Nutrition Promotion to Prevent Obesity in Young Adults.

Young adulthood is a vulnerable period for weight gain and the health consequences of becoming obese during this life-stage of serious concern. Some unhealthy dietary habits are typical of young adults in many developed nations encountering the obesity epidemic. These include high sugar-sweetened beverage consumption, lower vegetable intake and greater consumption of foods prepared outside the home including fast foods. Each of these dietary behaviours may place young adults at increased risk for overweight and obesity. Evidence suggests many young adults with unhealthy nutrition behaviours are not considering nor preparing to make changes. To improve their nutrition and health as they progress through the lifecycle requires approaches specifically targeted to this age group. Strategies and programs should include both individual level and population approaches. The evidence base for prevention of weight gain and halting overweight and obesity in young adulthood is currently small with few studies of high quality. Studies modifying food environments in colleges and universities are also of limited quality, but sufficiently promising to conduct further research employing better, more sophisticated, study designs and additionally to include health outcome measures. More research into programs tailored to the needs of young adults is warranted with several studies already underway.

Obesity and venous thrombosis: a review.

The world is experiencing an obesity pandemic, with rates of obesity rising for more than two decades. Obesity is defined as a body mass index (BMI) of 30 kg/m (2) or greater. Of particular concern are the risks that millions of obese people are likely to develop chronic diseases and at earlier ages than their parents might have. The risk of venous thrombosis increases with obesity, so that the incidence of this pathology is also expected to rise significantly. There is remarkable and consistent evidence from a systematic review, as well as cohort and case-control studies that obesity might predispose to venous thromboembolism (VTE). The risk appears to be at least double that for normal weight subjects (BMI 20 to 24.9 kg/m (2)). Plausible mechanisms exist to explain this relationship, including the physical effects of body fat limiting venous return and a proinflammatory, prothrombotic, and hypofibrinolytic milieu. Loss of body weight has been shown to reduce the concentrations of coagulation factors and plasminogen activator inhibitor-1 toward the normal range. Whether weight loss would prevent secondary occurrence of VTE in the absence of anticoagulant therapy could not be discerned from this literature search.

Occupational risk of overweight and obesity: an analysis of the Australian Health Survey.

BACKGROUND: Adults spend about one third of their day at work and occupation may be a risk factor for obesity because of associated socioeconomic and behavioral factors such as physical activity and sedentary time. The aim of this study was to examine body mass index (BMI) and prevalence of overweight and obesity by occupation and explore the contributions of socioeconomic factors and lifestyle behaviors (including leisure time and commuting physical activity, diet, smoking, and alcohol) to occupational risk. METHODS: Secondary analyses of the National Health Survey in Australia (2005) were conducted for working age adults (20 to 64 years). Linear and logistic regression models using BMI as either dichotomous or continuous response were computed for occupation type. Model 1 was age-adjusted, Model 2 adjusted for age and socioeconomic variables and Model 3 adjusted for age, socioeconomic variables and lifestyle behaviours. All models were stratified by gender. RESULTS: Age-adjusted data indicated that men in associate professional (OR 1.34, 95% CI 1.10-1.63) and intermediate production and transport (OR 1.24 95% CI 1.03-1.50) occupations had a higher risk of BMI >/= 25 kg/m2 than those without occupation, and women in professional (OR 0.71, 95% CI 0.61-0.82), management (OR 0.72, 95% CI 0.56-0.92) and advanced clerical and service occupations (OR 0.73 95% CI 0.58-0.93) had a lower risk. After adjustment for socioeconomic factors no occupational group had an increased risk but for males, professionals, tradesmen, laborers and elementary clerical workers had a lower risk as did female associate professionals and intermediate clerical workers. Adjustment for lifestyle factors explained the lower risk in the female professional and associate professionals but failed to account for the lower odds ratios in the other occupations. CONCLUSIONS: The pattern of overweight and obesity among occupations differs by gender. Healthy lifestyle behaviors appear to protect females in professional and associate professional occupations from overweight. For high-risk occupations lifestyle modification could be included in workplace health promotion programs. Further investigation of gender-specific occupational behaviors and additional lifestyle behaviors to those assessed in the current Australian Health Survey, is indicated.

Current and future costs of cancer, heart disease and stroke attributable to obesity in Australia - a comparison of two birth cohorts.

The obesity epidemic appears set to worsen the morbidity and mortality from leading causes of death in Australia - ischaemic heart disease, stroke and obesity-related cancers. The aim of this study was to compare hospital separations, deaths and direct health costs for middle-aged adults (45 to 54 years) in 2004/05 with those attaining age 45 to 54 years in 2024/25 who were born into an obesogenic environment. Using data from National Health Surveys, prevalence of obesity in 2004/05 was calculated for those born in 1950/51-59/60 and four scenarios were considered to project rates in 2024/25 for those born in 1970/71-79/80: an age-cohort model; a linear trend model; a steady state where rates increase to equal those of the older birth cohort at the same age; and a best case where rates remain at 2004/05 levels. Population attributable fractions were calculated by gender and disease using relative risks of disease from the literature, and applied to hospital separations, deaths, and direct health system costs data to estimate the proportion of each attributable to obesity. In 2024/25 the projected number of hospitalizations of 45 to 54 year olds due to the diseases of interest could be more than halved, over 200 lives rescued and $51.5 million (in 2004/05 dollars) saved if further gains in obesity in the younger birth cohort are halted. Instead, if the worst case scenario is realized there will be a more than doubling in costs (in 2004/05 dollars) compared with those born in 1950/51-59/60.

The effects of age, birth cohort and survey period on leisure-time physical activity by Australian adults: 1990-2005.

The prevalence of obesity continues to rise with many factors contributing to energy imbalance. Leisure-time physical activity (LTPA) has been proposed as one solution to counteract increasing energy intakes. The present study determined whether age, birth cohort and period of survey had independent effects on time, volume and energy expended in LTPA by Australian adults from 1990 to 2005. Adults were categorised into twelve age groups (5-year intervals from 20-24 years to >75 years), four survey periods (1990, 1995, 2000 and 2005) and fifteen birth cohorts (5-year intervals from pre-1916 to 1985). Time spent in three categories of LTPA was determined and metabolic equivalent (MET) values of 3.3, 4.0 and 8.0 were assigned for walking, moderate and vigorous activities, respectively, to calculate daily volume (MET minutes). Energy expended in LTPA was calculated using estimated BMR (from self-reported weight and published formulae), multiplied by the MET value. Regression models were fitted to the data. Age and period had independent effects on duration, volume and energy expenditure of LTPA for both males (P<0.01) and females (P<0.01), while birth cohort had independent effects for males only such that all three LTPA factors declined with recency of birth cohort (P<0.01). This indicates that more recent birth cohorts of males may need to be targeted to increase LTPA, but as duration, volume and energy expended in leisure time have been declining since 1990, both the sexes may benefit from the promotion of increased LTPA.

Mapping solutions to obesity: lessons from the Human Genome Project.

OBJECTIVE: To discuss appropriate endpoints for research designed to prevent obesity. Research investigating practical solutions to the complex multi-factorial global obesity epidemic may be stalled by undue emphasis on reduced body weight as the only acceptable endpoint. APPROACH: Considering prevention research in cardiovascular disease and tobacco control, we contend that investigations of intermediate endpoints make an important contribution to the multi-faceted approach needed to combat the complex problem of obesity. CONCLUSION: Intermediate endpoints are respected in other public health areas: reductions in risk factors such as high blood cholesterol or smoking are acceptable study endpoints for research aimed at reducing heart disease or lung cancer. Likewise, practical endpoints can be valuable in studies investigating interventions to reduce identified and potential intermediate risk factors for obesity, such as soft drink consumption. IMPLICATIONS: Reduced obesity is the global aim but obesity is not caused by one exposure and will not be solved by a single modality intervention. A wider debate about endpoint selection may assist research which identifies individual building blocks of obesity prevention in the same way as individual gene mapping contributed to the Human Genome Project.

A diet rich in high-oleic-acid sunflower oil favorably alters low-density lipoprotein cholesterol, triglycerides, and factor VII coagulant activity.

OBJECTIVE: To compare concentrations of factor VII coagulant activity (factor VIIc), fibrinogen, plasminogen activator inhibitor-1, and blood lipids on a saturated fat-rich diet with one rich in monounsaturated fat. DESIGN: Subjects were randomly allocated to two groups. The study design was an ABB/BAA extra-period crossover. One group consumed a diet rich in saturated fatty acid (SFA) with fat making up 20.8% of total energy, for 5 weeks and then one rich in monounsaturated fatty acid (MUFA), with fat making up 20.3% of total energy for 10 weeks. The other group consumed the MUFA diet for 5 weeks followed by the SFA diet for 10 weeks. SUBJECTS/SETTING: Men and women aged 35 to 69 years who were nonsmokers with no chronic illness and not on any medication were recruited to participate. Eighteen subjects were recruited and 15 (5 men, 10 women) completed the community-based study. INTERVENTION: Blood was sampled at the beginning and end point of each 5-week diet period for analysis of coagulation and fibrinolysis factors and blood lipids. Subjects kept 3-day food diaries twice during each of the three diet periods and were weighed on each visit for blood collection. Analysis of plasma fatty acids was used to indicate dietary compliance. MAIN OUTCOME MEASURES: Differences in fasting factor VIIc, fibrinogen, plasminogen activator inhibitor-1, insulin, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, apolipoproteins A-1 and B, and plasma oleic acid levels while receiving the SFA diet vs MUFA diet. STATISTICAL ANALYSIS: A general linear model allowing for the ABB/BAA extra-period crossover, was used for each of the outcome measures. RESULTS: Factor VIIc was lower on the MUFA diet ( P <.05) but fibrinogen and insulin concentrations and plasminogen activator inhibitor-1 activity did not differ between diets. Low-density lipoprotein cholesterol ( P <.001) and triglyceride ( P <.01) levels were lower on the MUFA diet compared with the SFA diet. A significant increase in both plasma phospholipid and neutral lipid oleic acid (P <.0001) occurred on the MUFA diet. CONCLUSIONS: Substitution of foods rich in saturated fat with foods rich in high-oleic-acid sunflower oil and margarine has favorable outcomes on blood lipids and factor VIIc. This oil presents another useful source of MUFA for diets aimed at prevention of heart disease.

Diet and aging: bearing on thrombosis and hemostasis.

Diet is one of the environmental factors that influences thrombosis and hemostasis. Macronutrients, micronutrients, and other bioactive food components alter the predisposition to thrombosis. The type and amount of dietary fat has been shown to alter thromboxane A2 production and platelet aggregation, bleeding time, factor VII, fibrinogen, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1). Both epidemiological studies and clinical trials indicate that the very long chain n-3 fatty acids lower thrombotic tendency and risk of heart disease. Other polyunsaturated fats and monounsaturated fat appear to have antithrombotic properties, but further studies are indicated. Hypercaloric diets and those with high glycemic loads are associated with elevations of PAI-1. Moderate consumption of alcohol is associated with decreased platelet aggregation. Low intakes of folate, vitamin B12, and vitamin B6 predispose to hyperhomocysteinemia, and the benefits of supplementation in decreasing vascular disease are under investigation. In a limited number of clinical and laboratory studies, vitamin E has been shown to decrease platelet aggregation and the concentration of PAI-1. Flavonoids and isoflavones appear to inhibit platelet aggregation at pharmacologic concentrations only. Nutritional status frequently declines with aging and may exacerbate the already increased risk for thrombosis. Diet presents an interesting area for research into thrombophilia, but additional work is indicated before specific recommendations are made.