<i>Background:</i> Components of the insulin-like growth factor (IGF) system have been associated with several cancers, but very few studies are available for ovarian cancer. <i>Methods:</i> A case-control study conducted between 1999 and 2003 in Italy, including a total of 59 women with incident, histologically confirmed ovarian cancer and 108 controls admitted to the same hospital network as cases, for acute non-neoplastic diseases. All subjects were interviewed using a validated questionnaire. <i>Results:</i> After adjustment for potential confounders, the multivariate odds ratios for the highest versus the lowest tertile of various IGF components were 0.6 (95% confidence interval, CI: 0.2–1.4) for free IGF-I, 0.4 (CI: 0.1–1.5) for total IGF-I, 2.6 (CI: 0.9–6.9) for IGF-binding protein (IGFBP)-1, and 0.2 (CI: 0.0–0.6) for IGFBP-3. <i>Conclusions:</i> This study suggests a protective role of IGFBP-3 and a positive association of IGFBP-1 with ovarian cancer. The complex role of the IGF system in ovarian carcinogenesis deserves further clarification.
Rare sugars are monosaccharides and disaccharides (found in small quantities in nature) that have slight differences in their chemical structure compared with traditional sugars. Little is known about their unique physiological and cardiometabolic effects in humans.
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.
<p>Background: The Dietary Approaches to Stop Hypertension (DASH) dietary pattern, which emphasizes fruit, vegetables, fat-free/low-fat dairy, whole grains, nuts and legumes, and limits saturated fat, cholesterol, red and processed meats, sweets, added sugars, salt and sugar-sweetened beverages, is widely recommended by international diabetes and heart association guidelines. Objective: To summarize the available evidence for the update of the European Association of the Study of Diabetes (EASD) guidelines, we conducted an umbrella review of existing systematic reviews and meta-analyses using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach of the relation of the DASH dietary pattern with cardiovascular disease and other cardiometabolic outcomes in prospective cohort studies and its effect on blood pressure and other cardiometabolic risk factors in controlled trials in individuals with and without diabetes. Methods: MEDLINE and EMBASE were searched through 3 January 2019. We included systematic reviews and meta-analyses assessing the relation of the DASH dietary pattern with cardiometabolic disease outcomes in prospective cohort studies and the effect on cardiometabolic risk factors in randomized and non-randomized controlled trials. Two independent reviewers extracted relevant data and assessed the risk of bias of individual studies. The primary outcome was incident cardiovascular disease (CVD) in the prospective cohort studies and systolic blood pressure in the controlled trials. Secondary outcomes included incident coronary heart disease, stroke, and diabetes in prospective cohort studies and other established cardiometabolic risk factors in controlled trials. If the search did not identify an existing systematic review and meta-analysis on a pre-specified outcome, then we conducted our own systematic review and meta-analysis. The evidence was summarized as risk ratios (RR) for disease incidence outcomes and mean differences (MDs) for risk factor outcomes with 95% confidence intervals (95% CIs). The certainty of the evidence was assessed using GRADE. Results: We identified three systematic reviews and meta-analyses of 15 unique prospective cohort studies (<em>n</em> = 942,140) and four systematic reviews and meta-analyses of 31 unique controlled trials (<em>n</em> = 4,414) across outcomes. We conducted our own systematic review and meta-analysis of 2 controlled trials (<em>n</em> = 65) for HbA1c. The DASH dietary pattern was associated with decreased incident cardiovascular disease (RR, 0.80 (0.76–0.85)), coronary heart disease (0.79 (0.71–0.88)), stroke (0.81 (0.72–0.92)), and diabetes (0.82 (0.74–0.92)) in prospective cohort studies and decreased systolic (MD, −5.2 mmHg (95% CI, −7.0 to −3.4)) and diastolic (−2.60 mmHg (−3.50 to −1.70)) blood pressure, Total-C (−0.20 mmol/L (−0.31 to −0.10)), LDL-C (−0.10 mmol/L (−0.20 to −0.01)), HbA1c (−0.53% (−0.62, −0.43)), fasting blood insulin (−0.15 μU/mL (−0.22 to −0.08)), and body weight (−1.42 kg (−2.03 to −0.82)) in controlled trials. There was no effect on HDL-C, triglycerides, fasting blood glucose, HOMA-IR, or CRP. The certainty of the evidence was moderate for SBP and low for CVD incidence and ranged from very low to moderate for the secondary outcomes. Conclusions: Current evidence allows for the conclusion that the DASH dietary pattern is associated with decreased incidence of cardiovascular disease and improves blood pressure with evidence of other cardiometabolic advantages in people with and without diabetes. More research is needed to improve the certainty of the estimates.</p>
Food components which are incompletely absorbed in the small intestine or not absorbed at all but are delivered to the colon have been part of the diet throughout the course of human evolution. Our great ape cousins may derive 30% or more of their dietary calories from colonic uptake of short-chain fatty acids (SCFAs) generated in the colon. The metabolic effects of dietary carbohydrate entering the colon are many and include taxation, the growth of the fecal biomass, nitrogen entrapment and SCFA generation. These SCFAs in turn may nourish mucosal cells, spare glutamine utilization, enhance hepatic gluconeogenesis and lipogenesis and possibly influence renal handling of uric acid. The health implications are significant in terms of modifying risk factors for disease and disease prevention and justify interest in the metabolic effects of non-absorbable sugars such as lactulose.
<p>This review synthesized the evidence from randomized controlled trials comparing the effect of meal replacements (MRs) as part of a weight loss intervention with conventional food-based weight loss diets on cardiometabolic risk in individuals with pre-diabetes and features of metabolic syndrome. MEDLINE, EMBASE, and Cochrane Library were searched through January 16, 2024. Data were pooled using the generic inverse variance method and expressed as mean difference [95% confidence intervals]. The overall certainty of the evidence was assessed using GRADE. Ten trials (n = 1254) met the eligibility criteria. MRs led to greater reductions in body weight (-1.38 kg [-1.81, -0.95]), body mass index (BMI, -0.56 kg/m2 [-0.78, -0.34]), waist circumference (-1.17 cm [-1.93, -0.41]), HbA1c (-0.11% [-0.22, 0.00]), LDL-c (-0.18 mmol/L [-0.28, -0.08]), non-HDL-c (-0.17 mmol/L [-0.33, -0.01]), and systolic blood pressure (-2.22 mmHg [-4.20, -0.23]). The overall certainty of the evidence was low to moderate owing to imprecision and/or inconsistency. The available evidence suggests that incorporating MRs into a weight loss intervention leads to small important reductions in body weight, BMI, LDL-c, non-HDL-c, and systolic blood pressure, and trivial reductions in waist circumference and HbA1c, beyond that seen with conventional food-based weight loss diets.</p>
<p><strong>Background and aims</strong></p> <p>Nut consumption has been associated with decreased risk of coronary heart disease (CHD) and type 2 diabetes which has been largely attributed to their healthy fatty acid profile, yet this has not been ascertained. Therefore, we investigated the effect of nut consumption on serum fatty acid concentrations and how these relate to changes in markers of glycemic control and calculated CHD risk score in type 2 diabetes.</p> <p><strong>Methods and results</strong></p> <p>117 subjects with type 2 diabetes consumed one of three iso-energetic (mean 475 kcal/d) supplements for 12 weeks: 1. full-dose nuts (50–100 g/d); 2. half-dose nuts with half-dose muffins; and 3. full-dose muffins. In this secondary analysis, fatty acid concentrations in the phospholipid, triacylglycerol, free fatty acid, and cholesteryl ester fractions from fasting blood samples obtained at baseline and week 12 were analyzed using thin layer and gas chromatography. Full-dose nut supplementation significantly increased serum oleic acid (OA) and MUFAs compared to the control in the phospholipid fraction (OA: P = 0.036; MUFAs: P = 0.024). Inverse associations were found with changes in CHD risk versus changes in OA and MUFAs in the triacylglycerol (r = −0.256, P = 0.011; r = −0.228, P = 0.024, respectively) and phospholipid (r = −0.278, P = 0.006; r = −0.260, P = 0.010, respectively) fractions. In the cholesteryl ester fraction, change in MUFAs was inversely associated with markers of glycemic control (HbA1c: r = −0.250, P = 0.013; fasting blood glucose: r = −0.395, P < 0.0001).</p> <p><strong>Conclusion</strong></p> <p>Nut consumption increased OA and MUFA content of the serum phospholipid fraction, which was inversely associated with CHD risk factors and 10-year CHD risk.</p> <p>Clinical Trial Reg. No.</p> <p>NCT00410722, clinicaltrials.gov.</p>
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