Association between sugar-sweetened and artificially sweetened soft drinks and type 2 diabetes: systematic review and dose-response meta-analysis of prospective studies.

The intake of sugar-sweetened soft drinks has been reported to be associated with an increased risk of type 2 diabetes, but it is unclear whether this is because of the sugar content or related lifestyle factors, whether similar associations hold for artificially sweetened soft drinks, and how these associations are related to BMI. We aimed to conduct a systematic literature review and dose-response meta-analysis of evidence from prospective cohorts to explore these issues. We searched multiple sources for prospective studies on sugar-sweetened and artificially sweetened soft drinks in relation to the risk of type 2 diabetes. Data were extracted from eleven publications on nine cohorts. Consumption values were converted to ml/d, permitting the exploration of linear and non-linear dose-response trends. Summary relative risks (RR) were estimated using a random-effects meta-analysis. The summary RR for sugar-sweetened and artificially sweetened soft drinks were 1·20/330 ml per d (95 % CI 1·12, 1·29, P< 0·001) and 1·13/330 ml per d (95 % CI 1·02, 1·25, P= 0·02), respectively. The association with sugar-sweetened soft drinks was slightly lower in studies adjusting for BMI, consistent with BMI being involved in the causal pathway. There was no evidence of effect modification, though both these comparisons lacked power. Overall between-study heterogeneity was high. The included studies were observational, so their results should be interpreted cautiously, but findings indicate a positive association between sugar-sweetened soft drink intake and type 2 diabetes risk, attenuated by adjustment for BMI. The trend was less consistent for artificially sweetened soft drinks. This may indicate an alternative explanation, such as lifestyle factors or reverse causality. Future research should focus on the temporal nature of the association and whether BMI modifies or mediates the association.

'My Meal Mate' (MMM): validation of the diet measures captured on a smartphone application to facilitate weight loss.

Accurate dietary assessment is an essential foundation of research in nutritional epidemiology. Due to the weaknesses in current methodology, attention is turning to strategies that automate the dietary assessment process to improve accuracy and reduce the costs and burden to participants and researchers. 'My Meal Mate' (MMM) is a smartphone application designed to support weight loss. The present study aimed to validate the diet measures recorded on MMM against a reference measure of 24 h dietary recalls. A sample of fifty volunteers recorded their food and drink intake on MMM for 7 d. During this period, they were contacted twice at random to conduct 24 h telephone recalls. Daily totals for energy (kJ) and macronutrients recorded on MMM were compared against the corresponding day of recall using t tests for group means and Pearson's correlations. Bland-Altman analysis was used to assess the agreement between the methods. Energy (kJ) recorded on MMM correlated well with the recalls (day 1: r 0·77 (95 % CI 0·62, 0·86), day 2: r 0·85 (95 % CI 0·74, 0·91)) and had a small mean difference (day 1 (MMM - recall): -68 kJ/d (95 % CI -553, 418 kJ) (-16 kcal/d, 95 % CI -127, 100 kcal); day 2 (MMM - recall): -441 kJ/d (95 % CI -854, -29 kJ) (-105 kcal/d, 95 % CI -204, -7 kcal)). Bland-Altman analysis showed wide limits of agreement between the methods: -3378 to 3243 kJ/d (-807 to 775 kcal/d) on day 1. At the individual level, the limits of agreement between MMM and the 24 h recall were wide; however, at the group level, MMM appears to have potential as a dietary assessment tool.

Body mass index, abdominal fatness and pancreatic cancer risk: a systematic review and non-linear dose-response meta-analysis of prospective studies.

BACKGROUND: Questions remain about the shape of the dose-response relationship between body mass index (BMI) and pancreatic cancer risk, possible confounding by smoking, and differences by gender or geographic location. Whether abdominal obesity increases risk is unclear. METHODS: We conducted a systematic review and meta-analysis of prospective studies of the association between BMI, abdominal fatness and pancreatic cancer risk and searched PubMed and several other databases up to January 2011. Summary relative risks (RRs) were calculated using a random-effects model. RESULTS: Twenty-three prospective studies of BMI and pancreatic cancer risk with 9504 cases were included. The summary RR for a 5-unit increment was 1.10 [95% confidence interval (CI) 1.07-1.14, I(2) = 19%] and results were similar when stratified by gender and geographic location. There was evidence of a non-linear association, P(non-linearity) = 0.005; however, among nonsmokers, there was increased risk even within the 'normal' BMI range. The summary RR for a 10-cm increase in waist circumference was 1.11 (95% CI 1.05-1.18, I(2) = 0%) and for a 0.1-unit increment in waist-to-hip ratio was 1.19 (95% CI 1.09-1.31, I(2) = 11%). CONCLUSIONS: Both general and abdominal fatness increases pancreatic cancer risk. Among nonsmokers, risk increases even among persons within the normal BMI range.

Dietary fructose, carbohydrates, glycemic indices and pancreatic cancer risk: a systematic review and meta-analysis of cohort studies.

BACKGROUND: Dietary carbohydrates, glycemic load and glycemic index have been hypothesized to influence pancreatic cancer risk, but epidemiological studies have been inconsistent. We conducted a systematic review and meta-analysis of prospective studies to clarify these results. METHODS: PubMed and several other databases were searched for prospective studies of intake of carbohydrates, glycemic index and glycemic load and pancreatic cancer up to September 2011. Summary relative risks were estimated using a random effects model. RESULTS: Ten cohort studies (13 publications) were included in the meta-analysis. The summary relative risk (RR) per 10 glycemic index units was 1.02 [95% confidence interval (CI): 0.93-1.12, I(2) = 0%], per 50 glycemic load units was 1.03 (95% CI: 0.93-1.14, I(2) = 10%), per 100 g/day of total carbohydrates was 0.97 (95% CI: 0.81-1.16, I(2) = 35%), and per 25 g/day of sucrose intake was 1.05 (95% CI: 0.85-1.23, I(2) = 53%). A positive association was observed with fructose intake, summary RR = 1.22 (95% CI: 1.08-1.37, I(2) = 0%) per 25 g/day. CONCLUSIONS: This meta-analysis does not support an association between diets high in glycemic index, glycemic load, total carbohydrates or sucrose and pancreatic cancer risk. The finding of an increased risk with fructose intake warrants further investigation in studies with better adjustment for confounding and in non-American populations.

Dietary acrylamide intake and risk of breast cancer in the UK women's cohort.

BACKGROUND: No studies to date have demonstrated a clear association with breast cancer risk and dietary exposure to acrylamide. METHODS: A 217-item food frequency questionnaire was used to estimate dietary acrylamide intake in 33,731 women aged 35-69 years from the UK Women's Cohort Study followed up for a median of 11 years. RESULTS: In all, 1084 incident breast cancers occurred during follow-up. There was no evidence of an overall association between acrylamide intake and breast cancer (hazard ratio=1.08 per 10 µg day(-1), 95% CI: 0.98-1.18, P(trend)=0.1). There was a suggestion of a possible weak positive association between dietary acrylamide intake and premenopausal breast cancer after adjustment for potential confounders (hazard ratio=1.2, 95% CI: 1.0-1.3, P(trend)=0.008). There was no suggestion of any association for postmenopausal breast cancer (hazard ratio=1.0, 95% CI: 0.9-1.1, P(trend)=0.99). CONCLUSIONS: There is no evidence of an association between dietary acrylamide intake and breast cancer. A weak association may exist with premenopausal breast cancer, but requires further investigation.

Alcohol intake and risk of colorectal cancer: results from the UK Dietary Cohort Consortium.

BACKGROUND: Epidemiological studies have suggested that excessive alcohol intake increases colorectal cancer (CRC) risk. However, findings regarding tumour subsites and sex differences have been inconsistent. METHODS: We investigated the prospective associations between alcohol intake on overall and site- and sex-specific CRC risk. Analyses were conducted on 579 CRC cases and 1996 matched controls nested within the UK Dietary Cohort Consortium using standardised data obtained from food diaries as a main nutritional method and repeated using data from food frequency questionnaire (FFQ). RESULTS: Compared with individuals in the lightest category of drinkers (>0-<5 g per day), the multivariable odds ratios of CRC were 1.16 (95% confidence interval (95% CI): 0.88, 1.53) for non-drinkers, 0.91 (95% CI: 0.67, 1.24) for drinkers with 5-<15 g per day, 0.90 (95% CI: 0.65, 1.25) for drinkers with 15-<30 g per day, 1.02 (95% CI: 0.66, 1.58) for drinkers with 30-<45 g per day and 1.19 (95% CI: 0.75, 1.91) for drinkers with >or=45 g per day. No clear associations were observed between site-specific CRC risk and alcohol intake in either sex. Analyses using FFQ showed similar results. CONCLUSION: We found no significantly increased risk of CRC up to 30 g per day of alcohol intake within the UK Dietary Cohort Consortium.

Gastric cancer: global pattern of the disease and an overview of environmental risk factors.

This first part of this chapter looks at the worldwide burden of gastric cancer at the beginning of the 21st century and summarises available population-based routine data that describes the variation in incidence of the disease in relation to age, sex, geography and time period. Consideration is also given to the differences in the descriptive epidemiology of gastric cancer arising in the proximal cardia region of the stomach. In the second part of the chapter, a brief review of the main identified environmental risk factors is conducted drawing, where available, on published systematic literature overviews and meta-analyses. Evidence relating the aetiology of gastric cancer to Helicobacter pylori infection, dietary factors, smoking, occupation, physical activity and anthropometry is presented.

Dietary fibre intake and risk of ischaemic and haemorrhagic stroke in the UK Women's Cohort Study.

BACKGROUND: Stroke risk is modifiable through many risk factors, one being healthy dietary habits. Fibre intake was associated with a reduced stroke risk in recent meta-analyses; however, data were contributed by relatively few studies, and few examined different stroke types. METHODS: A total of 27,373 disease-free women were followed up for 14.4 years. Diet was assessed with a 217-item food frequency questionnaire and stroke cases were identified using English Hospital Episode Statistics and mortality records. Survival analysis was applied to assess the risk of total, ischaemic or haemorrhagic stroke in relation to fibre intake. RESULTS: A total of 135 haemorrhagic and 184 ischaemic stroke cases were identified in addition to 138 cases where the stroke type was unknown or not recorded. Greater intake of total fibre, higher fibre density and greater soluble fibre, insoluble fibre and fibre from cereals were associated with a significantly lower risk for total stroke. For total stroke, the hazard ratio per 6 g/day total fibre intake was 0.89 (95% confidence intervals: 0.81-0.99). Different findings were observed for haemorrhagic and ischaemic stroke in healthy-weight or overweight women. Total fibre, insoluble fibre and cereal fibre were inversely associated with haemorrhagic stroke risk in overweight/obese participants, and in healthy-weight women greater cereal fibre was associated with a lower ischaemic stroke risk. In non-hypertensive women, higher fibre density was associated with lower ischaemic stroke risk. CONCLUSIONS: Greater total fibre and fibre from cereals are associated with a lower stroke risk, and associations were more consistent with ischaemic stroke. The different observations by stroke type, body mass index group or hypertensive status indicates potentially different mechanisms.

Dietary fat and the control of energy intake: evaluating the effects of fat on meal size and postmeal satiety.

Three separate experiments in lean subjects confirmed that a 1.52-MJ (362-kcal) carbohydrate supplement at breakfast suppressed appetite 90 min later but had no effect on a test meal given after 270 min. A 1.52-MJ (362-kcal) fat supplement produced no detectable action on measures of appetite at any time point. Therefore, fat and carbohydrate do not have identical effects on the appetite profile. In a further study in obese subjects, a novel experimental design was used to assess the satiating efficiency and compensatory response of fat. Eating from a range of either high-fat or high-carbohydrate foods, obese subjects voluntarily consumed twice as much energy from the fat items, thereby indicating a weak action of fat on satiation. In turn, this large intake of fat exerted a disproportionately weak effect on satiety. These studies suggest that the appetite-control system may have only weak inhibitory mechanisms to prevent the passive overconsumption of dietary fat. The results indicate how this action could induce a positive energy balance and lead to a gradual upward drift in body mass index.

Across-the-day monitoring of mood and energy intake before, during, and after a very-low-calorie diet.

Mood, hunger, and energy intake were monitored in eight obese women before, during, and after 2 wk on a very-low-calorie diet (VLCD). Energy intake was significantly lower by approximately 30% in the week after the VLCD compared with the prediet week, both from food diaries and at a controlled ad libitum test meal. There was a gradual reduction in hunger, irritability, and urge to eat after 1 wk on the VLCD, which persisted through the postdiet week. Hunger and discontent were greatest in the evening during the first few days of the VLCD but diminished as the duration of the VLCD increased.

Sugar consumption and cancers of the digestive tract.

In order to assess the relationship between dietary intake of sugar and cancers of the digestive tract a comprehensive search of the scientific literature was undertaken. Forty human studies (ecological, cohort or case-control) were found which assessed the intake of sugar or sucrose-containing foods and risk of cancer of the stomach, small intestine, colon or rectum. These were systematically reviewed and study quality criteria applied. No clear relationship between national or international estimates of sugar intake and risk of gastrointestinal cancers emerged. Two of eight studies for gastric cancer, and seven of 21 studies for colorectal cancer, reported risk estimates consistent with a positive association or trend for sugar consumption. Only one study was reported of the relationship between sugar intake and risk of small intestinal cancer. When study quality criteria were applied, none of the studies remaining showed a significant positive relationship between gastric cancer and intake of sugar, and of six studies of colorectal cancer only two showed a significant positive association. The balance of studies suggests that there is no relationship between intake of sugar and risk of developing cancer of the stomach. As a result of the limited number of well-conducted studies of small intestinal or colorectal cancer, however, there is insufficient information upon which to assess the degree of risk associated with sugar consumption and development of cancer of these sites.

Sugar consumption and human cancer in sites other than the digestive tract.

In order to assess the relationship between dietary intake of sugar and cancer a comprehensive search of the scientific literature was undertaken. An earlier publication details an analysis of studies relating to cancers of the digestive tract (Burley, 1997). Here, a total of 69 publications were reviewed which reported the results of ecological, case-control or cohort studies which had assessed the relationship between dietary sugar intake or sucrose-containing foods and risk of cancer at other sites. Cancer sites reviewed included the breast, pancreas, prostate, testis, female reproductive system, lung and upper aerodigestive tract and bladder. For most of these cancer sites the number of studies was insufficient to reach a conclusion. For breast cancer, the data on international per capita sugar intakes suggest a consistent positive correlation with breast cancer mortality rates. However, this relationship is not consistent in within-country ecological studies or in case-control studies, in which sugar intakes have been assessed as mono- and disaccharides or as sucrose. There is some suggestion of a weak increase in risk of breast cancer with high consumption of sucrose-containing foods, such as cakes and biscuits. However, these foods provide a range of other nutrients, particularly fat, which may also be implicated in the development of breast cancer, and further studies specifically designed to address this area are required. It is apparent that there is insufficient evidence to conclude whether sugar has a role in cancer at any site.

The specificity of satiety: the influence of foods of different macronutrient content on the development of satiety.

The effects of consuming equicaloric preloads with different macronutrient contents on the development of satiety were investigated. Ten normal-weight, nondieting women fasted overnight and then rated hunger, fullness, and food preferences, and the pleasantness of the taste of food samples before and after five different preloads. The greatest changes in the pleasantness of the taste of the food occurred for the eaten food relative to the uneaten food. Macronutrient content of the preloads did not significantly influence the magnitude of these changes or the pleasantness of foods with similar nutrient contents. Therefore, no evidence of nutrient-specificity was obtained. Nutrient composition had a differential effect on hunger, fullness and food intake. Ratings of hunger decreased and fullness increased following the high starch and high protein preloads to a greater extent than after the high fat, high sucrose and mixed content preloads. When a self-selection meal was offered 2 hours after the preloads energy intake and preference for high carbohydrate and high fat food items were significantly decreased by the high protein and high starch preloads. However, no specific reduction in macronutrient intake was observed. In conclusion, differential effects of the preloads were observed in subjective ratings of hunger, fullness, preferences and subsequent food intake, but there was no indication that satiety was macronutrient-specific.

Sensory stimulation and energy density in the development of satiety.

To determine the contribution of sensory stimulation to the changing hedonic response to foods, the effects of consuming very low-calorie and higher calorie versions of soup and jello on the subjective pleasantness of foods were compared. Subjects were 24 normal weight females with low dietary restraint. Half the subjects were given test meals of low- and high-calorie tomato soup and half were given low- and high-calorie orange jello. They rated the pleasantness of the appearance, smell, texture and taste of nine sample foods as well as hunger and stomach fullness before and 2, 20, 40 and 60 min after consumption of the test meal. After the 60 min rating subjects were offered as much as they wanted to eat of a second course of cheese on crackers. Despite differences in the energy density of the test meals, there were no significant differences in the weights of food eaten in either the first or second course and no significant compensation in the second course for the energy differences of the first course. No differential effects of the caloric manipulation were observed in terms of hunger or fullness or in the development, time course and magnitude of sensory-specific satiety. That very low-calorie foods can produce sensory-specific satiety indicates that the sensory properties of foods are important for the changing hedonic response to foods as they are consumed.

Postingestive inhibition of food intake by aspartame: importance of interval between aspartame administration and subsequent eating.

Aspartame administered in capsules (i.e., without tasting) 1 h before a meal significantly reduces the amount eaten in that meal. In the present study 36 young men and women were divided into 3 groups of 12 to receive aspartame (400 mg) or placebo (400 mg starch) on separate occasions either 5 min (Group A), 30 min (Group B) or 60 min (Group C) before beginning an ad lib test meal. Compared with placebo, aspartame reduced food intake in Group C (by 18.5%, p < 0.01), but did not reliably affect intake in Groups A or B. There were, in contrast, no significant effects of aspartame on premeal ratings of hunger, desire to eat or fullness for any of the groups. These results confirm a postingestive inhibitory action of aspartame on appetite, which may involve the amplification of the satiating effects of food. The lack of effect of aspartame administered at the shorter intervals before eating suggests a postgastric or even postabsorptive mechanism of action. This observation is also important in its implications for the possible therapeutic exploitation of the anorexic effect of capsulated aspartame.

Exercise-induced suppression of appetite: effects on food intake and implications for energy balance.

OBJECTIVE: To examine the effects of exercise on short term energy intake and to investigate the existence of exercise-induced anorexia. DESIGN: Two studies were conducted, both with three treatment conditions and employing a repeated measures design. SETTING: The Human Appetite Research Unit at Leeds University Psychology department. SUBJECTS: Twenty three healthy, lean male subjects (n = 11 and n = 12 respectively) were recruited from the student/staff population of Leeds University. INTERVENTIONS: Subjects were randomly assigned to a control, low intensity and high intensity exercise treatment in the first study and to a control, short duration and long duration exercise treatment (high intensity) in the second. Motivation to eat was measured by visual analogue rating scales and by the length of the time between the end of exercise and the volitional onset of eating. Energy and macronutrient intakes were measured by means of a free-selection test meal and by recorded intakes for the next 2 days. RESULTS: Subjective feelings of hunger were significantly suppressed during and after intense exercise sessions (P 0.01), but the suppression was short-lived. Exercise sessions had no significant effect on the total amount of food consumed in the test meal but intense exercise delayed the start of eating (P < 0.05). When energy intake was assessed relative to the energy expended during the exercise or control periods, only the long duration, high intensity session created a significant short-term negative energy balance (P < 0.001). CONCLUSIONS: These studies indicate that exercise-induced anorexia can be characterized by a brief suppression of hunger, accompanied by a delay to the onset of eating. The temporal aspects of exercise-induced anorexia may best be measured by the resistance to begin eating rather than the amount of food consumed.

Influence of a high-fibre food (myco-protein) on appetite: effects on satiation (within meals) and satiety (following meals).

The effect of meals containing Quorn myco-protein or chicken upon satiety and satiation were investigated in 18 lean, healthy male and female subjects using a within-subjects design. Both meals were designed to be similar in every respect with the exception of dietary fibre content (11 vs 3 g). Following consumption of a lunch containing Quorn myco-protein (high fibre) subsequent energy intake at an evening ad libitum test meal was reduced by 18% (P < 0.001) when compared with the response to an isocaloric chicken-containing (low-fibre) lunch. Using the Universal Eating Monitor (a device which weighs continuously the portion of food being consumed) the within-meal effects of a lunch containing Quorn or chicken were investigated. This study showed that during consumption, Quorn elicited similar eating behaviour when compared to a chicken meal. Amount selected, overall eating rate and the decrease in motivation to eat did not differ between the Quorn and control conditions. These two studies show that Quorn (high-protein, dietary fibre combination) has a strong impact on late satiety, but is similar in its effects during and immediately after consumption. These data have clear implications for the use of Quorn myco-protein for the control of appetite and body weight.

Effect of fat- and sucrose-containing foods on the size of eating episodes and energy intake in lean males: potential for causing overconsumption.

OBJECTIVE: This study compared the action of sucrose- and fat-containing foods on the size of eating episodes (satiation) and postingestive energy intake (satiety). DESIGN: The study was a 2 x 2 within-subjects design, each subject received each of four conditions in a counterbalanced order. SETTING: The study was carried out in the Human Appetite and Nutrition Research Unit. SUBJECTS: Eighteen normal-weight young male University students. INTERVENTIONS: Subjects consumed a low (2238 kJ) or high (3962 kJ) energy lunch followed 2 h later by the opportunity to eat freely from an ad libitum selection of high fat, low sucrose or high sucrose, low fat snacks. Visual analogue rating scales to record subjective feelings of hunger, fullness and related sensations were completed periodically through the test day. RESULTS: When offered a high sucrose, low fat selection of snacks subjects consumed less energy than when offered a high fat, low sucrose selection (P < 0.0001). However postingestive satiety was similar. The energy intake of snacks consumed was also determined by hunger; the low energy lunch gave rise to a higher level of hunger and greater intake (P < 0.01). Energy intake for the total day was significantly more when high fat, low sucrose snacks were consumed (P < 0.001). CONCLUSIONS: These results have indicated that the size of an eating episode is influenced by the level of hunger and the nutrient composition of the foods consumed. High fat foods (probably due to higher energy density) lead to a passive overconsumption which generates a relatively weak satiety.

Food-frequency questionnaires: a review of their design, validation and utilisation.

A review of the literature concerning the design, utilisation and validation of food-frequency questionnaires (FFQ) has been carried out using a semi-systematic approach to obtaining, reviewing and extracting data from articles. Databases were searched from 1980 to 1999. The present review identified 227 validation (from 1980 to September 1999) and 164 utilisation (for 1998 only) studies. A number of design issues have been evaluated through the present review. These include: the need to consider how portion sizes have been described, self-defined giving higher mean correlations; how an FFQ was administered, interviewer-administered giving higher mean correlations for some nutrients; how many items to include on an FFQ, those with the largest number of items having higher correlations. Validation techniques were described. Most validation studies involved comparing an FFQ against another dietary assessment method; only 19 % compared an FFQ to a biomarker. Measurement differences were most commonly assessed by correlation coefficients as opposed to other more appropriate methods. Mean correlation coefficients were highest for Ca and fat, and lowest for vitamin A and vegetables. The utilisation studies showed that FFQ were most commonly used in cross-sectional surveys, with ninety-three of the FFQ being designed to be disease-specific. The present review results were presented to a group of experts and a consensus arrived at concerning the development, validation and use of FFQ. Recommendations derived from the consensus arising from the literature review are presented as an appendix to the present paper.

Handheld Electronic Technology for Weight Loss in Overweight/Obese Adults.

Handheld electronic devices could offer a convenient and scalable platform with which to deliver a weight loss intervention. This paper aims to summarise the evidence provided by randomised trials of such interventions. There is heterogeneity among trials in terms of the components of the intervention package, the theoretical framework, the comparison groups and the duration of follow-up. While in the short term (<6 months) trials have shown some promising findings, two trials (one of a text message intervention and one of a PDA device for dietary self-monitoring) do not indicate clinically significant weight loss in the longer term (1-2 years). Topical issues are discussed including the importance of further research into dietary self-monitoring, the logistics of trialling smartphone applications and considerations of health literacy. There is currently no definitive randomised controlled trial of a smartphone app for weight loss in adults and further research into this approach is warranted.