Too Many Calories for All?
Ontology highlight
ABSTRACT:
SUBMITTER: Pecanha Antonio AC
PROVIDER: S-EPMC7528784 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC7528800 | biostudies-literature
Project description:Despite intensive research, the causes of the obesity epidemic remain incompletely understood and conventional calorie-restricted diets continue to lack long-term efficacy. According to the carbohydrate-insulin model (CIM) of obesity, recent increases in the consumption of processed, high-glycemic-load carbohydrates produce hormonal changes that promote calorie deposition in adipose tissue, exacerbate hunger, and lower energy expenditure. Basic and genetic research provides mechanistic evidence in support of the CIM. In animals, dietary composition has been clearly demonstrated to affect metabolism and body composition, independently of calorie intake, consistent with CIM predictions. Meta-analyses of behavioral trials report greater weight loss with reduced-glycemic load vs low-fat diets, though these studies characteristically suffer from poor long-term compliance. Feeding studies have lacked the rigor and duration to test the CIM, but the longest such studies tend to show metabolic advantages for low-glycemic load vs low-fat diets. Beyond the type and amount of carbohydrate consumed, the CIM provides a conceptual framework for understanding how many dietary and nondietary exposures might alter hormones, metabolism, and adipocyte biology in ways that could predispose to obesity. Pending definitive studies, the principles of a low-glycemic load diet offer a practical alternative to the conventional focus on dietary fat and calorie restriction.
| S-EPMC6082688 | biostudies-literature
Project description:Non-alcoholic fatty liver disease (NAFLD) is a growing epidemic, in parallel with the obesity crisis, rapidly becoming one of the commonest causes of chronic liver disease worldwide. Diet and physical activity are important determinants of liver fat accumulation related to insulin resistance, dysfunctional adipose tissue, and secondary impaired lipid storage and/or increased lipolysis. While it is evident that a hypercaloric diet (an overconsumption of calories) promotes liver fat accumulation, it is also clear that the macronutrient composition can modulate this risk. A number of other baseline factors modify the overfeeding response, which may be genetic or environmental. Although it is difficult to disentangle the effects of excess calories vs. specifically the individual effects of excessive carbohydrates and/or fats, isocaloric, and hypercaloric dietary intervention studies have been implemented to provide insight into the effects of different macronutrients, sub-types and their relative balance, on the regulation of liver fat. What has emerged is that different types of fat and carbohydrates differentially influence liver fat accumulation, even when diets are isocaloric. Furthermore, distinct molecular and metabolic pathways mediate the effects of carbohydrates and fat intake on hepatic steatosis. Fat accumulation appears to act through impairments in lipid storage and/or increased lipolysis, whereas carbohydrate consumption has been shown to promote liver fat accumulation through de novo lipogenesis. Effects differ dependent upon carbohydrate and fat type. Saturated fat and fructose induce the greatest increase in intrahepatic triglycerides (IHTG), insulin resistance, and harmful ceramides compared with unsaturated fats, which have been found to be protective. Decreased intake of saturated fats and avoidance of added sugars are therefore the two most important dietary interventions that can lead to a reduction in IHTG and potentially the associated risk of developing type 2 diabetes. A healthy and balanced diet and regular physical activity must remain the cornerstones of effective lifestyle intervention to prevent the development and progression of NAFLD. Considering the sub-type of each macronutrient, in addition to the quantity, are critical determinants of liver health.
| S-EPMC7921724 | biostudies-literature
Project description:Free sugars are a major source of calories in diets and contribute to the burden of many non-communicable diseases (NCDs). The World Health Organization (WHO) recommends reducing free sugars intake to less than 10% of total energy. This study aimed to estimate the number of diet-related NCD deaths which could be averted or delayed if Canadian adults were to reduce their calorie intake due to a systematic 20% reduction in the free sugars content in foods and beverages in Canada. We used the Preventable Risk Integrated ModEl (PRIME) to estimate the potential health impact. An estimated 6770 (95% UI 6184-7333) deaths due to diet-related NCDs could be averted or delayed, mostly from cardiovascular diseases (66.3%). This estimation would represent 7.5% of diet-related NCD deaths observed in 2019 in Canada. A 20% reduction in the free sugars content in foods and beverages would lead to a 3.2% reduction in calorie intake, yet an important number of diet-related NCD deaths could be averted or delayed through this strategy. Our findings can inform future policy decisions to support Canadians' free sugars intake reduction, such as proposing target levels for the free sugars content in key food categories.
| S-EPMC10140857 | biostudies-literature
Project description:The Food and Drug Administration's menu labeling rule requires chain restaurants to prominently display calories, while leaving other nutritional information (e.g., fat, sodium, sugar) to the request of consumers. We use rich micronutrient data from 257 large chain brands and 24,076 menu items to examine whether calories are correlated with widely used "nutrient profile" scores that measure healthfulness based on nutrient density. We show that calories are indeed statistically significant predictors of nutrient density. However, as a substantive matter, the correlation is highly attenuated (partial R2 < 0.01). Our findings (a) suggest that the promise of calorie labeling to improve nutrient intake quality at restaurants is limited and (b) clarify the basis for transparency of nutrient composition beyond calories to promote healthy menu choices.
| S-EPMC7205205 | biostudies-literature
Project description:ObjectiveHigh calorie foods and beverages, which often contain caffeine, contribute to child overweight/obesity. We evaluated the results of an educational intervention to promote healthy growth in very young children. Secondarily, we used detailed diet data to explore the association of nutrient intake with the early development of overweight and obesity.MethodsMothers were obese Latina women, enrolled prenatally, and their infants. Specially trained community health workers provided breastfeeding support and nutrition education during 10 home visits, birth to 24 months. At follow-up, age 18 to 36 months, we measured growth and completed detailed diet recalls (1-7 recall days/child).ResultsOf 174 infants randomized, 106 children were followed for 24 to 36 months. The educational intervention did not prevent overweight/obesity. Forty-two percent of children became overweight or obese. Fifty-eight percent of children consumed caffeine on at least 1 recall day. Mean intake was 0.48 mg/kg/day. Caffeine correlated with higher consumption of calories, and added sugar and decreased intake of protein, fiber and dairy. Compared with days without caffeine, on days when caffeine was consumed, children ingested 121 more calories and 3.8 gm less protein. Children frequently consumed less than the recommended daily intake of key nutrients such as fiber, vegetables, whole fruit, and vitamins.ConclusionsCaffeine was a marker for increased intake of calories and decreased intake of key nutrients. When discussing dietary intake in early childhood, practitioners should screen for nutrient deficiency in young children and recommend limiting the intake of caffeinated foods and beverages.
| S-EPMC7416448 | biostudies-literature
Project description:BackgroundPrior research on the restaurant environment and obesity risk is limited by cross-sectional data and a focus on specific geographic areas.ObjectiveTo measure the impact of changes in chain restaurant calories over time on body mass index (BMI).DesignWe used a first-difference model to examine whether changes from 2012 to 2015 in chain restaurant calories per capita were associated with percent changes in BMI. We also examined differences by race and county income, restaurant type, and initial body weight categories.SettingUSA (207 counties across 39 states).Participants447,873 adult patients who visited an athenahealth medical provider in 2012 and 2015 where BMI was measured.Main outcomes measuredPercent change in objectively measured BMI from 2012 to 2015.ResultsAcross all patients, changes in chain restaurant calories per capita were not associated with percent changes in BMI. For Black or Hispanic adults, a 10% increase in exposure to chain restaurant calories per capita was associated with a 0.16 percentage-point increase in BMI (95% CI 0.03, 0.30). This translates into a predicted weight increase of 0.89 pounds (or a 0.53% BMI increase) for an average weight woman at the 90th percentile of increases in the restaurant environment from 2012 to 2015 versus an increase 0.39 pounds (or 0.23% BMI increase) at the 10th percentile. Greater increases in exposure to chain restaurant calories also significantly increased BMI for Black or Hispanic adults receiving healthcare services in lower-income counties (0.26, 95% CI 0.04, 0.49) and with overweight/obesity (0.16, 95% CI 0.04, 0.29).LimitationsGeneralizability to non-chain restaurants is unknown and the sample of athenahealth patients is relatively homogenous.ConclusionsIncreased exposure to chain restaurant calories per capita was associated with increased weight gain among Black or Hispanic adults.
| S-EPMC7300171 | biostudies-literature
Project description:ObjectiveThe susceptibility to abdominal obesity and the metabolic syndrome is determined to a substantial extent during childhood and adolescence, when key adipose tissue characteristics are established. Although the general impact of postnatal nutrition is well known, it is not clear how specific dietary components drive adipose tissue growth and how this relates to the risk of metabolic dysfunction in adulthood.MethodsAdipose tissue growth including cell proliferation was analyzed in juvenile mice upon dietary manipulation with in vivo nucleotide labeling. The proliferative response of progenitors to specific fatty acids was assayed in primary cultures. Long-term metabolic consequences were assessed through transient dietary manipulation post-weaning with a second obesogenic challenge in adulthood.ResultsDietary lipids stimulated adipose tissue progenitor cell proliferation in juvenile mice independently of excess caloric intake and calorie-dependent adipocyte hypertrophy. Excess calories increased mitogenic IGF-1 levels systemically, whereas palmitoleic acid was able to enhance the sensitivity of progenitors to IGF-1, resulting in synergistic stimulation of proliferation. Early transient consumption of excess lipids promoted hyperplastic adipose tissue expansion in response to a second dietary challenge in adulthood and this correlated with abdominal obesity and hyperinsulinemia.ConclusionsDietary lipids and calories differentially and synergistically drive adipose tissue proliferative growth and the programming of the metabolic syndrome in childhood.
| S-EPMC6531874 | biostudies-literature
Project description:Background: Overfeeding can lead to multiple metabolic and clinical complications and has been associated with increased mortality in the critically ill. Continuous venovenous hemofiltration (CVVH) represents a potential source of calories that is poorly recognized and may contribute to overfeeding complications.Objective: We aimed to quantify the systemic caloric contribution of acid-citrate-dextrose regional anticoagulation and dextrose-containing replacement fluids in the CVVH circuit.Design: This was a prospective study in 10 critically ill adult patients who received CVVH from April 2014 to June 2014. Serial pre- and postfilter blood samples (n = 4 each) were drawn and analyzed for glucose and citrate concentrations on each of 2 consecutive days.Results: Participants included 5 men and 5 women with a mean ± SEM age of 61 ± 4 y (range: 42-84 y) and body mass index (in kg/m2) of 28 ± 2 (range: 18.3-36.2). There was generally good agreement between data on the 2 study days (CV: 7-11%). Mean ± SEM pre- and postfilter venous plasma glucose concentrations in the aggregate group were 152 ± 10 and 178 ± 9 mg/dL, respectively. Net glucose uptake from the CVVH circuit was 54 ± 5 mg/min and provided 295 ± 28 kcal/d. Prefilter plasma glucose concentrations were higher in patients with diabetes (n = 5) than in those without diabetes (168 ± 12 compared with 140 ± 14 mg/dL; P < 0.05); however, net glucose uptake was similar (46 ± 8 compared with 61 ± 6 mg/min; P = 0.15). Mean ± SEM pre- and postfilter venous plasma citrate concentrations were 1 ± 0.1 and 3.1 ± 0.2 mmol/L, respectively. Net citrate uptake from the CVVH circuit was 60 ± 2 mg/min and provided 218 ± 8 kcal/d.Conclusions: During CVVH there was a substantial net uptake of both glucose and citrate that delivered exogenous energy and provided ∼512 kcal/d. Failure to account for this source of calories in critically ill patients receiving nutrition on CVVH may result in overfeeding.
| S-EPMC6546225 | biostudies-literature
Project description:Dietary restriction (DR) extends life span in diverse organisms, including mammals, and common mechanisms may be at work. DR is often known as calorie restriction, because it has been suggested that reduction of calories, rather than of particular nutrients in the diet, mediates extension of life span in rodents. We here demonstrate that extension of life span by DR in Drosophila is not attributable to the reduction in calorie intake. Reduction of either dietary yeast or sugar can reduce mortality and extend life span, but by an amount that is unrelated to the calorie content of the food, and with yeast having a much greater effect per calorie than does sugar. Calorie intake is therefore not the key factor in the reduction of mortality rate by DR in this species.
| S-EPMC1140680 | biostudies-literature