cesse d'envoyer à votre corps des signaux de faim à tort et à travers. Oubliez les calories. Oubliez les envies de grignoter. Oubliez les régimes. L'approche du Dr Ludwig vous permettra de dompter votre faim une fois pour toutes et de perdre du poids... pour de bon!

ObjectiveThe relation of breakfast intake frequency to metabolic health is not well studied. The aim of this study was to examine breakfast intake frequency with incidence of metabolic conditions.Research design and methodsWe performed an analysis of 3,598 participants from the community-based Coronary Artery Risk Development in Young Adults (CARDIA) study who were free of diabetes in the year 7 examination when breakfast and dietary habits were assessed (1992-1993) and participated in at least one of the five subsequent follow-up examinations over 18 years.ResultsRelative to those with infrequent breakfast consumption (0-3 days/week), participants who reported eating breakfast daily gained 1.9 kg less weight over 18 years (P=0.001). In a Cox regression analysis, there was a stepwise decrease in risk across conditions in frequent breakfast consumers (4-6 days/week) and daily consumers. The results for incidence of abdominal obesity, obesity, metabolic syndrome, and hypertension remained significant after adjustment for baseline measures of adiposity (waist circumference or BMI) in daily breakfast consumers. Hazard ratios (HRs) and 95% CIs for daily breakfast consumption were as follows: abdominal obesity HR 0.78 (95% CI 0.66-0.91), obesity 0.80 (0.67-0.96), metabolic syndrome 0.82 (0.69-0.98), and hypertension 0.84 (0.72-0.99). For type 2 diabetes, the corresponding estimate was 0.81 (0.63-1.05), with a significant stepwise inverse association in black men and white men and women but no association in black women. There was no evidence of differential results for high versus low overall dietary quality.ConclusionsDaily breakfast intake is strongly associated with reduced risk of a spectrum of metabolic conditions.

ObjectiveThe relation of breakfast intake frequency to metabolic health is not well studied. The aim of this study was to examine breakfast intake frequency with incidence of metabolic conditions.Research design and methodsWe performed an analysis of 3,598 participants from the community-based Coronary Artery Risk Development in Young Adults (CARDIA) study who were free of diabetes in the year 7 examination when breakfast and dietary habits were assessed (1992-1993) and participated in at least one of the five subsequent follow-up examinations over 18 years.ResultsRelative to those with infrequent breakfast consumption (0-3 days/week), participants who reported eating breakfast daily gained 1.9 kg less weight over 18 years (P=0.001). In a Cox regression analysis, there was a stepwise decrease in risk across conditions in frequent breakfast consumers (4-6 days/week) and daily consumers. The results for incidence of abdominal obesity, obesity, metabolic syndrome, and hypertension remained significant after adjustment for baseline measures of adiposity (waist circumference or BMI) in daily breakfast consumers. Hazard ratios (HRs) and 95% CIs for daily breakfast consumption were as follows: abdominal obesity HR 0.78 (95% CI 0.66-0.91), obesity 0.80 (0.67-0.96), metabolic syndrome 0.82 (0.69-0.98), and hypertension 0.84 (0.72-0.99). For type 2 diabetes, the corresponding estimate was 0.81 (0.63-1.05), with a significant stepwise inverse association in black men and white men and women but no association in black women. There was no evidence of differential results for high versus low overall dietary quality.ConclusionsDaily breakfast intake is strongly associated with reduced risk of a spectrum of metabolic conditions.

Background. Fast-food consumption has increased greatly in the USA during the past three decades. However, the effect of fast food on risk of obesity and type 2 diabetes has received little attention. We aimed to investigate the association between reported fast-food habits and changes in bodyweight and insulin resistance over a 15-year period in the USA. Methods. Participants for the CARDIA study included 3031 young (age 18–30 years in 1985–86) black and white adults who were followed up with repeated dietary assessment. We used multiple linear regression models to investigate the association of frequency of fast-food restaurant visits (fast-food frequency) at baseline and follow-up with 15-year changes in bodyweight and the homoeostasis model (HOMA) for insulin resistance. Findings. Fast-food frequency was lowest for white women (about 1·3 times per week) compared with the other ethnic-sex groups (about twice a week). After adjustment for lifestyle factors, baseline fast-food frequency was directly associated with changes in bodyweight in both black (p=0·0050) and white people (p=0·0013). Change in fast-food frequency over 15 years was directly associated with changes in bodyweight in white individuals (p<0·0001), with a weaker association recorded in black people (p=0·1004). Changes were also directly associated with insulin resistance in both ethnic groups (p=0·0015 in black people, p<0·0001 in white people). By comparison with the average 15-year weight gain in participants with infrequent (less than once a week) fast-food restaurant use at baseline and follow-up (n=203), those with frequent (more than twice a week) visits to fast-food restaurants at baseline and follow-up (n=87) gained an extra 4·5 kg of bodyweight (p=0·0054) and had a two-fold greater increase in insulin resistance (p=0·0083). Interpretation. Fast-food consumption has strong positive associations with weight gain and insulin resistance, suggesting that fast food increases the risk of obesity