Sally D. Poppitt

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 24 h. Ad libitum food intake was covertly measured throughout the study and a reported food intake completed at the end of 24 h.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.

Short-term effects of macronutrient preloads on appetite and energy intake in lean women

This study investigated the relative satiating hierarchy of the four energy-providing macronutrients (fat, carbohydrate (CHO), protein, and alcohol) in lean women. On four separate occasions, the composition of an iso-energetic lunch preload was manipulated in 12 lean (BMI < 25 kg/m2) women. The four treatments comprised a 1-MJ baseline meal and drink (40% fat, 48% CHO, 12% protein) to which was covertly added: 1) + 1MJ protein; 2) + 1MJ alcohol; 3) + 1MJ CHO; and 4) + 1MJ fat. Prior to and at 30-min intervals, subjects completed 100-mm visual analogue scales rating subjective hunger and satiety. Ninety min following the preload, an ad lib. lunch meal was given (40% fat, 48% CHO, and 12% protein) and energy intake (EI) measured. Energy intake at the lunch meal was 2195 (880, SD) kJ, 2772 (1191, SD) kJ, 2502 (681, SD), kJ and 2558 (1050, SD) kJ for the protein, alcohol, CHO, and fat preloads, respectively. There was no significant difference between the pleasantness of the preloads (p > 0.05). Macronutrient composition had a significant effect on short-term hunger (F = 3.19; p < 0.05), subjects being less hungry after the protein preload. Subjects also had a lower energy intake after the protein preload (F = 3.11; p < 0.05). We conclude that only protein has a differential short-term satiating effect when incorporated iso-energetically and at a similar energy density into the diet.

Relationships of low serum vitamin D3 with anthropometry and markers of the metabolic syndrome and diabetes in overweight and obesity

Low serum 25 hydroxyvitamin D3 (vitamin D3) is known to perturb cellular function in many tissues, including the endocrine pancreas, which are involved in obesity and type II diabetes mellitus (TIIDM). Vitamin D3 insufficiency has been linked to obesity, whether obesity is assessed by body mass index (BMI) or waist circumference (waist). Central obesity, using waist as the surrogate, is associated with the metabolic syndrome (MetSyn), insulin resistance, TIIDM and atherosclerotic cardiovascular disease (CVD). We tested how vitamin D3 was related to measures of fat mass, MetSyn markers, haemoglobin A1c (HbA1c) and MetSyn in a cross-sectional sample of 250 overweight and obese adults of different ethnicities. There were modest inverse associations of vitamin D3 with body weight (weight) (r = -0.21, p = 0.0009), BMI (r = -0.18, p = 0.005), waist (r = -0.14, p = 0.03), [but not body fat % (r = -0.08, p = 0.24)], and HbA1c (r = -0.16, p = 0.01). Multivariable regression carried out separately for BMI and waist showed a decrease of 0.74 nmol/L (p = 0.002) in vitamin D3 per 1 kg/m2 increase in BMI and a decrease of 0.29 nmol/L (p = 0.01) per 1 cm increase in waist, with each explaining approximately 3% of the variation in vitamin D3 over and above gender, age, ethnicity and season.The similar relationships of BMI and waist with vitamin D3 may have been due to associations between BMI and waist, or coincidental, where different mechanisms relating hypovitaminosis D3 to obesity occur concurrently. Previously reviewed mechanisms include that 1) low vitamin D3, may impair insulin action, glucose metabolism and various other metabolic processes in adipose and lean tissue 2) fat soluble-vitamin D3 is sequestered in the large adipose compartment, and low in serum, 3) obese people may be sensitive about their body shape, minimising their skin exposure to view and sunlight (not tested). We showed evidence for the first theory but no evidence to support the second.In the current study, serum vitamin D3 was inversely related to weight, BMI and markers of TIIDM (large waist, raised HbA1c) but not to adipose mass nor to MetSyn per se.

Food intake and the menstrual cycle: A retrospective analysis, with implications for appetite research

The biological regulation of appetite is currently an important topic in nutrition, since hyperphagia has been implicated as the prime cause of obesity. Cyclical fluctuations in food intake occur in women across the menstrual cycle, with a periovulatory nadir and a peak in the luteal phase. These alterations in food intake, in response to ovarian steroid hormone changes may be more than 2.5 MJ/day, with the mean reported changes shown in 19 separate studies of 1.0 MJ/day. Hormonal induced fluctuations in food intake could, therefore, contribute to energy imbalance and consequent weight gain. Further, in nutrition studies involving women subjects where the menstrual cycle phase is not controlled, hormonally induced changes in food selection and intake may mask the often considerably smaller changes in response to experimental variables in appetite research.

Regeneration of the Heart in Diabetes by Selective Copper Chelation

Heart disease is the major cause of death in diabetes, a disorder characterized by chronic hyperglycemia and cardiovascular complications. Although altered systemic regulation of transition metals in diabetes has been the subject of previous investigation, it is not known whether changed transition metal metabolism results in heart disease in common forms of diabetes and whether metal chelation can reverse the condition. We found that administration of the Cu-selective transition metal chelator trientine to rats with streptozotocin-induced diabetes caused increased urinary Cu excretion compared with matched controls. A Cu(II)-trientine complex was demonstrated in the urine of treated rats. In diabetic animals with established heart failure, we show here for the first time that 7 weeks of oral trientine therapy significantly alleviated heart failure without lowering blood glucose, substantially improved cardiomyocyte structure, and reversed elevations in left ventricular collagen and beta(1) integrin. Oral trientine treatment also caused elevated Cu excretion in humans with type 2 diabetes, in whom 6 months of treatment caused elevated left ventricular mass to decline significantly toward normal. These data implicate accumulation of elevated loosely bound Cu in the mechanism of cardiac damage in diabetes and support the use of selective Cu chelation in the treatment of this condition.

Milk protein for improved metabolic health: a review of the evidence

Epidemiological evidence shows that consumption of dairy products is associated with decreased prevalence of metabolic related disorders, whilst evidence from experimental studies points towards dairy protein as a dietary component which may aid prevention of type 2 diabetes (T2DM). Poor metabolic health is a common characteristic of overweight, obesity and aging, and is the forerunner of T2DM and cardiovascular disease (CVD), and an ever increasing global health issue. Progressive loss of metabolic control is evident from a blunting of carbohydrate, fat and protein metabolism, which is commonly manifested through decreased insulin sensitivity, inadequate glucose and lipid control, accompanied by a pro-inflammatory environment and hypertension. Adverse physiological changes such as excess visceral adipose tissue deposition and expansion, lipid overspill and infiltration into liver, muscle and other organs, and sarcopaenia or degenerative loss of skeletal muscle mass and function all underpin this adverse profile. ‘Sarcobesity’ and sarcopaenic diabetes are rapidly growing health issues. As well as through direct mechanisms, dairy protein may indirectly improve metabolic health by aiding loss of body weight and fat mass through enhanced satiety, whilst promoting skeletal muscle growth and function through anabolic effects of dairy protein-derived branch chain amino acids (BCAAs). BCAAs enhance muscle protein synthesis, lean body mass and skeletal muscle metabolic function. The composition and processing of dairy protein has an impact on digestion, absorption, BCAA kinetics and function, hence the optimisation of dairy protein composition through selection and combination of specific protein components in milk may provide a way to maximize benefits for metabolic health.

Postprandial response of adiponectin, interleukin-6, tumor necrosis factor-α, and C-reactive protein to a high-fat dietary load

OBJECTIVE Circulating levels of adiponectin are low in obesity and metabolic disorders associated with increasing fat mass including insulin resistance and dyslipidemia. Body fat stores may be positively related to intake of dietary fat, but little is known of mechanisms by which serum adiponectin may be regulated through diet. We investigated acute effects of a high-fat load and changes in fatty acid saturation on circulating adiponectin and associated mediators of inflammation including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP). METHODS A high-fat test meal (59 +/- 4 g fat; 71% of energy as fat) containing a high ( approximately 71:29) or low ( approximately 55:45) ratio of saturated:unsaturated fatty acids was given at breakfast on two occasions. Blood samples were collected at 0 (baseline), 1, 3, and 6 h for measurement of adiponectin, IL-6, TNF-alpha, and high-sensitivity CRP. A fat-exclusion lunch, snack, and dinner were also given and blood samples collected at 10 and 24 h. RESULTS Eighteen healthy, lean men completed the trial. There was no evidence of acute change in circulating adiponectin in response to the lipid bolus or a differential effect of fatty acid saturation on adiponectin, high-sensitivity CRP, or IL-6 (P > 0.05). IL-6 increased over 6 h on both treatments (time, P < 0.05). TNF-alpha decreased on the high saturated:unsaturated fatty acid treatment (treatment by time, P < 0.05). There were no significant correlations between circulating adiponectin and insulin on either dietary treatment in these normoglycemic subjects. CONCLUSION Acute changes in the content of saturated and unsaturated fatty acids had no adverse effect on postprandial circulation of the adipose-related factors adiponectin, IL-6, TNF-alpha, or high-sensitivity CRP.

The effect of the dietary supplement, Chitosan, on body weight: a randomised controlled trial in 250 overweight and obese adults.

CONTEXT: Chitosan, a deacetylated chitin, is a widely available dietary supplement purported to decrease body weight and serum lipids through gastrointestinal fat binding. Although evaluated in a number of trials, its efficacy remains in dispute.OBJECTIVE: To evaluate the efficacy of chitosan for weight loss in overweight and obese adults.DESIGN AND SETTING: A 24-week randomised, double-blind, placebo-controlled trial, conducted at the University of Auckland between November 2001 and December 2002.PARTICIPANTS: A total of 250 participants (82% women; mean (s.d.) body mass index, 35.5 (5.1) kg/m2; mean age, 48 (12) y)INTERVENTIONS: Participants were randomly assigned to receive 3 g chitosan/day (n=125) or placebo (n=125). All participants received standardised dietary and lifestyle advice for weight loss. Adherence was monitored by capsule counts.MAIN OUTCOME MEASURES: The primary outcome measure was change in body weight. Secondary outcomes included changes in body mass index, waist circumference, body fat percentage, blood pressure, serum lipids, plasma glucose, fat-soluble vitamins, faecal fat, and health-related quality of life.RESULTS: In an intention-to-treat analysis with the last observation carried forward, the chitosan group lost more body weight than the placebo group (mean (s.e.), −0.4 (0.2) kg (0.4% loss) vs +0.2 (0.2) kg (0.2% gain), P=0.03) during the 24-week intervention, but effects were small. Similar small changes occurred in circulating total and LDL cholesterol, and glucose (P<0.01). There were no significant differences between groups for any of the other measured outcomes.CONCLUSION: In this 24-week trial, chitosan treatment did not result in a clinically significant loss of body weight compared with placebo.

Lipid-lowering effects of a modified butter-fat: a controlled intervention trial in healthy men

Objective: To investigate the lipid-lowering potential of a butter-fat modified through manipulations in bovine feeding to increase the unsaturated:saturated fatty acid ratio.Design: Double-blind, randomised, cross-over intervention trial.Setting: University of Auckland Human Nutrition Unit, New Zealand.Subjects: Twenty healthy, male subjects.Intervention: A residential trial in which all foods and beverages were provided during two intervention periods, comprising 3 weeks of high unsaturated ‘modified’ vs 3 weeks of saturated ‘control’ butter feeding separated by a 4 week washout. Diets were of typical composition of 39 percentage energy (en%) fat (20 en% butter-fat), 48 en% CHO, 13 en% protein.Results: There was a significant decrease in both total (P<0.05, −7.9%) and LDL-cholesterol (P<0.01, −9.5%) during modified butter feeding. There was no significant effect of treatment on a range of other risk factors including HDL-cholesterol, triglyceride, apolipoprotein A or B, nonesterified fatty acids (NEFA), haemostatic clotting factor VII and fibrinogen or glucose (P>0.05). Subjects were maintained in energy balance and there was no significant change in body weight during intervention. Butter-fat composition alone differed between treatments.Conclusions: A significant improvement in cardiovascular risk can be achieved by moderate changes in dietary fatty acid profile, achieved through a common and well accepted food source, butter-fat.Sponsorship: New Zealand Dairy Board, Wellington; Auckland Uniservices Ltd, Auckland; Maurice & Phyllis Paykel Trust, Auckland, New Zealand.

Energy-sparing strategies to protect human fetal growth

OBJECTIVES Our purpose was to test whether energy-sensitive adjustments in gestational metabolism, previously observed in studies of Gambian and British women, are a general phenomenon and to define the nutritional factors that direct them. STUDY DESIGN Retrospective analysis of data on basal metabolic rate and fat deposition in 360 pregnancies from 10 studies in a wide range of nutritional settings was performed. RESULTS The energy costs of pregnancy varied widely between different communities: maintenance costs from -45 to +210 MJ, fat deposition from -23 to +267 MJ, and total energy costs from -20 to +523 MJ. Total costs were correlated with prepregnancy fatness (r = 0.80, p < 0.01) and pregnancy weight gain (r = 0.94, p < 0.001). Marginally nourished women conserved energy by suppressing metabolic rate and by gaining little fat. CONCLUSIONS The energy needs of pregnancy are modulated over a wide range in response to maternal energy status. This may be an important means of protecting fetal growth.