Showing papers by "Thomas M.S. Wolever published in 2014"

Adiposity, gut microbiota and faecal short chain fatty acids are linked in adult humans

Abstract: High dietary fibre intakes may protect against obesity by influencing colonic fermentation and the colonic microbiota. Though, recent studies suggest that increased colonic fermentation contributes to adiposity. Diet influences the composition of the gut microbiota. Previous research has not evaluated dietary intakes, body mass index (BMI), faecal microbiota and short chain fatty acid (SCFA) in the same cohort. Our objectives were to compare dietary intakes, faecal SCFA concentrations and gut microbial profiles in healthy lean (LN, BMI⩽25) and overweight or obese (OWOB, BMI>25) participants. We collected demographic information, 3-day diet records, physical activity questionnaires and breath and faecal samples from 94 participants of whom 52 were LN and 42 OWOB. Dietary intakes and physical activity levels did not differ significantly between groups. OWOB participants had higher faecal acetate (P=0.05), propionate (P=0.03), butyrate (P=0.05), valerate (P=0.03) and total short chain fatty acid (SCFA; P=0.02) concentrations than LN. No significant differences in Firmicutes to Bacteroides/Prevotella (F:B) ratio was observed between groups. However, in the entire cohort, Bacteroides/Prevotella counts were negatively correlated with faecal total SCFA (r=−0.32, P=0.002) and F:B ratio was positively correlated with faecal total SCFA (r=0.42, P<0.0001). Principal component analysis identified distinct gut microbiota and SCFA–F:B ratio components, which together accounted for 59% of the variation. F:B ratio loaded with the SCFA and not with the microbiota suggesting that SCFA and F:B ratio vary together and may be interrelated. The results support the hypothesis that colonic fermentation patterns may be altered, leading to different faecal SCFA concentrations in OWOB compared with LN humans. More in-depth studies looking at the metabolic fate of SCFA produced in LN and OWOB participants are needed in order to determine the role of SCFA in obesity.

Evidence for greater production of colonic short-chain fatty acids in overweight than lean humans.

Abstract: Short-chain fatty acids (SCFA) are produced by colonic microbiota from dietary carbohydrates and proteins that reach the colon. It has been suggested that SCFA may promote obesity via increased colonic energy availability. Recent studies suggest obese humans have higher faecal SCFA than lean, but it is unclear whether this difference is due to increased SCFA production or reduced absorption. To compare rectal SCFA absorption, dietary intake and faecal microbial profile in lean (LN) versus overweight and obese (OWO) individuals. Eleven LN and eleven OWO individuals completed a 3-day diet record, provided a fresh faecal sample and had SCFA absorption measured using the rectal dialysis bag method. The procedures were repeated after 2 weeks. Age-adjusted faecal SCFA concentration was significantly higher in OWO than LN individuals (81.3±7.4 vs 64.1±10.4 mmol kg−1, P=0.023). SCFA absorption (24.4±0.8% vs 24.7±1.2%, respectively, P=0.787) and dietary intakes were similar between the groups, except for a higher fat intake in OWO individuals. However, fat intake did not correlate with SCFAs or bacterial abundance. OWO individuals had higher relative Firmicutes abundance (83.1±4.1 vs 69.5±5.8%, respectively, P=0.008) and a higher Firmicutes:Bacteriodetes ratio (P=0.023) than LN individuals. There was a positive correlation between Firmicutes and faecal SCFA within the whole group (r=0.507, P=0.044), with a stronger correlation after adjusting for available carbohydrate (r=0.615, P=0.005). The higher faecal SCFA in OWO individuals is not because of differences in SCFA absorption or diet. Our results are consistent with the hypothesis that OWO individuals produce more colonic SCFA than LN individuals because of differences in colonic microbiota. However, further studies are needed to prove this.

Total Fructose Intake and Risk of Hypertension: A Systematic Review and Meta-Analysis of Prospective Cohorts

Abstract: Objectives: Although most controlled feeding trials have failed to show an adverse effect of fructose on blood pressure, concerns continue to be raised regarding the role of fructose in hypertension To quantify the association between fructose-containing sugar (high-fructose corn syrup, sucrose, and fructose) intake and incident hypertension, a systematic review and meta-analysis of prospective cohort studies was undertakenMethods: MEDLINE, EMBASE, CINAHL and the Cochrane Library (through February 5, 2014) were searched for relevant studies Two independent reviewers reviewed and extracted relevant data Risk estimates were aggregated comparing the lowest (reference) quintile with highest quintile of intake using inverse variance random effect models and expressed as risk ratios (RR) with 95% confidence intervals (CIs) Interstudy heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic) The Newcastle–Ottawa Scale assessed study quality Clinicaltrialsgov NCT01608620Results: Elig

Kinetic model of acetate metabolism in healthy and hyperinsulinaemic humans

Abstract: The short chain fatty acid acetate (AC), may have a role in increasing insulin sensitivity, thus lowering risk for obesity and type 2 diabetes mellitus. It is unclear if AC kinetics is similar in normal (NI) and hyperinsulinaemic (HI) participants. Therefore, we studied AC absorption from the distal colon in participants with normal (<40 pmol/l) and high (⩾40 pmol/l) plasma insulin. This work was a part of a series of studies conceived to compute a kinetic model for AC. Kinetic parameters such as estimates of rate of entry into peripheral blood, hepatic uptake and endogenous/exogenous production were compared in the groups. Overnight fasted NI (n=9) and HI (n=8) participants were given rectal infusions containing sodium AC (90 mmol/l). The solutions were retained for 40 min, then voided for AC measurement. Total amount of AC infused was 27 mmols. AC absorption from the distal colon (279±103 vs 322±91 μmol/min, P=0.76) and hepatic uptake of AC (155±101 vs 146±85 μmol/min, P=0.94) were similar in the groups. Endogenous and exogenous AC production was significantly higher in NI than HI participants. Plasma AC was inversely proportional to plasma insulin concentrations in the entire cohort (y=k/x, where k=1813). There was low power to detect differences in AC absorption rate and hepatic AC uptake in NI vs HI. The rate of entry of AC into peripheral blood was similar in NI and HI participants. However, hyperinsulinaemia may alter endogenous and exogenous AC metabolism.

Glycaemic index: did Health Canada get it wrong? Position from the International Carbohydrate Quality Consortium (ICQC)

Abstract: On behalf of Health Canada, Aziz et al. ( 1 ) recently published their evaluation of the use of glycaemic index (GI) claims on food labels. Although the importance of controlling postprandial glycaemia (PPG) was recognised in the position statement, they expressed the view that the GI could be ‘misleading’ and ‘would not add value’ to the existing standards for nutrition labels. Unfortunately, several statements indicate a lack of understanding of the evidence base for current information on food labels and of the GI concept in particular. The clinical relevance of PPG is now recognised by health institutions worldwide( 2 , 3 ). Ideally, plasma glucose levels at the 2 h time point after a meal should be < 7·8 mmol/l since values above this level are considered to indicate the presence of impaired glucose tolerance (IGT), which may be indicative of pre-diabetes, a condition which is more prevalent than diabetes itself. Both type 2 diabetes mellitus and IGT are increasing at an alarming rate, largely due to obesity and sedentary lifestyles. Mitigating the risk of adverse outcomes associated with elevated PPG is an important target for population health. For food labelling purposes, the challenge is to find the best tool for evaluating a product's impact on PPG within the context of other health recommendations. Although the GI has a long history of use in research and clinical practice, Aziz et al. ( 1 ) concluded that the GI was not useful because: (1) it has poor accuracy and precision for labelling purposes, (2) it does not vary in response to the amount of food consumed and (3) it is not congruent with national nutritional policies and guidelines. To address the first issue, the GI methodology is recognised and described by the International Standards Organization (26 642:2010) and by the Food and Agriculture Organization of the United Nations( 4 ) as a method to assess the glycaemic impact of available carbohydrates. The GI value of one food is calculated from 640 data points (ten subjects, eight blood samples, in duplicate, one test series for the test food and three test series for the reference food). The margin of error of < 15 % (i.e. the standard error of the mean expressed as a percentage of the mean) is considered reliable in the context of the considerable day-to-day variation in glucose tolerance in healthy individuals ( ± 30–50 %)( 5 ). By testing a reference food, the GI method takes into account ‘between-person variation’. Concerning the accuracy and precision of any nutritional attribute, one cannot let perfect be the enemy of good. For example, both whole-grain and fibre claims are permitted on food labels, despite the fact that the definition and measurement of each varies among nations and is neither perfect nor precise. A whole-grain product may contain only 50 % whole grains according to the Food and Drug Administration, and there is marked disagreement of what fibre is and how it should be measured. Moreover, total carbohydrates on food labels are often described as ‘carbohydrate by difference’, which is calculated by subtracting the sum of the water, protein, fat, dietary fibre, ash and alcohol contents from 100. This method compounds the errors associated with all assays and often differs markedly from the direct measurement of the available carbohydrate. In addition, there is a permitted margin of error of < 20 % for any component listed in the nutrition panel, which is considerably higher than the margin of error considered reliable for the GI of a food ( < 15 %). In this context, the GI is being held to a much higher standard than other nutritional attributes. The second issue identified by Aziz et al. ( 1 ) was that the GI does not vary in response to the amount of food consumed. Informed consumers would anticipate that the greater the amount of the available carbohydrate consumed, the greater the increase in blood glucose. The key value of the GI therefore is that it allows comparisons between foods on a gram-for-gram carbohydrate basis, which is important for consumer choice. The glycaemic load (GL) per serving (the product of the available carbohydrate content × GI) varies in response to the amount consumed( 6 ), and could be included in the nutrient panel together with the GI. With respect to the third issue, Health Canada claims that the GI is not congruent with national nutritional policies and guidelines, implying that the GI would be used in isolation, irrespective of other important attributes such as saturated fat, fibre and whole grain content. We agree that the GI should not override sound dietary advice( 1 ). However, this concern relates to any dietary claim, including ‘low fat’ and ‘high fibre’. Of note, Health Canada's concern is inconsistent with their earlier statement that ‘low-GI diets have attributes of generally recognized healthy eating patterns’( 1 ). However, to address their concern that the composition of a low-GI food may not always be congruent with nutritional guidelines, our suggestion would be to consider a GI claim in conjunction with a healthy food profile. Programmes such as the GI symbol in Australia require the fulfilment of strict nutritional criteria that are consistent with dietary guidelines in order for a food to be eligible to use the certified GI logo. We agree with Aziz et al. ( 1 ) that ‘consumers are familiar with the concept, even though their understanding of it might not be accurate’. In our view, this largely reflects the lack of communication about the GI to the general public and health professionals. The assumption that the GI concept may be too difficult for the lay person is not supported by the Australian experience, where surveys indicate that one in four Australians look for healthy low-GI foods when shopping, simply substituting healthy low-GI varieties for regular high-GI variants within a food group/category( 7 ). Moreover, low-GI dietary advice in randomised clinical trials is associated with high completion rates (low attrition), suggesting that simple low-GI communications can be effective( 8 , 9 ). As in the case of quality of fat (saturated, monounsaturated and polyunsaturated), health agency advice preceded information now commonly listed in the nutritional panel( 10 ). Finally, in their conclusions, Aziz et al. ( 1 ) proposed that nutritional recommendations should take a food-based approach. We agree, yet Health Canada's recommendation to increase intakes of whole foods in the form of vegetables, fruits, grains and pulses does not address the main carbohydrate sources of most populations, i.e. breads, breakfast cereals, rice and ready-to-eat cereal products. Pasta, a staple carbohydrate food of the heart-healthy Mediterranean diet, is a refined yet low-GI carbohydrate food. Most basmati and parboiled rice are white yet have a low GI. There is also a need to distinguish high-GI from low-GI whole grains. Indeed, advice to ‘choose more intact, unprocessed or minimally processed whole-grain products instead of their highly processed counterparts’ is aimed at lowering overall dietary GI or GL. It is a common myth that all whole-grain products have low-GI values when in fact many are highly processed and correspondingly easy to digest( 11 ). In clinical trials, low-GI diets have produced superior outcomes compared with the high-fibre–high-GI diets( 8 , 9 , 12 ). We suggest that GI labels may in fact stimulate the food industry to produce genuinely healthier whole-grain products that retain the low GI of the original grain. Finally, if GI values are misleading and unreliable as Health Canada claims, then it is truly remarkable that a lower dietary GI/GL has been independently associated with a reduced risk of type 2 diabetes( 13 ) and cardiovascular disease( 14 ) in large prospective cohort studies of diverse populations( 15 ). Similarly, randomised controlled trials have shown the benefits of low-GI diets for weight management( 8 , 9 , 12 ), serum lipids( 9 , 12 , 16 ), insulin sensitivity( 17 ) and inflammatory markers( 18 ). Most importantly, the selection of low-GI foods has resulted in the successful improvements of glycaemic control, dyslipidaemia and inflammation in people with type 2 diabetes( 9 , 18 , 19 ). In this regard, these lines of evidence have been used to support the inclusion of low-GI and low-GL dietary patterns in the evidence-based nutrition recommendations of the Canadian Diabetes Association, American Diabetes Association, Diabetes UK, Diabetes Australia, International Diabetes Federation and the European Association for the Study of Diabetes( 20 ). If GI values were not precise, one would not expect to see distinct differences in PPG in response to low- or high-GI meals observed at different time points throughout the day( 12 ). These beneficial outcomes would not be possible if the GI concept were unduly undermined by large variability or differences among people of different ethnicity. Taken together, Health Canada's evaluation misinterprets and misrepresents current scientific evidence, in part by taking the GI outside the context of a healthy diet. In view of the proven health benefits of low-GI diets ‘as currently defined and measured’, every effort should be made to assist consumers in choosing carbohydrate foods that will not exacerbate PPG.

Revised food labeling in North America: the blind leading the blind?

Abstract: The US Food and Drug Administration (FDA) recently proposed that the Nutrition Facts label, the way North American consumers are informed about the nutritional composition of packaged foods, be redesigned.1 There are several good things to say about the proposed new label, which is easier to read, more clearly indicates the serving size and energy content of the food and includes welcome new information about potassium. However, recent comments hardly mention these things; instead, they focus on the proposal to declare the added sugars. Kessler2 argues that merely declaring added sugars does not go far enough, whereas Sylvetsky and Dietz3 argue that declaring added sugars goes too far and may confuse consumers. We are concerned that the rationale for declaring added sugars is based on popular misconceptions rather than high-quality evidence and may do harm.

Effect of Dietary Pulses in a Low Glycemic Index Diet on Renal Function in Participants with Type 2 Diabetes Mellitus

Abstract: BackgroundThere is uncertainty in the effects of dietary pulses so far tested. Reducing the glycemic (GI) of the diet using Acarbose, the α-glucosidase inhibitor, has been shown to be associated wi...