Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Sartorius K
PROVIDER: S-EPMC5829813 | biostudies-other | 2018 Feb
REPOSITORIES: biostudies-other
Publications
Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis.
Sartorius Kurt K Sartorius Benn B Madiba Thandinkosi E TE Stefan Cristina C
BMJ open 20180208 2
<h4>Objectives</h4>The present study aimed to test the association between high and low carbohydrate diets and obesity, and second, to test the link between total carbohydrate intake (as a percentage of total energy intake) and obesity.<h4>Setting, participants and outcome measures</h4>We sought MEDLINE, PubMed and Google Scholar for observation studies published between January 1990 and December 2016 assessing an association between obesity and high-carbohydrate intake. Two independent reviewer ...[more]
Similar Datasets
Project description:To conduct a systematic review of the literature and meta-analyses to fill the gaps in knowledge on potassium intake and health.Cochrane Central Register of Controlled Trials, Medline, Embase, WHO International Clinical Trials Registry Platform, Latin American and Caribbean Health Science Literature Database, and the reference lists of previous reviews.Randomised controlled trials and cohort studies reporting the effects of potassium intake on blood pressure, renal function, blood lipids, catecholamine concentrations, all cause mortality, cardiovascular disease, stroke, and coronary heart disease were included.Potential studies were independently screened in duplicate, and their characteristics and outcomes were extracted. When possible, meta-analysis was done to estimate the effects (mean difference or risk ratio with 95% confidence interval) of higher potassium intake by using the inverse variance method and a random effect model.22 randomised controlled trials (including 1606 participants) reporting blood pressure, blood lipids, catecholamine concentrations, and renal function and 11 cohort studies (127,038 participants) reporting all cause mortality, cardiovascular disease, stroke, or coronary heart disease in adults were included in the meta-analyses. Increased potassium intake reduced systolic blood pressure by 3.49 (95% confidence interval 1.82 to 5.15) mm Hg and diastolic blood pressure by 1.96 (0.86 to 3.06) mm Hg in adults, an effect seen in people with hypertension but not in those without hypertension. Systolic blood pressure was reduced by 7.16 (1.91 to 12.41) mm Hg when the higher potassium intake was 90-120 mmol/day, without any dose response. Increased potassium intake had no significant adverse effect on renal function, blood lipids, or catecholamine concentrations in adults. An inverse statistically significant association was seen between potassium intake and risk of incident stroke (risk ratio 0.76, 0.66 to 0.89). Associations between potassium intake and incident cardiovascular disease (risk ratio 0.88, 0.70 to 1.11) or coronary heart disease (0.96, 0.78 to 1.19) were not statistically significant. In children, three controlled trials and one cohort study suggested that increased potassium intake reduced systolic blood pressure by a non-significant 0.28 (-0.49 to 1.05) mm Hg.High quality evidence shows that increased potassium intake reduces blood pressure in people with hypertension and has no adverse effect on blood lipid concentrations, catecholamine concentrations, or renal function in adults. Higher potassium intake was associated with a 24% lower risk of stroke (moderate quality evidence). These results suggest that increased potassium intake is potentially beneficial to most people without impaired renal handling of potassium for the prevention and control of elevated blood pressure and stroke.
| S-EPMC4816263 | biostudies-other
Project description:OBJECTIVE:Excess body weight is associated with increased risk of developing hepatocellular cancer (HCC), but its effect on HCC-related mortality remains unclear. We performed a systematic review and meta-analysis to assess the association between premorbid obesity and HCC-related mortality. MATERIALS AND METHODS:Through a systematic literature search-up to March 2016, we identified 9 observational studies (1,599,453 individuals, 5705 HCC-related deaths) reporting the association between premorbid body mass index (BMI), and HCC-related mortality. We estimated summary adjusted hazard ratio (aHR) with 95% confidence intervals (CIs), comparing obese (BMI>30 kg/m(2)) and overweight (BMI, 25 to 29.9 kg/m(2)) individuals with normal BMI individuals using random-effects model. RESULTS:On meta-analysis, compared with individuals with normal BMI, obese (aHR, 1.95; 95% CI, 1.46-2.46), but not overweight individuals (aHR, 1.08; 95% CI, 0.97-1.21), had higher HCC-related mortality, with moderate heterogeneity. On subgroup analysis, magnitude of increased mortality was higher in obese men (aHR, 2.50; 95% CI, 2.02-3.09; 3 studies) as compared with obese women (aHR, 1.45; 95% CI, 1.08-1.97; 2 studies). The impact of premorbid obesity on HCC-related mortality was observed only in western populations (aHR, 2.10; 95% CI, 1.77-2.48; 4 studies), but not Asian populations (aHR, 1.10; 95% CI, 0.63-1.92; 1 study). There was limited assessment of competing risk because of advanced liver disease. CONCLUSIONS:On the basis of this meta-analysis, premorbid obesity may be independently associated with a 2-fold risk of HCC-related mortality. This association was more pronounced in men and western populations. Strategies targeting obesity-associated metabolic abnormalities may provide novel pathways for HCC therapy.
| S-EPMC5700876 | biostudies-literature
Project description:BackgroundResearch evidence has established the beneficial effects of diet in cancer prevention; various epidemiological studies have suggested that olive oil component could play a role in decreasing cancer risk. This systematic review and meta-analysis aims to investigate the association between olive oil consumption, cancer risk and prognosis.MethodsA systematic search was conducted in PubMed, EMBASE and Google Scholar databases (end-of-search: May 10, 2020). Pooled relative risk (RR) and 95% confidence intervals (95% CIs) were estimated with random-effects (DerSimonian-Laird) models. Subgroup analyses, sensitivity analyses and meta-regression analysis were also performed.Results45 studies were included in the meta-analysis; 37 were case-control (17,369 cases and 28,294 controls) and 8 were cohort studies (12,461 incident cases in a total cohort of 929,771 subjects). Highest olive oil consumption was associated with 31% lower likelihood of any cancer (pooled RR = 0.69, 95%CI: 0.62-0.77), breast (RR = 0.67, 95%CI: 0.52-0.86), gastrointestinal (RR = 0.77, 95%CI: 0.66-0.89), upper aerodigestive (RR = 0.74, 95%CI: 0.60-0.91) and urinary tract cancer (RR = 0.46, 95%CI: 0.29-0.72). Significant overall effects spanned both Mediterranean and non-Mediterranean participants, studies presenting a multivariate and a univariate analysis and all subgroups by study quality.ConclusionsOlive oil consumption seems to exert beneficial actions in terms of cancer prevention. Additional prospective cohort studies on various cancer types and survivors, as well as large randomized trials, seem desirable.
| S-EPMC8751986 | biostudies-literature
Project description:Overweight and obesity is a major public health concern that includes associations with the development of cardiovascular disease (CVD) risk factors during childhood and adolescence as well as premature mortality in adults. Despite the high prevalence of childhood and adolescent obesity as well as adult CVD, individual studies as well as previous systematic reviews examining the relationship between childhood obesity and adult CVD have yielded conflicting results. The purpose of this study was to use the aggregate data meta-analytic approach to address this gap.Studies were included if they met the following criteria: (1) longitudinal and cohort studies (including case-cohort), (2) childhood exposure and adult outcomes collected on the same individual over time, (3) childhood obesity, as defined by the original study authors, (4) English-language articles, (5) studies published up to June, 2015, (6) one or more of the following CVD risk factors [systolic blood pressure (SBP), diastolic blood pressure (DBP), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), non-high-density lipoprotein cholesterol (non-HDL), and triglycerides (TG)], (7) outcome(s) not self-reported, and (8) exposure measurements (child's adiposity) assessed by health professionals, trained investigators, or self-reported. Studies were retrieved by searching three electronic databases as well as citation tracking. Fisher's r to z score was calculated for each study for each outcome. Pooled effect sizes were calculated using random-effects models while risk of bias was assessed using the STROBE instrument. In order to try and identify sources of heterogeneity, random-effects meta-regression was also performed.Of the 4840 citations reviewed, a total of 23 studies were included in the systematic review and 21 in the meta-analysis. The findings suggested that childhood obesity is significantly and positively associated with adult SBP (Zr = 0.11; 95% CI: 0.07, 0.14), DBP (Zr = 0.11; 95% CI: 0.07, 0.14), and TG (Zr =0.08; 95% CI: 0.03, 0.13), and significantly and inversely associated with adult HDL (Zr = -0.06; 95% CI: -0.10, -0.02). For those studies that adjusted for adult body mass index (BMI), associations were reversed, suggesting that adult BMI may be a potential mediator. Nine studies had more than 33% of items that placed them at an increased risk for bias.The results of this study suggest that childhood obesity may be a risk factor for selected adult CVD risk factors. However, a need exists for additional, higher-quality studies that include, but are not limited to, both unadjusted and adjusted measures such as BMI before any definitive conclusions can be reached.PROSPERO 2015: CRD42015019763 .
| S-EPMC5575877 | biostudies-other
Project description:To examine the evidence underpinning recommendations to increase calcium intake through dietary sources or calcium supplements to prevent fractures.Systematic review of randomised controlled trials and observational studies of calcium intake with fracture as an endpoint. Results from trials were pooled with random effects meta-analyses.Ovid Medline, Embase, PubMed, and references from relevant systematic reviews. Initial searches undertaken in July 2013 and updated in September 2014.Randomised controlled trials or cohort studies of dietary calcium, milk or dairy intake, or calcium supplements (with or without vitamin D) with fracture as an outcome and participants aged >50.There were only two eligible randomised controlled trials of dietary sources of calcium (n=262), but 50 reports from 44 cohort studies of relations between dietary calcium (n=37), milk (n=14), or dairy intake (n=8) and fracture outcomes. For dietary calcium, most studies reported no association between calcium intake and fracture (14/22 for total, 17/21 for hip, 7/8 for vertebral, and 5/7 for forearm fracture). For milk (25/28) and dairy intake (11/13), most studies also reported no associations. In 26 randomised controlled trials, calcium supplements reduced the risk of total fracture (20 studies, n=58,573; relative risk 0.89, 95% confidence interval 0.81 to 0.96) and vertebral fracture (12 studies, n=48,967. 0.86, 0.74 to 1.00) but not hip (13 studies, n=56,648; 0.95, 0.76 to 1.18) or forearm fracture (eight studies, n=51,775; 0.96, 0.85 to 1.09). Funnel plot inspection and Egger's regression suggested bias toward calcium supplements in the published data. In randomised controlled trials at lowest risk of bias (four studies, n=44,505), there was no effect on risk of fracture at any site. Results were similar for trials of calcium monotherapy and co-administered calcium and vitamin D. Only one trial in frail elderly women in residential care with low dietary calcium intake and vitamin D concentrations showed significant reductions in risk of fracture.Dietary calcium intake is not associated with risk of fracture, and there is no clinical trial evidence that increasing calcium intake from dietary sources prevents fractures. Evidence that calcium supplements prevent fractures is weak and inconsistent.
| S-EPMC4784799 | biostudies-other
Project description:ObjectiveTo investigate dietary fibre intake and any potential dose-response association with coronary heart disease and cardiovascular disease.DesignSystematic review of available literature and dose-response meta-analysis of cohort studies using random effects models.Data sourcesThe Cochrane Library, Medline, Medline in-process, Embase, CAB Abstracts, ISI Web of Science, BIOSIS, and hand searching.Eligibility criteria for studiesProspective studies reporting associations between fibre intake and coronary heart disease or cardiovascular disease, with a minimum follow-up of three years and published in English between 1 January 1990 and 6 August 2013.Results22 cohort study publications met inclusion criteria and reported total dietary fibre intake, fibre subtypes, or fibre from food sources and primary events of cardiovascular disease or coronary heart disease. Total dietary fibre intake was inversely associated with risk of cardiovascular disease (risk ratio 0.91 per 7 g/day (95% confidence intervals 0.88 to 0.94)) and coronary heart disease (0.91 (0.87 to 0.94)). There was evidence of some heterogeneity between pooled studies for cardiovascular disease (I(2)=45% (0% to 74%)) and coronary heart disease (I(2)=33% (0% to 66%)). Insoluble fibre and fibre from cereal and vegetable sources were inversely associated with risk of coronary heart disease and cardiovascular disease. Fruit fibre intake was inversely associated with risk of cardiovascular disease.ConclusionsGreater dietary fibre intake is associated with a lower risk of both cardiovascular disease and coronary heart disease. Findings are aligned with general recommendations to increase fibre intake. The differing strengths of association by fibre type or source highlight the need for a better understanding of the mode of action of fibre components.
| S-EPMC3898422 | biostudies-literature
Project description:The results of prospective cohort studies regarding the role of salt intake and subsequent gastric cancer risk are inconsistent. Thus, we performed a systematic review and meta-analysis to summarize the strength of the association of salt intake with gastric cancer morbidity and mortality. PubMed, EmBase, and Cochrane Library were systematically searched to identify eligible studies published throughout September 2021. The effect estimates with 95% confidence intervals (CIs) for gastric cancer morbidity or mortality in each study were applied to calculate the pooled results; these analyses were performed using the random-effects model. Twenty-six prospective cohort studies involving 4,956,350 individuals were selected; these studies reported 19,301 cases of gastric cancer and 2,871 cases of gastric cancer-associated mortality. High (RR: 1.25; 95%CI: 1.10-1.41; P = 0.001) or moderate (RR: 1.20; 95%CI: 1.04-1.38; P = 0.012) salt intake was associated with a greater risk of gastric cancer. High pickled food intake was associated with an increased gastric cancer risk (RR: 1.28; 95%CI: 1.05-1.57; P = 0.017), while moderate pickled foods intake had no significant effect on gastric cancer risk (RR: 1.10; 95%CI: 0.88-1.37; P = 0.390). Neither high (RR: 1.14; 95%CI: 0.95-1.36; P = 0.161) nor moderate (RR: 1.10; 95%CI: 0.87-1.40; P = 0.436) salted fish intake were associated with gastric cancer risk. A high intake of processed meat was significantly associated with a higher risk of gastric cancer (RR: 1.24; 95%CI: 1.03-1.49; P = 0.023), while moderate processed meat intake had no significant effect on the gastric cancer risk (RR: 1.01; 95%CI: 0.92-1.11; P = 0.844). High (RR: 1.04; 95%CI: 0.90-1.19; P = 0.626) and moderate (RR: 1.02; 95%CI: 0.94-1.11; P = 0.594) miso-soup intake had no effects on the gastric cancer risk. High intakes of salt, pickled food, and processed meat are associated with significantly increased risks of gastric cancer; these increased risks are also seen when participants consumed moderate amounts of salt.
| S-EPMC8692376 | biostudies-literature
Project description:BackgroundWalnuts contain nutrients that are associated with improved cognitive health. To our knowledge, no review has systematically examined the effects of walnuts on cognitive function and risk for cognitive decline.ObjectiveTo conduct a systematic review and meta-analysis evaluating the effects of walnut intake on cognition-related outcomes and risk-factors for cognitive decline in adults.MethodsMedline®, Commonwealth Agricultural Bureau, and Cochrane Central Register of Controlled Trials were searched for randomized controlled trials (RCTs) and observational studies published until April 2020 on walnut intake, cognition (e.g. cognitive function, stroke, and mood), and selected risk factors for cognitive decline (e.g. glucose homeostasis and inflammation). Risk-of-bias and strength-of-evidence assessments were conducted using standard validated tools. Random-effects meta-analyses were conducted when ≥3 studies reported quantitative data for each outcome.Results32 RCT and 7 observational study publications were included. Meta-analysis of cognition-related outcomes could not be conducted due to heterogeneity of tests. None of the 5 cognition RCTs found significant effects of walnuts on overall cognition, although 3 studies found improvements on subdomains and/or subgroups. All 7 observational studies found significant associations and a dose-response relationship between walnut intake and cognition-related outcomes. Meta-analyses of 27 RCTs reporting glucose homeostasis and inflammation outcomes, selected risk factors for cognitive decline, did not show significant effects of walnut intake.ConclusionsDue to the non-uniformity of tests for cognition-related outcomes, definitive conclusions regarding the effect of walnut consumption on cognition could not be reached. Additionally, evidence does not show associations between walnut intake and glucose homeostasis or inflammation, cognitive decline risk-factors. High-quality studies with standardized measures are needed to clarify the role of walnuts in cognitive health.KEY MESSAGESThis is a systematic review and meta-analysis of 5 randomized clinical trials and 7 observational study articles of the impact of walnut intake on cognition decline and 27 randomized clinical trials of the effect of walnut intake on risk factors for cognitive decline including glucose homeostasis and inflammation.The non-uniformity of tests performed to measure cognitive function in the various studies did not allow for a meta-analysis of these studies. A definitive conclusion could therefore not be reached regarding the effect of walnut intake on cognitive decline.The evidence available does not show an association between walnut intake and glucose homeostasis or inflammation.
| S-EPMC8211141 | biostudies-literature
Project description:Several epidemiological studies have investigated the association between dietary flavonoid intake and digestive tract cancers risk; however, the results remain inconclusive. The aim of our study was to evaluate this association. PubMed and the Web of Knowledge were searched for relevant publications from inception to October 2015. The risk ratio (RR) or odds ratio (OR) with the 95% confidence interval (95% CI) for the highest versus the lowest categories of flavonoid intake were pooled using a fixed-effects model. A total of 15 articles reporting 23 studies were selected for the meta-analysis. In a comparison of the highest versus the lowest categories of dietary flavonoid intake, we found no significant association between flavonoid intake and oesophageal cancer (OR = 0.91, 95% CI = 0.75-1.10; I(2) = 0.0%), colorectal cancer (OR = 1.02, 95% CI = 0.92-1.14, I(2) = 36.2%) or gastric cancer (OR = 0.88; 95% CI = 0.74-1.04, I(2) = 63.6%). The subgroup analysis indicated an association between higher flavonoid intake and a decreased risk of gastric cancer in the European population (OR = 0.78, 95% CI = 0.62-0.97). In conclusion, the results of this meta-analysis do not strongly support an association between dietary flavonoid intake and oesophageal or colorectal cancer. Furthermore, the subgroup analysis suggested an association between higher dietary flavonoid intake and decreased gastric cancer risk in European population.
| S-EPMC4845003 | biostudies-other
Project description:The effects of dairy products on human health have been studied for years. However, the relationship between dairy products as well as calcium intake and the risk of lung cancer is still inconclusive. A total of 32 studies regarding this association were identified from the PubMed and Web of Science databases through April 1, 2015, including 12 cohort studies and 20 case-control studies. After pooling the results of individual studies, the summary RRs (relative risks) of lung cancer for the highest versus lowest intake were 1.05 (95%CI: 0.84-1.31) and 1.08 (95%CI: 0.80-1.46) for total dairy products and milk, respectively. The results on the consumption of cheese, yogurt and low-fat milk were also negative, and the RRs for total and dietary calcium intakes were 0.99 (95%CI: 0.70-1.38) and 0.85 (95%CI: 0.63-1.13), respectively. After stratifying by potential confounders, the results remained consistent in most subgroup analyses. Our study indicates that intake of dairy products or calcium was not statistically associated with the risk of lung cancer. This negative finding provides a conclusive answer to the disease association issue based on current evidence, and suggests that further efforts should be made to find other nutritional risk factors for lung cancer.
| S-EPMC4753428 | biostudies-literature