An "ecological" approach to the obesity pandemic.
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Biomedical subjects
Publications and source records attributed to B Swinburn.
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The prevalence of non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) is increasing worldwide. Although recent studies suggest that primary prevention of NIDDM is possible, strategies for controlling the NIDDM pandemic remain under development. Successful interventions to date have mainly relied upon the control of obesity and increased exercise, although pharmacological agents are being studied. While a mixture of both high risk and population-based approaches is likely to be required, the former will not prevent new high risk cases developing. Unfortunately, the success in the primary prevention of cardiovascular disease through risk factor reduction has not controlled obesity, the most important risk factor for NIDDM. New strategies are currently being developed and focus upon changes in the food supply of whole populations and a community development approach to altering attitudes to food and exercise. As these interventions are in the early stages of their development, formative, process, and quantitative evaluation remain essential components of any community-based programme aimed at the primary prevention of NIDDM.
OBJECTIVE: To estimate the costs of health care that are attributable to obesity in New Zealand. METHODS: The 1991 health care costs of non-insulin dependent diabetes, coronary heart disease, hypertension, gallstone disease, post-menopausal breast cancer and colon cancer were estimated and multiplied by the population attributable factor for obesity for each condition. The relative risk estimates were taken from the literature, the obesity prevalence from a 1990 New Zealand survey, and the costs and volumes of services were taken from a variety of sources and covered hospital (inpatient and outpatient) services, general practitioner consultations, pharmaceuticals, laboratory tests and ambulance services. Calculations were conservative and net of goods and services tax. RESULTS: A conservative estimate of the health care costs attributable to obesity for the six conditions was NZ$135 million. This represents about 2.5% of total health care costs which is similar to analyses from other countries. CONCLUSIONS: The health care costs of obesity as estimated are considerable. However, the total cost of overfatness to the New Zealand population is far greater than this because lesser degrees of overfatness, the health care costs of other obesity-related conditions such as arthritis, the costs to individuals of weight-loss programs and the indirect and intangible costs were not included in the analysis. A substantial and wide-ranging public health effort is needed to turn around the increasing prevalence and costs of obesity.
The reproducibility and validity of a self-administered 142-item food-frequency questionnaire (FFQ) was assessed in a population comprising 124 European and 52 Polynesian (17 Maori and 35 Pacific Island) New Zealanders aged 40-65 years. Reproducibility correlation coefficients, determined by administration of the same questionnaire on two occasions 3 years apart, were higher in European than Maori and Pacific Island participants, ranging from 0.47 to 0.87 in Europeans (median 0.66) and from 0.41 to 0.79 in Maori and Pacific Island people (median 0.44). In general, there were no significant differences in mean nutrient intakes calculated from the two FFQs by Europeans or Maori and Pacific Island participants despite their cultural and language differences. When the FFQ was compared with a 3-day food diary in a subsample of 101 Europeans, 15 Maori and 22 Pacific Islanders, the validity was good for most nutrients, with overestimation of a few nutrients in each ethnic group. Correlation coefficients between the 3-day food diary and FFQ ranged from 0.41 to 0.81 in Europeans (median 0.48) and from 0.36 to 0.56 in Maori and Pacific Island people (median 0.55). Ratios of energy intake to resting metabolic rate suggested that Maori and Pacific Island people were more likely to underestimate their habitual energy intake by the 3-day diet diary method compared to Europeans, but that Europeans were more likely to underestimate total energy intake by the food frequency method and Pacific Island participants to overestimate it. Obese Europeans and Maori were more likely to under-report dietary intakes by the 3-day diary method. We conclude that our FFQ performed better in European than Maori and Pacific Island participants.
AIMS: To describe recent trends in body mass in Auckland, and to determine whether associated changes in cigarette smoking and physical activity could explain these trends. METHODS: Risk factors for coronary heart disease were measured in three age-stratified random samples of Europeans aged 35-64 years using a standard protocol in 1982, 1986-8 and 1993-4. Body mass index (BMI) was calculated as weight in kg/(height in m2), with overweight or obese being defined as BMI>25. Results. The age-standardised mean BMI increased from 26.6 (25.4-25.8) to 26.4 (26.2-26.7) in men and from 24.6 (24.2-24.9) to 25.1 (24.8-25.5) in women between 1982 and 1993-4. The prevalence of overweight and obese people increased from 52.8% (48.1-57.7) to 64.2% (58.1-70.3) in men and from 36.5% (31.5-41.5) to 44.9% (39.7-50.1) in women. Self reported cigarette smoking declined between 1982 and 1993-94 with an associated increase in the prevalence of ex-smokers. The change in smoking status accounted for only 7% and 10% of the observed increase in BMI in men and women respectively. Most of the observed change in BMI was due to a general increase in BMI in all smoking categories in both sexes. The prevalence o leisure time physical activity increased in both sexes between 1986-88 and 1993-94 while work physical activity decreased. The change in physical activity should have decreased mean BMI by approximately 4% in men and 14% in women. As with smoking there was a trend towards increasing mean BMI irrespective of the activity undertaken. CONCLUSION: Recent trends in smoking cessation explain only a small percentage of the increase in body mass while the trends in physical activity would have predicted a small decrease in the prevalence of obesity, contrary to the observed trends. By exclusion, an increase in total energy intake, is the most likely explanation for the observed trends.
AIMS: This study compares recent coronary heart disease morbidity and mortality rates and ten year trends for Maori, Pacific Islands people and Europeans living in New Zealand. METHODS: Fatal coronary heart disease rates (mortality) and nonfatal hospitalisation rates for myocardial infarctions (morbidity) from 1983-92 were assessed and compared for males and females in each ethnic group, aged 35 to 64 years, using data from the Auckland Region Coronary or Stroke Study (ARCOS), a community-based coronary heart disease surveillance programme. RESULTS: The recent 1990-2 mean coronary heart disease mortality rate for Maori men (232/100 000) was almost double the rate for Pacific Islands men (135/100 000 p=0.008) and more than double the rate for European men (103/100 000 p=0.001). Maori women had a three-fold higher mean mortality rate (85/100 000) than European women (25/100 000 p=0.02). The morality rate for Pacific Islands women (42/100 000) was midway between the other ethnic groups. Over the decade 1983-92 coronary heart disease mortality rates have decreased significantly by approximately 5% per year for European men and women. Rates for Maori and Pacific Islands people also appear to have fallen although the precision of these estimates are low. Morbidity rates in 1990-2 were similar among men in all three ethnic groups. Among women, morbidity was approximately half the male rates and there were no clear differences between the ethnic groups. Between 1983 and 1992 morbidity rates declined significantly for European men (p=0.008) and women (p=0.02) by approximately 5% per year. Among Maori and Pacific Islands people the trends were variable. CONCLUSION: Maori men and women continue to experience more than double the coronary heart disease mortality rates than Europeans. Mortality rates for Pacific Islands people are intermediate between Maori and European. Both coronary heart disease mortality and morbidity rates are declining in Europeans; there appears to have been a decline in coronary heart disease mortality for Maori and Pacific Islands groups but not in morbidity rates which may have increased. Given the trend towards a decline in coronary heart disease mortality for Maori and Pacific Islands people, the most likely explanation for the apparent increase in morbidity is improved access to secondary health care services and greater awareness of coronary health disease symptoms.
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Under normal conditions, carbohydrate, protein, and alcohol are not converted to fat. Glycogen and protein stores are closely controlled, and increasing the intake of nonfat nutrients stimulates their oxidation rates proportionally. Thus, chronic imbalance between intake and oxidation of nonfat nutrients cannot lead to obesity. On the other hand, fat stores are not controlled and their capacity for expansion is enormous. Because an increase in fat intake does not stimulate fat oxidation, a positive fat balance results, which has the potential to become chronic. Obesity is therefore due to a long-standing positive fat balance, which may simply be due to a high-fat diet. The use of the fat-balance equation instead of the energy-balance equation adds another option for the treatment of obesity--that of changing the quality of the diet, ie, lowering the fat content.
Lipid and apoprotein composition of four very low density lipoprotein (VLDL) subfractions decreasing in Sf value were evaluated in the fasting state in 12 normolipidemic Pima Indians (6 M, 6 F, age 39 +/- 1.7 yrs) (mean +/- SEM) with non-insulin-dependent diabetes mellitus (NIDDM) in poor glycemic control (HbA1 9.8 +/- 2.9%) and in 14 normoglycemic Pima controls matched for age, BMI and lipid values. Total cholesterol (CHOL), triglyceride (TG), phospholipids (PL), total protein (TP), apo B, apo CII, apo CIII and apoE were assayed in total VLDL and in each of the four VLDL subfractions designed as A (Sf greater than 400), B (Sf 175-400), C (Sf 100-175), and D (Sf 20-100). Diabetics compared to nondiabetics had higher concentrations of all constituents of VLDL D, with the largest changes being in TG (38.0 +/- 3.8 vs 28.0 +/- 2.5 mg/dl, P less than 0.04), PL (14.0 +/- 1.3 vs 10.0 +/- 1.0 mg/dl, P less than 0.04), TP (9.8 +/- 0.8 vs 7.6 +/- 2.4 mg/dl, P less than 0.05), apo B (6.3 +/- 0.5 vs 4.7 +/- 0.4 mg/dl, P less than 0.03) and apoE (0.73 +/- 0.09 vs 0.52 +/- 0.04 mg/dl, P less than 0.04). Since no difference was found between the groups in percentage composition of lipids or apoproteins in total VLDL and in all VLDL subfractions, the data suggest that in diabetics, even when normolipidemic, there is an increase in the number rather than in the composition of the smallest VLDL subfraction (VLDL D), which are usually considered to be more atherogenic.
To assess the validity of bioelectrical resistance (BR) in an obese population, body composition was determined by both hydrostatic weighing and by BR in 156 Pima Indian volunteers representing a wide range of body weight (46.1-202.6 kg) and body composition (11-52% fat). A predictive equation was derived by use of data on height, BR, weight, age, and sex from 130 randomly selected volunteers and was applied to the remaining 26 volunteers. When compared with the manufacturer's software, the new equation increased correlations with hydrostatic weighing for predicting percent body fat and fat-free mass (FFM) from 0.70 to 0.92 and 0.79 to 0.97, respectively. The manufacturer's software underestimated FFM by 5.3 +/- 8.6 kg (P less than 0.05) when compared with FFM derived from hydrostatic weighing whereas the new equation improved the accuracy to -0.1 +/- 3.3 kg (NS). There were no significant effects of fluid intake (700 mL) or breakfast consumption on body composition as determined by BR. BR represents a simple and accurate way to assess body composition in Pima Indians with our newly derived equation.
The energy cost of physical activity on a metabolic ward was derived from the difference between the energy requirement to maintain body weight on a metabolic ward and sedentary 24-h energy expenditure measured in a respiratory chamber in 56 nondiabetic male subjects. The cost of physical activity was negatively correlated with body weight (r = -0.67, P less than 0.0001) and with percent body fat (r = -0.48, P less than 0.0005). In a subgroup of 15 subjects selected for strict weight stability (rate of daily weight change less than +/- 35 g/d), similar negative correlations were observed between energy cost of activity and body weight (r = -0.61, P less than 0.01) and percent body fat (r = -0.51, P = 0.05). The ratio of active to sedentary energy expenditure, an index of physical activity, was also negatively correlated with body weight and percent body fat (r = -0.74, P less than 0.002 and r = -0.61, P less than 0.02, respectively). These results suggest that heavier subjects on a metabolic ward are less active and expend less energy in physical activity than do lighter subjects.
The mechanisms by which high-carbohydrate, low-saturated-fat diets lower LDL cholesterol (LDLC) concentrations are unknown. In this study, kinetics of VLDL, intermediate density lipoprotein (IDL), and LDL apoprotein B and VLDL triglyceride were determined in seven nondiabetic (ND) and seven non-insulin-dependent diabetic (NIDDM) Pima Indian subjects on high-fat and high-carbohydrate (HICHO) diets. Metabolic changes were similar in ND and NIDDM. On the HICHO diet, LDLC decreased (131 +/- 8 vs. 110 +/- 7 mg/dl, P less than 0.0001) in all subjects. Mean fasting and 24-h triglyceride (TG) concentrations were unchanged, as were mean production rates and fractional clearance rates (FCR) of VLDL apoB and VLDL TG. The mean VLDL apoB pool size (303 +/- 20 vs. 371 +/- 38 mg, P = 0.01) increased owing to a decrease in the mean transport rate (10.7 +/- 1.1 vs. 8.4 +/- 0.9 mg/kg fat-free mass (ffm) per day, P less than 0.0001) and the mean rate constant (2.3 +/- 0.2 vs. 1.5 +/- 0.2, P less than 0.001) for the VLDL apoB to IDL apoB conversion pathway. The mean transport rate of VLDL apoB to LDL apoB via IDL (10.2 +/- 0.9 vs. 8.0 +/- 0.8 mg/kg ffm per day, P less than 0.001) decreased. Mean LDL apoB concentrations decreased (70 +/- 5 vs. 61 +/- 5 mg/dl, P less than 0.001) on the HICHO diet. Means for total LDL apoB transport rate, LDL apoB FCR, and LDLC/apoB ratios were unchanged. In summary, the HICHO diet decreased the activity of mechanisms that convert VLDL to LDL, which contributed to the decrease in LDLC in all subjects. There was also evidence in some subjects for increased activity of LDL apoB clearance mechanisms, and a decrease in the LDLC to apoB ratio.
If a single gene produced insulin resistance, with environmental effects creating some additional variance, insulin action might be distributed as a mixture of two normal distributions if the gene is dominant or recessive or as a mixture of three normal distributions if the gene is codominant. To estimate maximal insulin-stimulated glucose uptake rates (MaxMs), hyperinsulinemic-euglycemic clamps were performed on 245 nondiabetic Pima Indians (126 men, 119 women). Five models (for 1, 2, 3, 4, or 5 components each, normally distributed with a common variance) were fitted to the frequency distribution of MaxM by iterative maximum-likelihood estimation. The three-component model fit the data significantly better than a single normal distribution (chi 2 = 14.3 with 4 df P less than .01) or a mixture of two normal distributions (chi 2 = 9.9 with 2 df, P less than .01). Mixtures of four or five normal distributions did not fit the data significantly better than a mixture of three normal distributions. The first component of the distribution comprised 23%, the second 48%, and the third 29% of the total distribution. Similarly, the frequency distributions of fasting plasma insulin concentrations and a principal component score derived from MaxM and fasting insulin were best fitted by a mixture of three normal distributions. These results are consistent with the hypothesis that among Pimas, insulin resistance is determined by a single gene with a codominant mode of inheritance. Segregation analyses of studies performed in pedigrees are indicated to prove or disprove this genetic hypothesis.
Impaired glucose tolerance often presages the development of non-insulin-dependent diabetes mellitus. We have studied insulin action and secretion in 24 Pima Indians before and after the development of impaired glucose tolerance and in 254 other subjects representing the whole spectrum of glucose tolerance, including subjects with overt non-insulin-dependent diabetes. The transition from normal to impaired glucose tolerance was associated with a decrease in glucose uptake during hyperinsulinemia, from 0.018 to 0.016 mmol per minute (from 3.3 to 2.8 mg per kilogram of fat-free body mass per minute) (P less than 0.0003). Mean plasma insulin concentrations increased during an oral glucose-tolerance test, from 1200 to 1770 pmol per liter (from 167 to 247 microU per milliliter). In 151 subjects with normal glucose tolerance, the insulin concentration measured during an oral glucose-tolerance test correlated with the plasma glucose concentration (r = 0.48, P less than or equal to 0.0001). This relation was used to predict an insulin concentration of 1550 pmol per liter (216 microU per milliliter) in subjects with impaired glucose tolerance (actual value, 1590 pmol per liter [222 microU per milliliter]; P not significant), suggesting that these subjects had normal secretion of insulin. In contrast, plasma insulin concentrations in the diabetics decreased as glucose concentrations increased (r = -0.75, P less than or equal to 0.0001), suggesting deficient secretion of insulin. This relative insulin deficiency first appears at the lower end of the second (diabetic) mode seen in population frequency distributions of plasma glucose concentrations. Our data show that impaired glucose tolerance in our study population is primarily due to impaired insulin action. In patients with non-insulin-dependent diabetes mellitus, by contrast, impaired insulin action and insulin secretory failure are both present.
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A 23 year old man presented with hepatic veno-occlusive disease and severe portal hypertension and subsequently died from liver failure. Light microscopy and hepatic angiography showed occlusion of sublobular veins and small venous radicles of the liver, associated with widespread haemorrhagic necrosis of hepatocytes. The patient had been on a predominantly vegetarian diet and, prior to his illness, took comfrey leaves which are known to contain hepatotoxic pyrrolizidine alkaloids. Comfrey is widely used as a herbal remedy, but so far has only been implicated in two other documented cases of human hepatic veno-occlusive disease. A possible causal association of comfrey and this patient's veno-occlusive disease is suggested by the temporal relationship of the ingestion of comfrey to his presentation, the histological changes in the liver and the exclusion of other known causes of the disease.