Aims/hypothesisType 2 diabetes is regarded as inevitably progressive, with irreversible beta cell failure. The hypothesis was tested that both beta cell failure and insulin resistance can be reversed by dietary restriction of energy intake.MethodsEleven people with type 2 diabetes (49.5 ± 2.5 years, BMI 33.6 ± 1.2 kg/m2, nine male and two female) were studied before and after 1, 4 and 8 weeks of a 2.5 MJ (600 kcal)/day diet. Basal hepatic glucose output, hepatic and peripheral insulin sensitivity and beta cell function were measured. Pancreas and liver triacylglycerol content was measured using three-point Dixon magnetic resonance imaging. An age-, sex- and weight-matched group of eight non-diabetic participants was studied.ResultsAfter 1 week of restricted energy intake, fasting plasma glucose normalised in the diabetic group (from 9.2 ± 0.4 to 5.9 ± 0.4 mmol/l; p = 0.003). Insulin suppression of hepatic glucose output improved from 43 ± 4% to 74 ± 5% (p = 0.003 vs baseline; controls 68 ± 5%). Hepatic triacylglycerol content fell from 12.8 ± 2.4% in the diabetic group to 2.9 ± 0.2% by week 8 (p = 0.003). The first-phase insulin response increased during the study period (0.19 ± 0.02 to 0.46 ± 0.07 nmol min−1 m−2; p < 0.001) and approached control values (0.62 ± 0.15 nmol min−1 m−2; p = 0.42). Maximal insulin response became supranormal at 8 weeks (1.37 ± 0.27 vs controls 1.15 ± 0.18 nmol min−1 m−2). Pancreatic triacylglycerol decreased from 8.0 ± 1.6% to 6.2 ± 1.1% (p = 0.03).Conclusions/interpretationNormalisation of both beta cell function and hepatic insulin sensitivity in type 2 diabetes was achieved by dietary energy restriction alone. This was associated with decreased pancreatic and liver triacylglycerol stores. The abnormalities underlying type 2 diabetes are reversible by reducing dietary energy intake.

(2011) 'Tracking of obesity-related behaviours from childhood to adulthood : a systematic review. ', Maturitas., 70 (3). pp. 266-284. Further information on publisher's website:http://dx.doi.org/10.1016/j.maturitas. 2011.08.005 Publisher's copyright statement: NOTICE: this is the author's version of a work that was accepted for publication in Maturitas. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reected in this document. Changes may have been made to this work since it was submitted for publication. A denitive version was subsequently published in Maturitas, 70/3, 2011Maturitas, 70/3, , 10.1016Maturitas, 70/3, /j.maturitas.2011 Additional information: Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-prot purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details. Key words: tracking; diet; physical activity; childhood obesity; adult obesity. ABSTRACTObesity in childhood carries a wide range of physical, psychological and social disbenefits and also increases the risk of adult obesity with its well-recognised, enhanced risk of several common complex diseases as well as adverse socioeconomic and psychosocial sequelae. Understanding the tracking of the two key modifiable behaviours, food consumption and physical activity, between childhood and adulthood may illuminate the childhood determinants of adult obesity and contribute to the development of effective interventions.We performed a systematic review of the available literature on tracking of both physical activity and of dietary intake between childhood and adulthood by searching MEDLINE, EMBASE, CINAHL, PSYCInfo, Google and Google Scholar. For inclusion, studies had to report baseline measurements when the children were less than, or equal to, 18 years and to report follow-up for at least 5 years to any age over 18 years.After removal of duplicates, 9625 search hits were screened by title and/or abstract and 79 potentially relevant papers were identified and full papers obtained. In total 39 papers were included in this analysis. Of these, 11 papers (from 5 studies) reported data on tracking of diet from childhood to adulthood and 28 papers (from 16 studies) reported data on tracking of physical activity or inactivity.Despite the diversity of study design and measurement methodology, we found evidence of tracking of both physical activity and of diet between childhood and adulthood with estimates of strength of tracking of a similar order for both behaviours. Because of the inherent methodological difficulties...

SummaryBackgroundObservational studies report reduced colorectal cancer in regular aspirin consumers. Randomised controlled trials have shown reduced risk of adenomas but none have employed prevention of colorectal cancer as a primary endpoint. The CAPP2 trial aimed to investigate the antineoplastic effects of aspirin and a resistant starch in carriers of Lynch syndrome, the major form of hereditary colorectal cancer; we now report long-term follow-up of participants randomly assigned to aspirin or placebo.MethodsIn the CAPP2 randomised trial, carriers of Lynch syndrome were randomly assigned in a two-by-two factorial design to 600 mg aspirin or aspirin placebo or 30 g resistant starch or starch placebo, for up to 4 years. Randomisation was in blocks of 16 with provision for optional single-agent randomisation and extended postintervention double-blind follow-up; participants and investigators were masked to treatment allocation. The primary endpoint was development of colorectal cancer. Analysis was by intention to treat and per protocol. This trial is registered, ISRCTN59521990.Results861 participants were randomly assigned to aspirin or aspirin placebo. At a mean follow-up of 55·7 months, 48 participants had developed 53 primary colorectal cancers (18 of 427 randomly assigned to aspirin, 30 of 434 to aspirin placebo). Intention-to-treat analysis of time to first colorectal cancer showed a hazard ratio (HR) of 0·63 (95% CI 0·35–1·13, p=0·12). Poisson regression taking account of multiple primary events gave an incidence rate ratio (IRR) of 0·56 (95% CI 0·32–0·99, p=0·05). For participants completing 2 years of intervention (258 aspirin, 250 aspirin placebo), per-protocol analysis yielded an HR of 0·41 (0·19–0·86, p=0·02) and an IRR of 0·37 (0·18–0·78, p=0·008). No data for adverse events were available postintervention; during the intervention, adverse events did not differ between aspirin and placebo groups.Interpretation600 mg aspirin per day for a mean of 25 months substantially reduced cancer incidence after 55·7 months in carriers of hereditary colorectal cancer. Further studies are needed to establish the optimum dose and duration of aspirin treatment.FundingEuropean Union; Cancer Research UK; Bayer Corporation; National Starch and Chemical Co; UK Medical Research Council; Newcastle Hospitals trustees; Cancer Council of Victoria Australia; THRIPP South Africa; The Finnish Cancer Foundation; SIAK Switzerland; Bayer Pharma.

In order to establish firm evidence for the health effects of dietary polyphenol consumption, it is essential to have quantitative information regarding their dietary intake. The usefulness of the current methods, which rely mainly on the assessment of polyphenol intake using food records and food composition tables, is limited as they fail to assess total intake accurately. This review highlights the problems associated with such methods with regard to polyphenol-intake predictions. We suggest that the development of biological biomarkers, measured in both blood and urine, are essential for making accurate estimates of polyphenol intake. However, the relationship between dietary intakes and nutritional biomarkers are often highly complex. This review identifies the criteria that must be considered in the development of such biomarkers. In addition, we provide an assessment of the limited number of potential biomarkers of polyphenol intake currently available. In the last decade, there has been intense interest in the potential health benefits of dietary-derived plant polyphenols. An everincreasing number of studies have described their antioxidant properties and linked this to their proposed role in the prevention of human disease. Plant polyphenols are abundant in the human diet, particularly in fruit, vegetables and pulses which have been consistently associated with a decreased risk of cancer 1 -3 , CVD 4 -6 and a range of other chronic disorders. The likely active components of fruits, vegetables and pulses are a group of phytochemicals, known as polyphenols. However, it has proved extremely difficult to quantitatively establish the benefit afforded by polyphenols for a number of reasons: (1) there is a great diversity of polyphenol content between foods; (2) there is limited data regarding the polyphenol content of specific foods within the commonly-used food composition databases; (3) there are challenges in characterising and quantifying habitual food intake; and (4) there is a limited understanding regarding the extent of absorption and metabolic fate of individual polyphenols from particular foods.Biological markers of nutrient exposure, as an alternative to the more traditional dietary assessment tools, have been used for many years. In this approach one or more biochemical moieties are measured in an accessible fluid or tissue to provide a semi-quantitative index of the exposure to individual food constituents. For polyphenols, this may appear to be an attractive approach. However, the relationship between dietary intake and resulting concentrations of biomarkers in body fluids is highly complex. Before a particular dietary component, or its metabolite, can be used as a sensitive and accurate biomarker of exposure to a specific polyphenol, a number of factors must be realised. Firstly, a full understanding of the metabolism of polyphenols in human subjects is required in order to select credible biomarkers. Secondly, it is important to understand the time -response relationship between polyphenol int...

Background and ObjectivesPhysical activity is associated with lower cardiovascular and all-cause mortality. However, the effects of different exercise modalities on arterial stiffness are currently unclear. Our objectives were to investigate the effects of exercise modalities (aerobic, resistance or combined) on pulse wave velocity (PWV) and augmentation index (AIx), and to determine whether the effects on these indices differed according to the participants' or exercise characteristics.MethodsWe searched the Medline, Embase and Cochrane Library databases from inception until April 2014 for randomized controlled trials lasting ≥4 weeks investigating the effects of exercise modalities on PWV and AIx in adults aged ≥18 years.ResultsForty-two studies (1627 participants) were included in this analysis. Aerobic exercise improved both PWV (WMD: −0.63 m/s, 95% CI: −0.90, −0.35) and AIx (WMD:−2.63%, 95% CI: −5.25 to −0.02) significantly. Aerobic exercise training showed significantly greater reduction in brachial-ankle (WMD: −1.01 m/s, 95% CI: −1.57, −0.44) than in carotid-femoral (WMD: -0.39 m/s, 95% CI: −0.52, −0.27) PWV. Higher aerobic exercise intensity was associated with larger reductions in AIx (β: −1.55%, CI −3.09, 0.0001). In addition, aerobic exercise had a significantly larger effect in reducing PWV (WMD:−1.0 m/s, 95% CI: −1.43, −0.57) in participants with stiffer arteries (PWV ≥8 m/s). Resistance exercise had no effect on PWV and AIx. There was no significant effect of combined exercise on PWV and AIx.ConclusionsWe conclude that aerobic exercise improved arterial stiffness significantly and that the effect was enhanced with higher aerobic exercise intensity and in participants with greater arterial stiffness at baseline.Trial Registration PROSPERODatabase registration: CRD42014009744,.