Editorial : which weight loss diet?

Full editorial: A recent study evaluating the long-term (2 yr) weight reducing efficacy of different types of diets – high or low in carbohydrates (CHOs), protein or fat - confirmed that it is calorie deficit not dietary composition that determines the loss and maintenance of body weight.1 Is there any advantage in following a specific weight loss diet? Short-term use of nutritionally complete commercially available (very) low calorie diets has benefited people with diabetes when  supported by education programmes.2 Initial weight loss has been encouraging with some fad diets eg the Atkins and the South Beach diets, but these diets are difficult to maintain and there are safety issues regarding their short- and long-term use – especially in people with diabetes.3 The types of macronutrients consumed can have a considerable impact on glycaemic control and energy metabolism. Although a low CHO diet additionally enhances initial weight loss by reducing cellular water content, if fat is not proportionally reduced the diet may not benefit the lipid profile for vascular disease risk. High fat and high protein diets – which are simultaneously low in CHOs – increase vulnerability to hypoglycaemia in people taking insulin secretagogues or on insulin therapy, and may promote excess fat metabolism and ketogenesis, particularly in people vulnerable to lack of insulin. Very low protein diets are not recommended as lean body mass tends to be reduced in diabetes. Altering the macronutrient balance has implications for the micronutrient mix: deficiencies are higher if more foods are excluded and conversely specific micronutrient excess can occur with some fad diets. The altered nutrient mix affects intestinal fauna and flora, and gut motility and glycaemic control are influenced by the quantity and type of fibre consumed. Support programmes help individuals achieve long term weight loss and there is mounting evidence that community schemes which educate and promote lifestyle changes may stem the rising tide of obesity and consequent type 2 diabetes.4 Consuming smaller portions of a balanced diet (and adjusting antidiabetic medications accordingly) will create an energy deficit to promote healthy weight loss. Increased movement/exercise will enhance this energy deficit. Knowledge (eg 1g fat has 2.25 times more energy than 1g CHO) allows sensible food choices and compensation for inclusion of small volumes of  ‘naughty but nice’ foods. Ultimately weight control requires self control. References 1. Sacks FM, Bray GA, Carey VJ et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med 2009;360:859–73. 2. Bennett P. Obesity, diabetes and VLCD. Br J Diabetes Vasc Dis 2004;4:328–30. 3. Baldwin EJ. Fad diets in diabetes. Br J Diabetes Vasc DIs 2004;4:333–7. 4. Romon M, Lommoz A, Tafflet M et al. Downward trends in the prevalence of childhood overweight in the setting of 12-year school- and community-based programmes. Public Health Nutr 2008; Dec 28, 1–8 [Epub ahead of print].

Treatment of lean and diet-induced obesity (DIO) mice with a novel stable obestatin analogue alters plasma metabolite levels as detected by untargeted LC–MS metabolomics

Introduction: Obestatin is a controversial gastrointestinal peptide purported to have metabolic actions.

Objectives: This study investigated whether treatment with a stable obestatin analogue (PEG-OB(Cys10, Cys13)) changed plasma metabolite levels firstly in lean and subsequently in diet-induced obesity (DIO) C57BL6/J mice.

Methods: Untargeted LC-HRMS metabolomics experiments were carried out in ESI + mode with plasma extracts from both groups of animals. Data were normalised, multivariate and univariate statistical analysis performed and metabolites of interest putatively identified.

Results: In lean mice, 39 metabolites were significantly changed by obestatin treatment and the majority of these were increased, including various C16 and C18 moieties of phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and monoacylglycerol, along with vitamin A, vitamin D3, tyrosine, acetylcarnitine and 2α-(hydroxymethyl)-5α-androstane-3β,17β-diol. Decreased concentrations of glycolithocholic acid, 3-dehydroteasterone and various phospholipids were observed. In DIO mice, 25 metabolites were significantly affected and strikingly, the magnitudes of changes here were generally much greater in DIO mice than in lean mice, and in contrast, the majority of metabolite changes were decreases. Four metabolites affected in both groups included glycolithocholic acid, and three different long-chain (C18) phospholipid molecules (phosphatidylethanolamine, platelet activating factor (PAF), and monoacylglycerol). Metabolites exclusively affected in DIO mice included various phosphatidylcholines, lysophosphatidylcholines and fatty acyls, as well as creatine and oxidised glutathione.

Conclusion: This investigation demonstrates that obestatin treatment affects phospholipid turnover and influences lipid homeostasis, whilst providing convincing evidence that obestatin may be acting to ameliorate diet-induced impairments in lipid metabolism, and it may influence steroid, bile acid, PAF and glutathione metabolism.

A Palatable Hyperlipidic Diet Causes Obesity and Affects Brain Glucose Metabolism in Rats

Background We have previously shown that either the continuous intake of a palatable hyperlipidic diet (H) or the alternation of chow (C) and an H diet (CH regimen) induced obesity in rats. Here, we investigated whether the time of the start and duration of these feeding regimens are relevant and whether they affect brain glucose metabolism. Methods Male Wistar rats received C, H, or CH diets during various periods of their life spans: days 30-60, days 30-90, or days 60-90. Experiments were performed the 60th or the 90th day of life. Rats were killed by decapitation. The glucose, insulin, leptin plasma concentration, and lipid content of the carcasses were determined. The brain was sliced and incubated with or without insulin for the analysis of glucose uptake, oxidation, and the conversion of [1-14C]-glucose to lipids. Results The relative carcass lipid content increased in all of the H and CH groups, and the H30-60 and H30-90 groups had the highest levels. Groups H30-60, H30-90, CH30-60, and CH30-90 exhibited a higher serum glucose level. Serum leptin increased in all H groups and in the CH60-90 and CH30-90 groups. Serum insulin was elevated in the H30-60, H60-90, CH60-90, CH30-90 groups. Basal brain glucose consumption and hypothalamic insulin receptor density were lower only in the CH30-60 group. The rate of brain lipogenesis was increased in the H30-90 and CH30-90 groups. Conclusion These findings indicate that both H and CH diet regimens increased body adiposity independent treatment and the age at which treatment was started, whereas these diets caused hyperglycemia and affected brain metabolism when started at an early age.

Exercise and Lifestyle Therapy Improves Weight Maintenance in Young People With Psychosis: A Service Evaluation

INTRODUCTION Young people with psychosis typically have higher rates of premature cardiovascular disease and metabolic disorders compared to non-psychotic peers. This has been primarily due to a sedentary lifestyle, poor diet composition, misuse of harmful substances and higher rates of obesity and smoking. When prescribed obesogenic antipsychotic medication, a weight gain of >12 kg within 2 years is typical. PURPOSE: To examine the benefits of a 12 wk exercise and lifestyle intervention entitled ‘Supporting Health and Promoting Exercise’ (SHAPE) for young people recently diagnosed with psychosis. METHODS Participants (n=26; 8 females; mean age 27.7 ± 5.1) engaged in weekly 45’ education sessions on healthy lifestyle behaviors, including: managing anxiety and depression, mindfulness and relaxation training, substance misuse, smoking cessation, healthy eating and nutritional advice, dental and sexual health care. This was followed by a 45’ exercise session including activities such as circuit and resistance training, yoga, and badminton, led by qualified exercise instructors. Anthropometric data were measured at baseline, 12 wk and 12 month post-intervention. Lifestyle behaviors and clinical measurements, including resting heart rate, blood pressure, total cholesterol, triglycerides, HbA1c and prolactin, were assessed at baseline and 12 months post-intervention as part of their routine clinical care plan. Significant differences over time were assessed using Paired Sample t-tests. RESULTS SHAPE participants (n=26) presented with first episode psychosis (n=11), schizophrenia (n=11), bipolar disorder (n=2), at risk mental state (n=1), and persistent delusion disorder (n=1) of which 52% were prescribed highly obesogenic antipsychotic medications (Clozapine and Olanzepine). Mean baseline data suggests participants were at an increased health risk due to elevated values in mean BMI (70% were overweight or obese), waist circumference, resting heart rate, and triglycerides (see Table 1 & 2). Over 50% reported smoking daily and 85% had elevated resting blood pressure (>120/80 mm Hg). At 12 wk post-intervention, no changes were observed in mean BMI or waist circumference (see Table 1); 19 participants either maintained (mean 0.5 kg: range ± 2 kg) or decreased (mean -5.7 kg: range 2-7 kg) weight; 7 participants increased weight (mean 4.9 kg: range 2.0-9.6 kg). At 12 month post-intervention (n=16), no change was evident in mean BMI, waist circumference, or any other clinical variable (see Table 2). Positive impacts on lifestyle behaviors included 7 participants eating ~400g of fruit/vegetables daily, 2 ceased substance use, 2 ceased alcohol use, 4 ceased smoking and 5 were less sedentary. CONCLUSION At the start of the programme, participants were already at an increased risk for cardiometabolic disorders. Findings suggest that SHAPE supported young people with psychosis to: -attenuate their physical health risk following a 12 wk exercise and lifestyle intervention which were sustained at 12 months follow up. -make positive lifestyle behavior changes leading to sustained improvements in weight maintenance and physical health.

A systematic review of environmental correlates of obesity-related dietary behaviors in youth

There is increasing interest in the role the environment plays in shaping the dietary behavior of youth, particularly in the context of obesity prevention. An overview of environmental factors associated with obesity-related dietary behaviors among youth is needed to inform the development of interventions. A systematic review of observational studies on environmental correlates of energy, fat, fruit/ vegetable, snack/fast food and soft drink intakes in children (4–12 years) and adolescents (13–18 years) was conducted. The results were summarized using the analysis grid for environments linked to obesity. The 58 papers reviewed mostly focused on sociocultural and economical–environmental factors at the household level. The most consistent associations were found between parental intake and children’s fat, fruit/vegetable intakes, parent and sibling intake with adolescent’s energy and fat intakes and parental education with adolescent’s fruit/ vegetable intake. A less consistent but positive association was found for availability and accessibility on children’s fruit/vegetable intake. Environmental factors are predominantly studied at the household level and focus on sociocultural and economic aspects. Most consistent associations were found for parental influences (parental intake and education).More studies examining environmental factors using longitudinal study designs and validated measures are needed for solid evidence to inform interventions.

Trends in demographic, health behaviour factors, and self-perceived weight status : influences on obesity in Australia from 1995 to 2005

Overweight and obesity are two of the most important emerging public health issues in our time and regarded by the World Health Organisation [WHO] (1998) as a worldwide epidemic. The prevalence of obesity in the USA is the highest in the world, and Australian obesity rates fall into second place. Currently, about 60% of Australian adults are overweight (BMI „d 25kg/m2). The socio-demographic factors associated with overweight and/or obesity have been well demonstrated, but many of the existing studies only examined these relationships at one point of time, and did not examine whether significant relationships changed over time. Furthermore, only limited previous research has examined the issue of the relationship between perception of weight status and actual weight status, as well as factors that may impact on people¡¦s perception of their body weight status. Aims: The aims of the proposed research are to analyse the discrepancy between perceptions of weight status and actual weight status in Australian adults; to examine if there are trends in perceptions of weight status in adults between 1995 to 2004/5; and to propose a range of health promotion strategies and furth er research that may be useful in managing physical activity, healthy diet, and weight reduction. Hypotheses: Four alternate hypotheses are examined by the research: (1) there are associations between independent variables (e.g. socio -demographic factors, physical activity and dietary habits) and overweight and/or obesity; (2) there are associations between the same independent variables and the perception of overweight; (3) there are associations between the same independent variables and the discrepancy between weight status and perception of weight status; and (4) there are trends in overweight and/or obesity, perception of overweight, and the discrepancy in Australian adults from 1995 to 2004/5. Conceptual Framework and Methods: A conceptual framework is developed that shows the associations identified among socio -demographic factors, physical activity and dietary habits with actual weight status, as well as examining perception of weight status. The three latest National Health Survey data bases (1995 , 2001 and 2004/5) were used as the primary data sources. A total of 74,114 Australian adults aged 20 years and over were recruited from these databases. Descriptive statistics, bivariate analyses (One -Way ANOVA tests, unpaired t-tests and Pearson chi-square tests), and multinomial logistic regression modelling were used to analyse the data. Findings: This research reveals that gender, main language spoken at home, occupation status, household structure, private health insurance status, and exercise are related to the discrepancy between actual weight status and perception of weight status, but only gender and exercise are related to the discrepancy across the three time point s. The current research provides more knowledge about perception of weight status independently. Factors which affect perception of overweight are gender, age, language spoken at home, private health insurance status, and diet ary habits. The study also finds that many factors that impact overweight and/or obesity also have an effect on perception of overweight, such as age, language spoken at home, household structure, and exercise. However, some factors (i.e. private health insurance status and milk consumption) only impact on perception of overweight. Furthermore, factors that are rel ated to people’s overweight are not totally related to people’s underestimation of their body weight status in the study results. Thus, there are unknown factors which can affect people’s underestimation of their body weight status. Conclusions: Health promotion and education activities should provide education about population health education and promotion and education for particular at risk sub -groups. Further research should take the form of a longitudinal study design ed to examine the causal relationship between overweight and/or obesity and underestimation of body weight status, it should also place more attention on the relationships between overweight and/or obesity and dietary habits, with a more comprehensive representation of SES. Moreover, further research that deals with identification of characteristics about perception of weight status, in particular the underestimation of body weight status should be undertaken.

Interactions between energy intake and expenditure in the development and treatment of obesity.

Summary There are four interactions to consider between energy intake (EI) and energy expenditure (EE) in the development and treatment of obesity. (1) Does sedentariness alter levels of EI or subsequent EE? and (2) Do high levels of EI alter physical activity or exercise? (3) Do exercise-induced increases in EE drive EI upwards and undermine dietary approaches to weight management and (4) Do low levels of EI elevate or decrease EE? There is little evidence that sedentariness alters levels of EI. This lack of cross-talk between altered EE and EI appears to promote a positive EB. Lifestyle studies also suggest that a sedentary routine actually offers the opportunity for over-consumption. Substantive changes in non exercise activity thermogenesis are feasible, but not clearly demonstrated. Cross talk between elevated EE and EI is initially too weak and takes too long to activate, to seriously threaten dietary approaches to weight management. It appears that substantial fat loss is possible before intake begins to track a sustained elevation of EE. There is more evidence that low levels of EI does lower physical activity levels, in relatively lean men under conditions of acute or prolonged semi-starvation and in dieting obese subjects. During altered EB there are a number of small but significant changes in the components of EE, including (i) sleeping and basal metabolic rate, (ii) energy cost of weight change alters as weight is gained or lost, (iii) exercise efficiency, (iv) energy cost of weight bearing activities, (v) during substantive overfeeding diet composition (fat versus carbohydrate) will influence the energy cost of nutrient storage by ~ 15%. The responses (i-v) above are all “obligatory” responses. Altered EB can also stimulate facultative behavioural responses, as a consequence of cross-talk between EI and EE. Altered EB will lead to changes in the mode duration and intensity of physical activities. Feeding behaviour can also change. The degree of inter-individual variability in these responses will define the scope within which various mechanisms of EB compensation can operate. The relative importance of “obligatory” versus facultative, behavioural responses -as components of EB control- need to be defined.

Molecular markers of obesity and diabetes

Recently it has been shown that the consumption of a diet high in saturated fat is associated with impaired insulin sensitivity and increased incidence of type 2 diabetes. In contrast, diets that are high in monounsaturated fatty acids (MUFAs) or polyunsaturated fatty acids (PUFAs), especially very long chain n-3 fatty acids (FAs), are protective against disease. However, the molecular mechanisms by which saturated FAs induce the insulin resistance and hyperglycaemia associated with metabolic syndrome and type 2 diabetes are not clearly defined. It is possible that saturated FAs may act through alternative mechanisms compared to MUFA and PUFA to regulate of hepatic gene expression and metabolism. It is proposed that, like MUFA and PUFA, saturated FAs regulate the transcription of target genes. To test this hypothesis, hepatic gene expression analysis was undertaken in a human hepatoma cell line, Huh-7, after exposure to the saturated FA, palmitate. These experiments showed that palmitate is an effective regulator of gene expression for a wide variety of genes. A total of 162 genes were differentially expressed in response to palmitate. These changes not only affected the expression of genes related to nutrient transport and metabolism, they also extend to other cellular functions including, cytoskeletal architecture, cell growth, protein synthesis and oxidative stress response. In addition, this thesis has shown that palmitate exposure altered the expression patterns of several genes that have previously been identified in the literature as markers of risk of disease development, including CVD, hypertension, obesity and type 2 diabetes. The altered gene expression patterns associated with an increased risk of disease include apolipoprotein-B100 (apo-B100), apo-CIII, plasminogen activator inhibitor 1, insulin-like growth factor-I and insulin-like growth factor binding protein 3. This thesis reports the first observation that palmitate directly signals in cultured human hepatocytes to regulate expression of genes involved in energy metabolism as well as other important genes. Prolonged exposure to long-chain saturated FAs reduces glucose phosphorylation and glycogen synthesis in the liver. Decreased glucose metabolism leads to elevated rates of lipolysis, resulting in increased release of free FAs. Free FAs have a negative effect on insulin action on the liver, which in turn results in increased gluconeogenesis and systemic dyslipidaemia. It has been postulated that disruption of glucose transport and insulin secretion by prolonged excessive FA availability might be a non-genetic factor that has contributed to the staggering rise in prevalence of type 2 diabetes. As glucokinase (GK) is a key regulatory enzyme of hepatic glucose metabolism, changes in its activity may alter flux through the glycolytic and de novo lipogenic pathways and result in hyperglycaemia and ultimately insulin resistance. This thesis investigated the effects of saturated FA on the promoter activity of the glycolytic enzyme, GK, and various transcription factors that may influence the regulation of GK gene expression. These experiments have shown that the saturated FA, palmitate, is capable of decreasing GK promoter activity. In addition, quantitative real-time PCR has shown that palmitate incubation may also regulate GK gene expression through a known FA sensitive transcription factor, sterol regulatory element binding protein-1c (SREBP-1c), which upregulates GK transcription. To parallel the investigations into the mechanisms of FA molecular signalling, further studies of the effect of FAs on metabolic pathway flux were performed. Although certain FAs reduce SREBP-1c transcription in vitro, it is unclear whether this will result in decreased GK activity in vivo where positive effectors of SREBP-1c such as insulin are also present. Under these conditions, it is uncertain if the inhibitory effects of FAs would be overcome by insulin. The effects of a combination of FAs, insulin and glucose on glucose phosphorylation and metabolism in cultured primary rat hepatocytes at concentrations that mimic those in the portal circulation after a meal was examined. It was found that total GK activity was unaffected by an increased concentration of insulin, but palmitate and eicosapentaenoic acid significantly lowered total GK activity in the presence of insulin. Despite the fact that total GK enzyme activity was reduced in response to FA incubation, GK enzyme translocation from the inactive, nuclear bound, to active, cytoplasmic state was unaffected. Interestingly, none of the FAs tested inhibited glucose phosphorylation or the rate of glycolysis when insulin is present. These results suggest that in the presence of insulin the levels of the active, unbound cytoplasmic GK are sufficient to buffer a slight decrease in GK enzyme activity and decreased promoter activity caused by FA exposure. Although a high fat diet has been associated with impaired hepatic glucose metabolism, there is no evidence from this thesis that FAs themselves directly modulate flux through the glycolytic pathway in isolated primary hepatocytes when insulin is also present. Therefore, although FA affected expression of a wide range of genes, including GK, this did not affect glycolytic flux in the presence of insulin. However, it may be possible that a saturated FA-induced decrease in GK enzyme activity when combined with the onset of insulin resistance may promote the dys-regulation of glucose homeostasis and the subsequent development of hyperglycaemia, metabolic syndrome and type 2 diabetes.

The Eat Smart Study : a randomised controlled trial of a reduced carbohydrate versus a low fat diet for weight loss in obese adolescents

Background Despite the recognition of obesity in young people as a key health issue, there is limited evidence to inform health professionals regarding the most appropriate treatment options. The Eat Smart study aims to contribute to the knowledge base of effective dietary strategies for the clinical management of the obese adolescent and examine the cardiometablic effects of a reduced carbohydrate diet versus a low fat diet. Methods and design Eat Smart is a randomised controlled trial and aims to recruit 100 adolescents over a 2½ year period. Families will be invited to participate following referral by their health professional who has recommended weight management. Participants will be overweight as defined by a body mass index (BMI) greater than the 90th percentile, using CDC 2000 growth charts. An accredited 6-week psychological life skills program ‘FRIENDS for Life’, which is designed to provide behaviour change and coping skills will be undertaken prior to volunteers being randomised to group. The intervention arms include a structured reduced carbohydrate or a structured low fat dietary program based on an individualised energy prescription. The intervention will involve a series of dietetic appointments over 24 weeks. The control group will commence the dietary program of their choice after a 12 week period. Outcome measures will be assessed at baseline, week 12 and week 24. The primary outcome measure will be change in BMI z-score. A range of secondary outcome measures including body composition, lipid fractions, inflammatory markers, social and psychological measures will be measured. Discussion The chronic and difficult nature of treating the obese adolescent is increasingly recognised by clinicians and has highlighted the need for research aimed at providing effective intervention strategies, particularly for use in the tertiary setting. A structured reduced carbohydrate approach may provide a dietary pattern that some families will find more sustainable and effective than the conventional low fat dietary approach currently advocated. This study aims to investigate the acceptability and effectiveness of a structured reduced dietary carbohydrate intervention and will compare the outcomes of this approach with a structured low fat eating plan. Trial Registration: The protocol for this study is registered with the International Clinical Trials Registry (ISRCTN49438757).

Children’s food and activity patterns following a six-month child weight management program

Objective To describe the impact of a parent-led, family focused child weight management program on the food intake and activity patterns of pre-pubertal children. Methods n assessor-blinded, randomized controlled trial involving 111 (64% female) overweight, pre-pubertal children 6 to 9 years of age randomly assigned to parenting-skills training plus intensive lifestyle education, parenting-skills training alone, or a 12-month wait-listed control. Study outcomes were assessed at baseline, 6 months, and 12 months. This paper presents data on food intake assessed via a validated 54-item parent completed dietary questionnaire and activity behaviours assessed via a parent-report 20-item activity questionnaire. Results Intake of energy-dense nutrient poor foods was lower in both intervention groups at 6 months (mean difference, P+DA -1.5 serves [CI -2.0;-1.0]; P -1.0 serves [-2.0;-0.5]) and 12 months (mean difference P+DA -1.0 serves [CI -2.0;-0.5]; P -1.0 serves [-1.5; 0.0]) compared to baseline. Intake of vegetables, fruit, breads and cereals, meat and alternatives and dairy foods remained unchanged. Regardless of study group there were significant reductions over time in the reported time spent engaged in small screen activities and an increase in the time reported spent in active play. Conclusion Child weight management intervention that promotes food intake in line with national dietary guidelines achieves a reduction in children’s intake of energy dense, nutrient poor foods. This was achieved without compromising intake of nutrient-rich food and changes in were maintained even once the intervention ceased.

A systematic review of studies on socioeconomic inequalities in dietary intakes associated with weight gain and overweight/obesity conducted among European adults

This Review examined socioeconomic inequalities in intakes of dietary factors associated with weight gain, overweight/obesity among adults in Europe. Literature searches of studies published between 1990 and 2007 examining socioeconomic position (SEP) and the consumption of energy, fat, fibre, fruit, vegetables, energy-rich drinks and meal patterns were conducted. Forty-seven articles met the inclusion criteria. The direction of associations between SEP and energy intakes were inconsistent. Approximately half the associations examined between SEP and fat intakes showed higher total fat intakes among socioeconomically disadvantaged groups. There was some evidence that these groups consume a diet lower in fibre. The most consistent evidence of dietary inequalities was for fruit and vegetable consumption; lower socioeconomic groups were less likely to consume fruit and vegetables. Differences in energy, fat and fibre intakes (when found) were small-to-moderate in magnitude; however, differences were moderate-to-large for fruit and vegetable intakes. Socioeconomic inequalities in the consumption of energy-rich drinks and meal patterns were relatively under-studied compared with other dietary factors. There were no regional or gender differences in the direction and magnitude of the inequalities in the dietary factors examined. The findings suggest that dietary behaviours may contribute to socioeconomic inequalities in overweight/obesity in Europe. However, there is only consistent evidence that fruit and vegetables may make an important contribution to inequalities in weight status across European regions.

Cognitive behavior therapy and dialectical behavior therapy for treating obese emotional eaters

This study describes the treatment of obese individuals who rated high on emotional eating using four case studies that involved 22 sessions of either cognitive behavioral therapy (CBT) or dialectical behavioral therapy (DBT). Outcomes measures relating to weight, body mass index, emotional eating, depression, anxiety, and stress were all assessed with each participant prior to each baseline (three weekly sessions), during treatment and posttherapy. At the 8-week follow-up, the two cases that had received DBT had lost 10.1% and 7.6% of their initial body weight, whereas the two cases that had received CBT had lost 0.7% and 0.6% of their initial body weight. The two DBT cases also exhibited reductions in emotional distress, frequency of emotional eating or quantity of food eating in response to emotions, whereas the two CBT cases showed no overall reductions in these areas. Important processes from all four cases are described as are the implications to clinicians for developing more effective interventions for obese clients who engage in emotional eating.

Does metabolic compensation explain the majority of less-than-expected weight loss in obese adults during a short-term severe diet and exercise intervention?

Objective: We investigated to what extent changes in metabolic rate and composition of weight loss explained the less-than-expected weight loss in obese men and women during a diet-plus-exercise intervention. Design: 16 obese men and women (41 ± 9 years; BMI 39 ± 6 kg/m2) were investigated in energy balance before, after and twice during a 12-week VLED (565–650 kcal/day) plus exercise (aerobic plus resistance training) intervention. The relative energy deficit (EDef) from baseline requirements was severe (74-87%). Body composition was measured by deuterium dilution and DXA and resting metabolic rate (RMR) by indirect calorimetry. Fat mass (FM) and fat-free mass (FFM) were converted into energy equivalents using constants: 9.45 kcal/gFM and 1.13 kcal/gFFM. Predicted weight loss was calculated from the energy deficit using the '7700 kcal/kg rule'. Results: Changes in weight (-18.6 ± 5.0 kg), FM (-15.5 ± 4.3 kg), and FFM (-3.1 ± 1.9 kg) did not differ between genders. Measured weight loss was on average 67% of the predicted value, but ranged from 39 to 94%. Relative EDef was correlated with the decrease in RMR (R=0.70, P<0.01) and the decrease in RMR correlated with the difference between actual and expected weight loss (R=0.51, P<0.01). Changes in metabolic rate explained on average 67% of the less-than-expected weight loss, and variability in the proportion of weight lost as FM accounted for a further 5%. On average, after adjustment for changes in metabolic rate and body composition of weight lost, actual weight loss reached 90% of predicted values. Conclusion: Although weight loss was 33% lower than predicted at baseline from standard energy equivalents, the majority of this differential was explained by physiological variables. While lower-than-expected weight loss is often attributed to incomplete adherence to prescribed interventions, the influence of baseline calculation errors and metabolic down-regulation should not be discounted.

Drugs for diabetes and obesity

14.1 Drugs for diabetes 14.1.1 Diabetes mellitus 14.1.2 Physiology of the pancreas 14.1.3 Insulin replacement therapy 14.1.4 Metformin 14.1.5 Acarbose 14.1.6 Sulfonylureas 14.1.7 Glitazones 14.1.8 Glucagon-like peptide-1, exenatide and sitagliptin 14.2 Drugs for obesity 14.2.1 Introduction 14.2.2 Amphetamine 14.2.3 Phentermine 14.2.5 Orlistat