94 research outputs found

    Satiety. No way to slim

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    The issue: satiety as a slimming claim Vigorous attempts are being made to obtain regulatory approval for products claiming to help reduction of weight by satiating appetite for food. There are increasing numbers of reviews, books and grants on satiety as an aid to slimming. 1 Yet, on scientific principle, such a general implication can never be true. Definitions and measurements of satiety are beside the point. Two widely neglected facts are fundamental to the control of body weight. The first is that average rates, not cumulative amounts, of energy intake and expenditure determine how much weight is lost or gained. This is the physics of fatness, an inescapable fact of the thermodynamics of energy balance. The second fact is that any alteration in those rates of energy exchange produces a change in weight that comes to an asymptote while the altered rate of energy intake and/or expenditure persists. As the fat content of the body changes, lean mass changes in the same direction and hence also the rate of use of energy to keep those tissues working It follows that any dietary way to slim must lower the rate of intake of energy for the weeks needed for a step reduction in body fat content. In addition, that way of losing weight must be maintained (or replaced by an equally effective means) in order to avoid regaining the initial fatness. Less food eaten or greater fullness rated over a test period does not in itself slow the daily rate of intake of energy. Even repeated observation of an acute suppression of intake does nothing to show a smaller total amount of energy intake over the period of the study. Feeling fuller after every meal is no guarantee of lower daily energy intake. It follows that no augmentation of satiety by a medically prescribed or commercially marketed material can be relied on by itself to reduce obesity or to prevent overweight for the years required to reduce the risks to health. The science of support to effective weight-controlling food choices Weight-controlling satiety therefore is not an effect of any sort of medication, food group or food product. Rather, satiety that slims is eating less often in ways that fatten by raising the average daily rate of intake of energy. That is, a 'slimming satiety' is an habitual pattern of eating and drinking that reduces weight when its frequency increases and is maintained throughout life at that new frequenc

    The role of working memory sub-components in food choice and dieting success

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    Evidence suggests a role for self-reported working memory (WM) in self-reported food intake, but it is not known which WM sub-components are involved. It is also important to consider how individual differences in dietary restraint and disinhibition influence WM and the impact of this on food choice. The current study assessed the relationship between WM sub-components and food choice, using computerised measures of WM sub-components and a direct assessment of food intake. The role of dieting success (measured by restraint and disinhibition) as a distal predictor of food choice that influences food choices via WM, and the role of WM more generally in dieting success were investigated. Female undergraduate students (N = 117, mean age: 18.9 years, mean BMI: 21.6 kg/m2) completed computer tasks assessing three components of WM (updating, phonological loop and visuospatial sketchpad) and a snack food taste-test. Greater visuospatial WM span was associated with a higher (lower) percentage of food intake that was low (high) energy dense. It was also found that unsuccessful dieters (high restraint, high disinhibition) had poorer visuospatial WM span and consumed a lower (higher) percentage of low (high) energy dense food. Visuospatial WM span significantly mediated the relationship between dieting success and percentage of low energy dense food intake. Further, dietary restraint was associated with poorer updating ability, irrespective of disinhibition. These findings suggest that better visuospatial WM is associated with a greater (reduced) preference for low (high) energy dense foods, and that deficits in visuospatial WM may undermine dieting attempts. Future work should assess whether the ability to deal with food cravings mediates the relationship between visuospatial WM and dieting success and investigate how WM may influence the mechanisms underlying behavioural control

    Microstructural abnormalities in white and gray matter in obese adolescents with and without type 2 diabetes

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    Aims/hypotheses In adults, type 2 diabetes and obesity have been associated with structural brain changes, even in the absence of dementia. Some evidence suggested similar changes in adolescents with type 2 diabetes but comparisons with a non-obese control group have been lacking. The aim of the current study was to examine differences in microstructure of gray and white matter between adolescents with type 2 diabetes, obese adolescents and healthy weight adolescents. Methods Magnetic resonance imaging data were collected from 15 adolescents with type 2 diabetes, 21 obese adolescents and 22 healthy weight controls. Volumetric differences in the gray matter between the three groups were examined using voxel based morphology, while tract based spatial statistics was used to examine differences in the microstructure of the white matter. Results Adolescents with type 2 diabetes and obese adolescents had reduced gray matter volume in the right hippocampus, left putamen and caudate, bilateral amygdala and left thalamus compared to healthy weight controls. Type 2 diabetes was also associated with significant regional changes in fractional anisotropy within the corpus callosum, fornix, left inferior fronto-occipital fasciculus, left uncinate, left internal and external capsule. Fractional anisotropy reductions within these tracts were explained by increased radial diffusivity, which may suggest demyelination of white matter tracts. Mean diffusivity and axial diffusivity did not differ between the groups. Conclusion/interpretation Our data shows that adolescent obesity alone results in reduced gray matter volume and that adolescent type 2 diabetes is associated with both white and gray matter abnormalities

    Validation of the Turkish Version of the Problem Areas in Diabetes Scale

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    The Problem Areas in Diabetes (PAID) scale is a widely used self-report measure that can facilitate detection of diabetes-specific emotional distress in clinical practice. The aim of this study was to assess the factor structure and validity of the Turkish version of the PAID. A validation study was conducted among 154 patients with insulin-naïve type 2 diabetes. Participants completed the PAID, Centre for Epidemiological Studies Depression Scale (CES-D), Insulin Treatment Appraisal Scale (ITAS), and World Health Organization-Five Well-Being Index (WHO-5) questionnaires. Exploratory factor analyses yielded a 2-factor structure, identifying a 15-item “diabetes distress” factor and a 5-item “support-related issues” factor. The total PAID-score and the two dimensions were associated with higher levels of depression and poor emotional well-being. In the present study, the Turkish version of the PAID had satisfactory psychometric properties, however, the factorial structure was found to differ from factor solutions from other countries

    The mediating role of comorbid conditions in the association between type 2 diabetes and cognition: a cross-sectional observational study using the UK Biobank cohort

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    Aims: Using the UK Biobank cohort, a large sample of middle aged and older adults in the UK, the present study aimed to examine the cross-sectional association between type 2 diabetes and cognition and to assess the hypothesised mediating role of common comorbid conditions, whilst controlling for important demographic and lifestyle factors. Methods: Using regression models and general structural equation models, we examined the cross-sectional association between type 2 diabetes status and: fluid intelligence; reaction time; visual memory; digit span and prospective memory; and the hypothesised mediating role of common comorbid conditions: visceral obesity; sleep problems; macrovascular problems; respiratory problems,; cancer and depressive symptoms in 47,468 participants from the UK Biobank cohort, of whom 1,831 have type 2 diabetes. We controlled for ethnicity, sex, age, deprivation, smoking status, alcohol consumption, physical activity levels and use of diabetes medication. Results: Participants with type 2 diabetes had a significantly shorter digit span, b = -0.14, 99.2% CIs [-0.27, -0.11] than those without type 2 diabetes. Those with type 2 diabetes did not differ from those without type 2 diabetes on fluid intelligence, reaction time, visual memory and prospective memory. The associations that do exist between type 2 diabetes and cognition are consistently mediated via macrovascular problems, depressive symptoms, and to a lesser extent visceral obesity. Respiratory problems, sleep disturbances and cancer did not mediate the association between type 2 diabetes status and measures of cognition. Conclusions: Comorbid conditions explain some of the observed association between type 2 diabetes and cognitive deficits. This suggests that prevention, management or treatment of these comorbid conditions may be important to reduce the likelihood of cognitive decline. Treatment studies with long follow-ups are needed to examine this. Tweet: Comorbid conditions explain the association between type 2 diabetes and cognitive deficits. Prevention, management or treatment of these comorbid conditions may prevent or delay the onset of cognitive decline in people with type 2 diabetes

    Does working memory training improve dietary self-care in type 2 diabetes mellitus? Results of a double blind randomised controlled trial

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    Aims: Controlling food intake despite adequate knowledge remains a struggle for many people with type 2 diabetes. The present study investigated whether working memory training can reduce food intake and improve glycaemic control. It also examined training effects on cognition, food cravings, and dietary self-efficacy and self-care. Methods: In a double-blind multicentre parallel-group randomised controlled trial, adults with type 2 diabetes mellitus were randomly allocated to receive 25 sessions of either active (n = 45) or control (n = 36) working memory training. Assessments at baseline, post-training and 3-month follow-up measured cognition, food intake (primary outcomes), glycaemic control (HbA1c) and cholesterol (secondary outcomes). Semi-structured interviews assessed participants’ experiences of the training. Results: Intention-to-treat ANOVAs (N = 81) showed improved non-trained updating ability in active compared to control training from pre-test (active M = 34.37, control M = 32.79) to post-test (active M = 31.35, control M = 33.53) and follow-up (active M = 31.81, control M = 32.65; g2 = 0.05). There were no overall effects of training on other measures of cognition, food intake, HbA1c, cholesterol, food cravings and dietary self-efficacy and self-care. In post-hoc analyses, those high in dietary restraint in the active training group showed a greater reduction in fat intake pre to post-test compared to controls. Interviews revealed issues around acceptability and performance of the training. Conclusions: Transfer of working memory training effects to non-trained behaviour were limited, but do suggest that training may reduce fat intake in those who are already motivated to do so. Trial registration: Current Controlled Trials ISRCTN22806944
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