Despite the widespread use of ginseng in the management of diabetes, supporting evidence of its anti-hyperglycemic efficacy is limited, necessitating the need for evidence-based recommendations for the potential inclusion of ginseng in diabetes management.To elucidate the effect of ginseng on glycemic control in a systematic review and meta-analysis of randomized controlled trials in people with and without diabetes.MEDLINE, EMBASE, CINAHL and the Cochrane Library (through July 3, 2013).Randomized controlled trials ≥30 days assessing the glycemic effects of ginseng in people with and without diabetes.Relevant data were extracted by 2 independent reviewers. Discrepancies were resolved by consensus. The Heyland Methodological Quality Score and the Cochrane risk of bias tool were used to assess study quality and risk of bias respectively.Sixteen trials were included, in which 16 fasting blood glucose (n = 770), 10 fasting plasma insulin (n = 349), 9 glycated hemoglobin (n = 264), and 7 homeostasis model assessment of insulin resistance (n = 305) comparisons were reported. Ginseng significantly reduced fasting blood glucose compared to control (MD = -0.31 mmol/L [95% CI: -0.59 to -0.03], P = 0.03). Although there was no significant effect on fasting plasma insulin, glycated hemoglobin, or homeostasis model assessment of insulin resistance, a priori subgroup analyses did show significant reductions in glycated hemoglobin in parallel compared to crossover trials (MD = 0.22% [95%CI: 0.06 to 0.37], P = 0.01).Most trials were of short duration (67% trials<12wks), and included participants with a relatively good glycemic control (median HbA1c non-diabetes = 5.4% [2 trials]; median HbA1c diabetes = 7.1% [7 trials]).Ginseng modestly yet significantly improved fasting blood glucose in people with and without diabetes. In order to address the uncertainty in our effect estimates and provide better assessments of ginseng's anti-diabetic efficacy, larger and longer randomized controlled trials using standardized ginseng preparations are warranted.ClinicalTrials.gov NCT01841229.
Background Tree nut consumption is associated with reduced diabetes risk, however, results from randomized controlled trials (RCTs) on glycemia have been inconsistent. Aim We conducted a systematic review and meta‐analysis of RCTs to assess the effect of tree nuts on glycemic control. Methods We searched MEDLINE, EMBASE, CINAHL, and Cochrane databases through 8 August 2014 for relevant RCTs 蠅3‐weeks reporting HbA1c, fasting glucose (FBG), fasting insulin (FPI), and/or HOMA‐IR. Two independent reviewers extracted relevant data. Data were pooled using generic inverse variance random effects models and expressed as mean differences (MD) with 95% confidence intervals (CI). Heterogeneity was assessed (Cochran's Q) and quantified (I 2 ). Results 31 trials (n=1645) met the eligibility criteria. Diets emphasizing tree nuts significantly lowered FBG (MD=‐0.11 mmol/L, 95% CI:‐0.18, ‐0.03 mmol/L), FPI (MD=‐4.79 pmol/L, 95% CI:‐8.12, ‐1.46 pmol/L) and HOMA‐IR (MD=‐0.45, 95% CI:‐0.81, ‐0.09) compared with isocaloric control diets. No effects were observed for HbA1c, however the direction of effect favoured tree nuts. Limitations Majority of trials were of poor quality and short duration. Conclusion Pooled analyses show diets higher in tree nuts improve glycemic control. Longer, higher quality trials are needed. Funding International Tree Nut Council Nutrition Research & Education Foundation
Objective To systematically review associations between intake of saturated fat and trans unsaturated fat and all cause mortality, cardiovascular disease (CVD) and associated mortality, coronary heart disease (CHD) and associated mortality, ischemic stroke, and type 2 diabetes. Design Systematic review and meta-analysis. Data sources Medline, Embase, Cochrane Central Registry of Controlled Trials, Evidence-Based Medicine Reviews, and CINAHL from inception to 1 May 2015, supplemented by bibliographies of retrieved articles and previous reviews. Eligibility criteria for selecting studies Observational studies reporting associations of saturated fat and/or trans unsaturated fat (total, industrially manufactured, or from ruminant animals) with all cause mortality, CHD/CVD mortality, total CHD, ischemic stroke, or type 2 diabetes. Data extraction and synthesis Two reviewers independently extracted data and assessed study risks of bias. Multivariable relative risks were pooled. Heterogeneity was assessed and quantified. Potential publication bias was assessed and subgroup analyses were undertaken. The GRADE approach was used to evaluate quality of evidence and certainty of conclusions. Results For saturated fat, three to 12 prospective cohort studies for each association were pooled (five to 17 comparisons with 90 501-339 090 participants). Saturated fat intake was not associated with all cause mortality (relative risk 0.99, 95% confidence interval 0.91 to 1.09), CVD mortality (0.97, 0.84 to 1.12), total CHD (1.06, 0.95 to 1.17), ischemic stroke (1.02, 0.90 to 1.15), or type 2 diabetes (0.95, 0.88 to 1.03). There was no convincing lack of association between saturated fat and CHD mortality (1.15, 0.97 to 1.36; P=0.10). For trans fats, one to six prospective cohort studies for each association were pooled (two to seven comparisons with 12 942-230 135 participants). Total trans fat intake was associated with all cause mortality (1.34, 1.16 to 1.56), CHD mortality (1.28, 1.09 to 1.50), and total CHD (1.21, 1.10 to 1.33) but not ischemic stroke (1.07, 0.88 to 1.28) or type 2 diabetes (1.10, 0.95 to 1.27). Industrial, but not ruminant, trans fats were associated with CHD mortality (1.18 (1.04 to 1.33) v 1.01 (0.71 to 1.43)) and CHD (1.42 (1.05 to 1.92) v 0.93 (0.73 to 1.18)). Ruminant trans-palmitoleic acid was inversely associated with type 2 diabetes (0.58, 0.46 to 0.74). The certainty of associations between saturated fat and all outcomes was "very low." The certainty of associations of trans fat with CHD outcomes was "moderate" and "very low" to "low" for other associations. Conclusions Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations. Trans fats are associated with all cause mortality, total CHD, and CHD mortality, probably because of higher levels of intake of industrial trans fats than ruminant trans fats. Dietary guidelines must carefully consider the health effects of recommendations for alternative macronutrients to replace trans fats and saturated fats.
Industrial, not fruit fructose intake is associated with the severity of liver fibrosis in genotype 1 chronic hepatitis C patientsJournal of HepatologyVol. 59Issue 6PreviewUnhealthy food intake, specifically fructose, has been associated with metabolic alterations and with the severity of liver fibrosis in patients with non-alcoholic fatty liver disease. In a cohort of patients with genotype 1 chronic hepatitis C (G1 CHC), we tested the association of fructose intake with the severity of liver histology. Full-Text PDF Reply to: "Is industrial fructose just a marker of an unhealthy dietary pattern?"Journal of HepatologyVol. 61Issue 1PreviewWe recently reported a link between fructose intake and the severity of liver fibrosis in a cohort of Italian patients with genotype 1 (G1) chronic hepatitis C (CHC) [1]. In particular, the association holds true for "industrial" only, not for "fruit" fructose intake. Full-Text PDF Open Access We read with interest the cross-sectional study by Petta et al. [[1]Petta S. Marchesini G. Caracausi L. Macaluso F.S. Camma C. Ciminnisi S. et al.Industrial, not fruit fructose intake is associated with the severity of liver fibrosis in genotype 1 chronic hepatitis C patients.J Hepatol. 2013; 59: 1169-1176Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar] showing that "industrial" fructose and not fruit fructose intake is associated with liver fibrosis in biopsy-proven genotype 1 chronic hepatitis C (G1CHC) patients. We are concerned that important confounders were not included in their analytical models. The authors selected their multivariate models based on the significance of variables in univariate models. Taking this approach, important confounders may have been missed. One of the most important confounders in nutrition is that of energy, a factor intrinsic to all foods. Although neither "hypercaloric" nor "energy intake" were significant in univariate models, both were significantly associated with fructose intake. Excess energy has also been shown to be an important mediating factor in the effects of fructose on cardiometabolic risk. In a series of systematic reviews and meta-analyses of controlled feeding trials, we found that fructose in isocaloric exchange for other carbohydrates (energy matched conditions) showed no signal for harm in relation to markers of non-alcoholic fatty liver disease (NAFLD) [[2]Chiu S. Sievenpiper J.L., de Souza R.J. Cozma A.I. Mirrahimi A. Carleton A.J. et al.Effect of fructose on markers of Non-Alcoholic Fatty Liver Disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials.Eur J Clin Nutr. 2014; ([Epub ahead of print])https://doi.org/10.1038/ejcn.2014.8Crossref PubMed Scopus (219) Google Scholar] as well as body weight [[3]Sievenpiper J.L. de Souza R.J. Mirrahimi A. Yu M.E. Carleton A.J. Beyene J. et al.Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis.Ann Intern Med. 2012; 21: 291-304Crossref Scopus (234) Google Scholar], glycemic control [[4]Cozma A.I. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Ha V. Wang D.D. et al.Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials.Diabetes Care. 2012; 35: 1611-1620Crossref PubMed Scopus (165) Google Scholar], insulin [[4]Cozma A.I. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Ha V. Wang D.D. et al.Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials.Diabetes Care. 2012; 35: 1611-1620Crossref PubMed Scopus (165) Google Scholar], serum fasting lipids [[5]Sievenpiper J.L. Carleton A.J. Chatha S. Jiang H.Y. de Souza R.J. Beyene J. et al.Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans.Diabetes Care. 2009; 32: 1930-1937Crossref PubMed Scopus (141) Google Scholar], postprandial triglycerides [[6]Wang D.D. Sievenpiper J.L. De Souza R.J. Cozma A.I. Chiavaroli L. Ha V. et al.Effect of fructose on postprandial triglycerides: a systematic review and meta-analysis of controlled feeding trials.Atherosclerosis. 2014; 232: 125-133Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar], blood pressure [[7]Ha V. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Wang D.D. Cozma A.I. et al.Effect of fructose on blood pressure: a systematic review and meta-analysis of controlled feeding trials.Hypertension. 2012; 59: 787-795Crossref PubMed Scopus (149) Google Scholar], and uric acid [[8]Wang D.D. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Ha V. Cozma A.I. et al.The effects of fructose intake on serum uric acid vary among controlled dietary trials.J Nutr. 2012; 142: 916-923Crossref PubMed Scopus (166) Google Scholar]. A lack of harm is seen even under conditions of fructose overfeeding (positive energy balance) at high doses, as long as the comparison with the carbohydrate comparator remains matched for the excess calories. There may, however, be a dose threshold for some fasting lipid effects in some high dose subgroup analyses [[5]Sievenpiper J.L. Carleton A.J. Chatha S. Jiang H.Y. de Souza R.J. Beyene J. et al.Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans.Diabetes Care. 2009; 32: 1930-1937Crossref PubMed Scopus (141) Google Scholar]. A consistent signal for harm is not seen until one examines fructose in imbalanced, hypercaloric comparisons. If fructose supplements background diets with excess energy compared with the same diets without the excess energy, then one sees adverse effects on markers of NAFLD and other cardiometabolic risk factors [2Chiu S. Sievenpiper J.L., de Souza R.J. Cozma A.I. Mirrahimi A. Carleton A.J. et al.Effect of fructose on markers of Non-Alcoholic Fatty Liver Disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials.Eur J Clin Nutr. 2014; ([Epub ahead of print])https://doi.org/10.1038/ejcn.2014.8Crossref PubMed Scopus (219) Google Scholar, 3Sievenpiper J.L. de Souza R.J. Mirrahimi A. Yu M.E. Carleton A.J. Beyene J. et al.Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis.Ann Intern Med. 2012; 21: 291-304Crossref Scopus (234) Google Scholar, 4Cozma A.I. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Ha V. Wang D.D. et al.Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials.Diabetes Care. 2012; 35: 1611-1620Crossref PubMed Scopus (165) Google Scholar, 5Sievenpiper J.L. Carleton A.J. Chatha S. Jiang H.Y. de Souza R.J. Beyene J. et al.Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans.Diabetes Care. 2009; 32: 1930-1937Crossref PubMed Scopus (141) Google Scholar, 6Wang D.D. Sievenpiper J.L. De Souza R.J. Cozma A.I. Chiavaroli L. Ha V. et al.Effect of fructose on postprandial triglycerides: a systematic review and meta-analysis of controlled feeding trials.Atherosclerosis. 2014; 232: 125-133Abstract Full Text Full Text PDF PubMed Scopus (134) Google Scholar, 7Ha V. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Wang D.D. Cozma A.I. et al.Effect of fructose on blood pressure: a systematic review and meta-analysis of controlled feeding trials.Hypertension. 2012; 59: 787-795Crossref PubMed Scopus (149) Google Scholar, 8Wang D.D. Sievenpiper J.L. de Souza R.J. Chiavaroli L. Ha V. Cozma A.I. et al.The effects of fructose intake on serum uric acid vary among controlled dietary trials.J Nutr. 2012; 142: 916-923Crossref PubMed Scopus (166) Google Scholar]. In the absence of a clear effect on markers of NAFLD and its related cardiometabolic risk factors in isocaloric comparisons (especially under conditions of positive energy balance), the effects seen in the hypercaloric comparisons appear to relate more to the excess energy than the fructose. Adjustment for total energy intake would therefore seem essential in understanding whether an association with fructose exists beyond the energy it contributes. Other lifestyle factors associated with NAFLD were also not adjusted for in their multivariate models. These include smoking, exercise, total fat, trans fat, saturated fat, cholesterol, the n-6:-3 ratio of polyunsaturated fatty acids, total carbohydrate, animal protein, dietary fibre, and an overall Western dietary pattern which embodies these variables. Even if some of these factors were not significant in univariate analyses, each has been shown to have an equal or stronger association with NAFLD [9Mouzaki M. Allard J.P. The role of nutrients in the development, progression, and treatment of nonalcoholic fatty liver disease.J Clin Gastroenterol. 2012; 46: 457-467Crossref PubMed Scopus (88) Google Scholar, 10Zein C.O. Unalp A. Colvin R. Liu Y.C. McCullough A.J. Nonalcoholic steatohepatitis clinical research network. Smoking and severity of hepatic fibrosis in nonalcoholic fatty liver disease.J Hepatol. 2011; 54: 753-759Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar] and may contribute to residual confounding. These factors individually and collectively may also contribute to important collinearity effects, as high consumers of added sugars (in the form of sugar sweetened beverages) tend to smoke more, exercise less, and eat more calories in the form of a Western dietary pattern characterized by increased red meat, processed meat, potato products, and refined grains. The lack of adjustment for these factors greatly complicates the interpretation of the results. In the absence of adjustment for factors associated with NAFLD, one cannot conclude with confidence that "industrial" fructose is a risk factor for liver fibrosis in biopsy-proven G1CHC patients. Added fructose from industrial sources may simply represent a marker of an unhealthy lifestyle pattern in these patients. To understand whether fructose is an independent predictor of liver fibrosis, the authors must address these confounders in future models. There also remains an urgent need for higher quality evidence from well-conducted prospective observational studies with good measurements of exposure and the ability to adjust for known confounders as well as longer, larger, higher quality randomized controlled trials of the effect of fructose on the progression of NAFLD. LC has received research support from the Canadian Institutes of Health Research (CIHR) and is a clinical research coordinator at Glycemic Index Laboratories, Toronto, Ontario, Canada. VH has received a Province of Ontario Graduate Scholarship and research support from the Canadian Institutes of Health Research (CIHR) and World Health Organization (WHO) for work on a systematic review and meta-analysis commissioned by the WHO of the relation of saturated fatty acids with health outcomes. She also received a travel award to attend the "Journey Through Science Day" hosted by PepsiCo and the New York Academy of Sciences (NYAS). RJdS is funded by a CIHR Postdoctoral Fellowship Award and has received research support from the CIHR, Calorie Control Council, the Canadian Foundation for Dietetic Research (CFDR), and The Coca-Cola Company (investigator initiated, unrestricted grant). He has served as an external resource person to the World Health Organization's (WHO) Nutrition Guidelines Advisory Group (NUGAG), and is the lead author of two systematic reviews and meta-analyses commissioned by the WHO of the relation of saturated fatty acids and trans fatty acids with health outcomes. The WHO paid for his travel and accommodation to attend NUGAG Meetings in Hangzhou, China and Copenhagen, Denmark. CWCK has received research grants, travel funding, consultant fees, honoraria, or has served on the scientific advisory board for Abbott Laboratories, Advanced Food Materials Network, Agrifoods and Agriculture Canada (AAFC), Almond Board of California, American Peanut Council, American Pistachio Growers, Barilla, California Strawberry Commission, Bayer, Calorie Control Council, Canadian Institutes of Health Research (CIHR), Canola Council of Canada, The Coca Cola Company (investigator initiated, unrestricted), Danone, General Mills, Hain Celestial, International Tree Nut Council, Kellogg, Kraft, Loblaw Brands Ltd, Nutrition Foundation of Italy, Oldways Preservation Trust, Orafti, Paramount Farms, Peanut Institute, Pepsi-Co, Pulse Canada, Sabra Dipping Co., Saskatchewan Pulse Growers, Solae, Sun-Maid, Tate & Lyle and Unilever. JLS has received research support from the Canadian Institutes of Health Research (CIHR), Calorie Control Council, The Coca-Cola Company (investigator initiated, unrestricted educational grant), Dr. Pepper Snapple Group (investigator initiated, unrestricted educational grant), Pulse Canada, and The International Tree Nut Council Nutrition Research & Education Foundation. He has received travel funding, speaker fees, and/or honoraria from the American Heart Association (AHA), American College of Physicians (ACP), American Society for Nutrition (ASN), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH), Canadian Diabetes Association (CDA), Canadian Nutrition Society (CNS), University of South Carolina, University of Alabama at Birmingham, Calorie Control Council, Diabetes and Nutrition Study Group (DNSG) of the European Association for the Study of Diabetes (EASD), International Life Sciences Institute (ILSI) North America, ILSI Brazil, Abbott Laboratories, Pulse Canada, Canadian Sugar Institute, Dr. Pepper Snapple Group, and The Coca-Cola Company. He is on the Clinical Practice Guidelines Expert Committee for Nutrition Therapy of both the CDA and EASD, as well as being on the ASN writing panel for a scientific statement on the metabolic and nutritional effects of fructose, sucrose and high fructose corn syrup. He is a member of the International Carbohydrate Quality Consortium (ICQC) and an unpaid scientific advisor for the ILSI North America, Food, Nutrition, and Safety Program (FNSP). His wife is an employee of Unilever Canada.
Current guidelines recommend diet and lifestyle modifications for primary prevention and treatment of hypertension, but do not encourage dietary pulses specifically for lowering blood pressure (BP). To quantify the effect of dietary pulse interventions on BP and provide evidence for their inclusion in dietary guidelines, a systematic review and meta-analysis of controlled feeding trials was conducted. MEDLINE, EMBASE, Cochrane Library, and CINAHL were each searched from inception through 5 May 2013. Human trials ≥3 weeks that reported data for systolic, diastolic, and/or mean arterial BPs were included. Two reviewers independently extracted data and assessed methodological quality and risk of bias of included studies. Effect estimates were pooled using random effects models, and reported as mean differences (MD) with 95% confidence intervals (CIs). Heterogeneity was assessed (χ2 test) and quantified (I2). Eight isocaloric trials (n = 554 participants with and without hypertension) were included in the analysis. Dietary pulses, exchanged isocalorically for other foods, significantly lowered systolic (MD = −2.25 mm Hg (95% CI, −4.22 to −0.28), P = 0.03) and mean arterial BP (MD = −0.75 mm Hg (95% CI, −1.44 to −0.06), P = 0.03), and diastolic BP non-significantly (MD = −0.71 mm Hg (95% CI, −1.74 to 0.31), P = 0.17). Heterogeneity was significant for all outcomes. Dietary pulses significantly lowered BP in people with and without hypertension. Higher-quality large-scale trials are needed to support these findings. NCT01594567
Although there is a call for patient-centred prenatal care, women’s preferences for and concerns about preterm birth (PTB) prevention have not been well-studied. Therefore, we conducted a cross-sectional survey to determine women’s preferences for PTB prevention and their likelihood of following their healthcare provider’s recommendations for PTB prevention, as well as factors associated with these responses. A piloted self-administered questionnaire was completed by pregnant women who could read English. Data were collected about their preferences for and concerns about PTB prevention, and the likelihood of following their healthcare provider’s recommendations, using multivariable logistic regression to control for other factors. Three hundred and eleven women at a median of 32-weeks of gestation completed the survey, a response rate of 85.2%. Most women reported that if they were told they were at increased risk for PTB, they preferred not to use PTB prevention (65.8%), of whom almost all (93.4%) reported they preferred close-monitoring and 6.6% preferred neither monitoring nor prevention. A much smaller proportion of women reported that they would not follow their healthcare provider’s recommendation for progesterone (10.9%) compared to pessary (28.7%) or cerclage (50.2%). Women who were neither married nor in a common-law relationship were more likely to report that they would not follow recommendations for progesterone (aOR = 5.88 [95% CI: 1.72, 20.00]). Most women (84.5%) reported they would use other sources of information other than their main healthcare provider to learn more about PTB prevention, with the most popular source being the internet. Most women reported that if they were told they were at increased risk of PTB, they preferred close-monitoring over using PTB prevention. Their reported likelihood of not following their healthcare provider’s recommendations for PTB prevention varied from 10.9% for progesterone to 50.2% for cerclage. These findings suggest that more education about the risk of PTB, PTB preventions, as well as compliance with progesterone is needed and that the internet would be an important source of information. However as our study was completed by women at a median of 32 weeks of gestation, future surveys targeted at women earlier in their pregnancy are needed.
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