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Biomedical subjects

A M Prentice

Publications and source records attributed to A M Prentice.

At least 55 records · Page 3Linked to original sources
PubMed1998

Assessment of selective under-reporting of food intake by both obese and non-obese women in a metabolic facility.

OBJECTIVE: To investigate the degree of bias in under-reporting of food intake in obese and non-obese subjects, hypothesising that under-reporting may be selective for either macronutrient content (carbohydrate (CHO), fat, protein, alcohol), specific food types or eating occasions (meals, snacks). DESIGN: Thirty-three women (18 obese, 15 non-obese) were recruited to a long-stay metabolic facility for 24h. Ad libitum food intake was covertly measured throughout the study and a reported food intake completed at the end of 24h. RESULTS: Reported total daily energy intake was significantly lower than measured intake. Whilst meals were accurately reported, energy from snack foods eaten between meals was significantly under-reported. (P< 0.001) Reported total carbohydrate and added sugar intakes were significantly lower than measured, whilst reported protein and fat intakes were not significantly different from measured. Reported alcohol intake was also considerably lower than measured, but high variability prevented significance. CONCLUSIONS: In both obese and non-obese women the major cause of under-reporting, as assessed by covert study design in subjects restricted within a metabolic facility, is the failure to report between-meal snack foods. There is some evidence for increased under-reporting in high CHO, but no evidence of a bias in under-reporting towards high fat or high protein foods.

Adult↗
PubMed1998

Leptin: physiology and pathophysiology.

The identification and sequencing of the ob gene and its product, leptin, in late 1994 opened new insights in the study of the mechanisms controlling body weight and led to a surge of research activity. During this time, a considerable body of knowledge regarding leptin's actions has been accumulated and the field continues to expand rapidly. Currently there is particular interest in the interaction of leptin with other peripheral and neural mechanisms to regulate body weight, reproduction and immunological response. In this review, we attempt to place the current state of knowledge about leptin in the broader perspective of physiology, including its structural characteristics, receptors, binding proteins, signalling pathways, regulation of adipose tissue expression and production, secretion patterns, clearance mechanisms and functional effects. In addition, leptin's involvement in the pathophysiology of obesity, anorexia nervosa, diabetes mellitus, polycystic ovary syndrome, acquired immunodeficiency syndrome, cancer, nephropathy, thyroid disease, Cushing's syndrome and growth hormone deficiency will be reviewed.

Animals↗
PubMed1998

Manipulation of dietary fat and energy density and subsequent effects on substrate flux and food intake.

Dietary fat has traditionally been viewed as being particularly lipogenic because of its high energy density, metabolic efficiency, and palatability. If these attributes of dietary fat were counteracted by a high satiating power, or if the body made autoregulatory adjustments in fat utilization in response to high fat intakes, energy balance would not necessarily be displaced. However, recent experiments have shown that neither of these hold true: human and animal trials consistently show that covert manipulation of dietary fat can induce hyperphagia, which can readily lead to spontaneous fat storage of 50-100 g/d in humans. Experiments with isoenergy-dense diets show that this high-fat hyperphagia (with diets of similar palatability) is caused by the high energy density of fatty foods rather than by their other attributes. Hyperphagia has therefore been termed passive overconsumption because it occurs unintentionally and without the consumption of excess bulk. When palatability is allowed to vary normally, high-fat foods may additionally induce active overconsumption in response to the enhanced organoleptic qualities of fats. In terms of substrate flux, fat is at the bottom of an oxidative hierarchy that determines fuel selection. Whereas alcohol, carbohydrates, and protein elicit powerful autoregulatory adjustments in their oxidation in response to changes in intake, fat fails to elicit such a response and fat balance is therefore easily displaced. These physiologic observations provide mechanistic support for secular-trend, cross-cultural, and cross-sectional epidemiologic studies investigating the role of energy-dense diets in the etiology of obesity.

Diet↗
PubMed1998

Effect of dietary manipulation on substrate flux and energy balance in obese women taking the appetite suppressant dexfenfluramine.

BACKGROUND: Studies in lean men show poor regulation of energy (EB) and fat balance (FB) during manipulation of dietary ratios of fat to carbohydrate. High-fat (HF), high-energy diets cause hyperphagia and a positive EB and FB. OBJECTIVE: The protocol was designed to measure substrate flux and EB in obese women taking dexfenfluramine (DF) or placebo (PL) during an HF (50% of energy) or low-fat (25% of energy; LF) diet. We hypothesized that alterations in dietary fat would not be regulated and would lead to a positive EB and FB. DESIGN: The study was double-blind, randomized, and placebo-controlled, with 4 treatments (LF/DF, HF/DF, LF/PL, and HF/PL) and a crossover. Five days of continuous, whole-body calorimetry measurements were made in 6 subjects after 8 d of home DF/PL treatment. Macronutrient balance and EB were measured within the chamber as the cumulative difference between ad libitum intake and oxidation. RESULTS: The HF diet increased energy (HF, 10.50 MJ/d; LF, 8.13 MJ/d; P < 0.0001) and fat intakes (HF, 5.34 MJ/d; LF, 2.06 MJ/d; P < 0.0001), leading to a positive EB (delta = 2.37 MJ/d) and FB (delta = 2.31 MJ/d). DF reduced energy (DF, 8.96 MJ/d; PL, 9.66 MJ/d; P < 0.01) and macronutrient intakes, but did not increase energy expenditure (delta = -0.31 MJ/d; P < 0.01), or 24-h fat oxidation (delta = 0.03 MJ/d; P = 0.46). CONCLUSIONS: EB and FB are poorly regulated with HF, energy-dense diets in obese women, which leads to fat deposition and weight gain.

Appetite Depressants↗
PubMed1998

Dietary compensation in response to covert imposition of negative energy balance by removal of fat or carbohydrate.

Compensatory changes in energy intake (EI) and macronutrient metabolism in response to modest covert underfeeding were tested by whole-body calorimetry in eight lean men. Each was studied on three occasions comprising a controlled stabilization day followed by manipulation and outcome days in a whole-body calorimeter. On the manipulation day EI was fixed, and calculated to maintain energy balance (CONTROL) or to provide 85% of CONTROL BY removing energy as carbohydrate (CHOred) or as fat (FATred). On the outcome day, ad libitum EI was allowed at fixed mealtimes. CHOred and FATred manipulations generated significantly different energy balances (-1.10 (SE 0.13) MJ, P = 0.000; -1.10 (SE 0.12) MJ, P = 0.000) and fat balances (-0.61 (SE 0.23) MJ, P = 0.03; -1.09 (SE 0.20) MJ, P = 0.000), but not carbohydrate balances (-0.39 (SE 0.22) MJ, NS; 0.11 (SE 0.23) MJ, NS) by the end of the manipulation day compared with CONTROL. On the outcome day, EI was significantly higher than CONTROL after CHOred (+1.58 (SE 0.33) MJ, P = 0.004) and FATred (+1.21 (SE 0.49) MJ, P = 0.022) with no differences between treatments. Overall 48 h energy balances averaged close to zero at -0.14, +0.34, +0.04 MJ on CONTROL, CHOred and FATred respectively. Total 48 h energy intakes on CHOred and FATred averaged 101 (SE 1.7)% and 99 (SE 2.5)% of CONTROL, thus demonstrating accurate detection of a mild energy deficit and efficient next-day compensation. Despite significant differences in macronutrient oxidation rates, the energy homeostatic mechanism appeared to be independent of specific macronutrient deficits.

Adult↗
PubMed1997

Effects on birth weight and perinatal mortality of maternal dietary supplements in rural Gambia: 5 year randomised controlled trial .

OBJECTIVE: To test the efficacy in terms of birth weight and infant survival of a diet supplement programme in pregnant African women through a primary healthcare system. DESIGN: 5 year controlled trial of all pregnant women in 28 villages randomised to daily supplementation with high energy groundnut biscuits (4.3 MJ/day) for about 20 weeks before delivery (intervention) or after delivery (control). SETTING: Rural Gambia. SUBJECTS: Chronically undernourished women (twin bearers excluded), yielding 2047 singleton live births and 35 stillbirths. MAIN OUTCOME MEASURES: Birth weight; prevalence of low birth weight (< 2500 g); head circumference; birth length; gestational age; prevalence of stillbirths; neonatal and postneonatal mortality. RESULTS: Supplementation increased weight gain in pregnancy and significantly increased birth weight, particularly during the nutritionally debilitating hungry season (June to October). Weight gain increased by 201 g (P < 0.001) in the hungry season, by 94 g (P < 0.01) in the harvest season (November to May), and by 136 g (P < 0.001) over the whole year. The odds ratio for low birthweight babies in supplemented women was 0.61 (95% confidence interval 0.47 to 0.79, P < 0.001). Head circumference was significantly increased (P < 0.01), but by only 3.1 mm. Birth length and duration of gestation were not affected. Supplementation significantly reduced perinatal mortality: the odds ratio was 0.47 (0.23 to 0.99, P < 0.05) for stillbirths and 0.54 (0.35 to 0.85, P < 0.01) for all deaths in first week of life. Mortality after 7 days was unaffected. CONCLUSION: Prenatal dietary supplementation reduced retardation in intrauterine growth when effectively targeted at genuinely at-risk mothers. This was associated with a substantial reduction in the prevalence of stillbirths and in early neonatal mortality. The intervention can be successfully delivered through a primary healthcare system.

Birth Weight↗
PubMed1997

Carbohydrates and energy balance.

In the early 1970s carbohydrates (CHOs) were believed to induce overconsumption and excess fat deposition. They are now perceived to protect against these consequences. This paper evaluates the evidence for this change of interpretation by considering (1) the energy content of CHOs, (2) the energetic efficiency with which they are handled by the body, and (3) their effects on appetite, relative to other macronutrients. CHOs are the least energy-dense macronutrients (delta Hc) and exhibit the greatest variability in digestibility. Doubling the usual levels of nonstarch polysaccharides (fiber) may decrease digestibility of a Western diet by 5%. De novo lipogenesis from dietary CHO is energetically inefficient but very limited on Western diets, which are relatively high in fat. There appears to be a hierarchy (protein > CHO > fat) in the extent to which the stores of the macronutrients are autoregulated by oxidation. Excess CHO intake tends to promote storage (but not de novo synthesis) of fat. The thermogenic effects of CHO are therefore relatively limited on Western diets. Per MJ of energy ingested, macronutrients differentially affect satiety (protein > CHO > fat) under conditions where fat is disproportionately energy dense. Isoenergetically dense loads of fat and CHO exert less pronounced differences on satiety. Under some conditions HC diets promote excess energy intakes. There is little evidence that a CHO-rich diet, or one with intense sweeteners, promotes spontaneous weight loss.

Dietary Carbohydrates↗
PubMed1997

Meal frequency and energy balance.

Several epidemiological studies have observed an inverse relationship between people's habitual frequency of eating and body weight, leading to the suggestion that a 'nibbling' meal pattern may help in the avoidance of obesity. A review of all pertinent studies shows that, although many fail to find any significant relationship, the relationship is consistently inverse in those that do observe a relationship. However, this finding is highly vulnerable to the probable confounding effects of post hoc changes in dietary patterns as a consequence of weight gain and to dietary under-reporting which undoubtedly invalidates some of the studies. We conclude that the epidemiological evidence is at best very weak, and almost certainly represents an artefact. A detailed review of the possible mechanistic explanations for a metabolic advantage of nibbling meal patterns failed to reveal significant benefits in respect of energy expenditure. Although some short-term studies suggest that the thermic effect of feeding is higher when an isoenergetic test load is divided into multiple small meals, other studies refute this, and most are neutral. More importantly, studies using whole-body calorimetry and doubly-labelled water to assess total 24 h energy expenditure find no difference between nibbling and gorging. Finally, with the exception of a single study, there is no evidence that weight loss on hypoenergetic regimens is altered by meal frequency. We conclude that any effects of meal pattern on the regulation of body weight are likely to be mediated through effects on the food intake side of the energy balance equation.

Adolescent↗
PubMed1997

Feasibility of heart-rate monitoring to estimate total level and pattern of energy expenditure in a population-based epidemiological study: the Ely Young Cohort Feasibility Study 1994-5.

Increasing the precision of measurements of total energy expenditure in population-based epidemiological studies is important for accurately quantifying the relationship between this exposure and disease. Current questionnaire-based methods cannot accurately quantify total energy expenditure, although they may provide an estimate of the frequency of vigorous activities. Heart rate monitoring with individual calibration has been advocated as a method for assessing energy expenditure in field studies and has been compared with the 'gold standard' techniques of doubly-labelled water and indirect calorimetry. However the method has previously only been used on small and selected populations. This study was, therefore, established to test the feasibility of using heart rate monitoring in a population-based study of adults. A total of 167 individuals aged 30-40 years were randomly selected and underwent 4 d heart-rate monitoring. Only three individuals could not complete the protocol. The mean physical activity level (PAL) measured over 4 d was 1.89 (SD 0.40) in men and 1.76 (sd 0.31) in women. There was no difference between mean PAL on weekend days compared with weekdays (mean paired difference 0.0008, 95% CI -0.06 +0.06). The estimate of mean PAL was not correlated with BMI, percentage body fat or the waist:hip ratio. It was, however, correlated with cardio-respiratory fitness as measured by VO2(max) per kg (Spearman rank correlation coefficient 0.50 in men and 0.42 in women). The pattern of energy expenditure was assessed by calculating the percentage of daytime hours in which PAL was greater than five times basal energy expenditure. This measure was strongly correlated with the mean PAL in both men (Spearman correlation coefficient 0.77) and women (0.71). We conclude that heart-rate monitoring is a feasible method for assessing the pattern and total level of energy expenditure in medium-sized epidemiological studies. It may also prove useful as the reference technique for calibrating questionnaires to estimate energy expenditure in larger scale studies.

Adult↗
PubMed1996

Energy density and its role in the control of food intake: evidence from metabolic and community studies.

This review discusses the role that dietary composition and energy density play in the control of eating behaviour. The effect of dietary manipulations of fat and carbohydrate on energy intake remains controversial. We suggest this to be largely a consequence of different study designs. When low-fat foods are included in the diet and thus only some items manipulated subsequent food choice commonly ensures compensation and energy intake remains constant. However, when all items are manipulated and macronutrient composition fixed, an alteration in the energy density results in a parallel change in energy intake and there is no energy compensation. In addition, we hypothesise that hyperphagia on high-fat diets is a consequence of a high energy density rather than fat content per se. Independent of fat content, low energy dense diets generate greater satiety than high energy dense diets, suggesting that an important regulatory signal may be the weight or volume of food consumed. Epidemiological studies confirm that energy intake increases with energy density and thus weight loss may be best achieved on a low energy dense diet. Although the use of low-fat items may not reduce intake during covert manipulation, it may be successful during periods of deliberate dieting, providing that food-substitutions are not counter-balanced by other high density items.

Dietary Carbohydrates↗
PubMed1996

Short-term effects of alcohol consumption on appetite and energy intake.

The relationship between alcohol intake and obesity remains uncertain. Evidence suggesting that alcohol-derived energy may be unregulated points to an inability to maintain appetite, energy balance and, hence, body weight when alcohol is introduced to the diet. This study investigated the short-term effects of alcohol on hunger and energy intake in 20 lean women. On 4 occasions, subjects were given a randomised preload drink ('alcohol', 'no alcohol', 'carbohydrate', 'water') followed by visual analogue scales (VAS) rating hunger and an ad lib test meal. There was no difference in hunger ratings (p > 0.05) nor in the amount of energy consumed during the test meal (F = 1.66, p > 0.05) following any of the 4 preloads. Consumption of the 2 high energy preload drinks ('alcohol', 0.91 MJ; 'CHO', 0.72 MJ) did not result in a compensatory decrease in the amount of energy subsequently eaten (ad lib intake: 'alcohol' = 2.62 MJ, 0.32 SEM; 'no alcohol' = 2.98 MJ, 0.28 SEM; 'CHO' = 2.93 MJ, 0.21 SEM; 'water' = 2.82 MJ, 0.25 SEM), suggesting either no physiological recognition or no regulation of energy consumed within a drink in quantities of less than 1 MJ. The addition of either alcoholic or CHO-containing carbonated beverages into the diet will result, in the short-term, to an overall increase in energy intake.

Adult↗
PubMed1996

Dietary supplementation and rapid catch-up growth after acute diarrhoea in childhood.

Diarrhoea is a major cause of short-term growth faltering in children of the developing world. If catch-up weight gain is delayed by inadequate dietary intake, or by further bouts of diarrhoea, progressive growth failure occurs. To test the hypothesis that early refeeding is as effective as later feeding after acute diarrhoea with weight loss, we measured the effects of a timed dietary intervention on weight gain after acute diarrhoea in underweight Gambian children. Thirty-four children aged 4-22 months with weight loss following acute diarrhoea were given a high-energy-protein supplement for 14 d beginning either immediately after rehydration or a fortnight later. With a 50% increase in energy intake and a 100% increase in protein intake there was a rapid and highly significant (P < 0.001) gain in weight within a fortnight whether the supplement was given immediately or 2 weeks after presentation. Rates of weight increase were similar whether supplementation was provided early or late, but over the full 28 d (of intervention and non-intervention) children who received late supplementation had greater overall weight gain (P < 0.02) than those supplemented early. Vigorous and early feeding with a high-energy-protein supplement should be central to the management of malnourished children with acute diarrhoea in developing countries, and may be as important as control of diarrhoea in preventing malnutrition and growth failure. This may be achieved in the community using locally available foods, in the face of continuing diarrhoea.

Acute Disease↗
PubMed1996

Alcohol and the regulation of energy balance: overnight effects on diet-induced thermogenesis and fuel storage.

The effect of alcohol on overnight energy expenditure and substrate disposal was studied in eleven subjects (five men, six women) using whole-body indirect calorimetry for 15.5 h after test meals. Three test meals were studied in random order with at least 48 h between treatments: control, 50% of maintenance energy needs provided as 14, 40 and 46% energy from protein, fat and carbohydrate respectively; alcohol addition, control plus 23% energy as alcohol; alcohol substitution, control with alcohol replacing 23% of carbohydrate energy. ANOVA revealed no significant sex effects. Alcohol-induced thermogenesis dissipated only 15 (SD 14)% of the alcohol energy. Alcohol addition had no significant effect on protein or carbohydrate oxidation but fat oxidation was suppressed (P < 0.0005) to an extent equivalent to storing 74 (SD 51)% of the alcohol energy as fat. Alcohol substitution reduced carbohydrate oxidation (P < 0.009) to an equivalent of 42 (SD 41)% and also spared fat (P < 0.005) to an equivalent of 59 (SD 37)% of the alcohol energy. It is concluded that alcohol has no special thermogenic capacity, and that its energy can be accounted for in a similar way to carbohydrate.

Adult↗
PubMed1996

Changes in macronutrient balance during over- and underfeeding assessed by 12-d continuous whole-body calorimetry.

Alterations in energy balance must be accommodated by adjustments in the net storage of the major energy-yielding macronutrients: carbohydrate, protein, and fat. This study used continuous whole-body calorimetry to measure changes in energy expenditure and substrate oxidation during a 12-d imposed energy imbalance in six lean men on mixed diets (overfeeding: 16.5 MJ/d, +33%, n = 3; underfeeding: 3.5 MJ/d, -67%, n = 3). Changes in total energy expenditure (TEE) and its components were modest; TEE changed by +6.2% (overfeeding) and -10.5% (underfeeding). In consequence, body weight changed by +2.90 and -3.18 kg. Marked changes in metabolic fuel selection occurred over the course of the study. Carbohydrate intake (540 and 83 g/d for overfeeding and underfeeding, respectively) exerted direct autoregulatory feedback on carbohydrate oxidation (551 and 106 g/d at day 12 for overfeeding and underfeeding, respectively). Subjects were close to balance by day 5. Changes in protein oxidation were small and not sufficient to prevent the oxidation of body protein mass, or its accretion, in response to energy deficit or surplus. Fat oxidation (59 and 177 g/d for overfeeding and underfeeding, respectively) was not sensitive to dietary fat intake (150 and 20 g/d, for overfeeding and underfeeding, respectively), rather, its oxidation was inversely related to the oxidation of other substrates. Changes in fat balance accounted for 74.1% and 84.0% of the energy imbalance during overfeeding and underfeeding, respectively. This study shows a clear oxidative hierarchy for the macronutrients. Metabolic fuel selection is dominated by the need to maintain carbohydrate balance. This induces inappropriate counterregulatory alterations in fat oxidation during energy surplus.

Adult↗