Obesity: Rankin JW

Donnelly JE, Blair SN, Jakicic JM, Manore MM, Rankin JW, Smith BK, Anonymous00019. · No affiliation provided · Med Sci Sports Exerc. · Pubmed #19127177 No free full text.

Abstract: Overweight and obesity affects more than 66% of the adult population and is associated with a variety of chronic diseases. Weight reduction reduces health risks associated with chronic diseases and is therefore encouraged by major health agencies. Guidelines of the National Heart, Lung, and Blood Institute (NHLBI) encourage a 10% reduction in weight, although considerable literature indicates reduction in health risk with 3% to 5% reduction in weight. Physical activity (PA) is recommended as a component of weight management for prevention of weight gain, for weight loss, and for prevention of weight regain after weight loss. In 2001, the American College of Sports Medicine (ACSM) published a Position Stand that recommended a minimum of 150 min wk(-1) of moderate-intensity PA for overweight and obese adults to improve health; however, 200-300 min wk(-1) was recommended for long-term weight loss. More recent evidence has supported this recommendation and has indicated more PA may be necessary to prevent weight regain after weight loss. To this end, we have reexamined the evidence from 1999 to determine whether there is a level at which PA is effective for prevention of weight gain, for weight loss, and prevention of weight regain. Evidence supports moderate-intensity PA between 150 and 250 min wk(-1) to be effective to prevent weight gain. Moderate-intensity PA between 150 and 250 min wk(-1) will provide only modest weight loss. Greater amounts of PA (>250 min wk(-1)) have been associated with clinically significant weight loss. Moderate-intensity PA between 150 and 250 min wk(-1) will improve weight loss in studies that use moderate diet restriction but not severe diet restriction. Cross-sectional and prospective studies indicate that after weight loss, weight maintenance is improved with PA >250 min wk(-1). However, no evidence from well-designed randomized controlled trials exists to judge the effectiveness of PA for prevention of weight regain after weight loss. Resistance training does not enhance weight loss but may increase fat-free mass and increase loss of fat mass and is associated with reductions in health risk. Existing evidence indicates that endurance PA or resistance training without weight loss improves health risk. There is inadequate evidence to determine whether PA prevents or attenuates detrimental changes in chronic disease risk during weight gain.

Peairs AT, Rankin JW. · Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, Virginia, USA. · Obesity (Silver Spring). · Pubmed #18451774 No free full text.

Abstract: The objective of this study was to test the hypothesis that the inflammatory response to a high-fat, low-carbohydrate weight loss diet (HF) we previously observed was due to oxidative stress. Nineteen overweight subjects (BMI>27 kg/m(2)) were randomly assigned to either an antioxidant supplement (AS) (1 g vitamin C/800 IU vitamin E) or a placebo (P) group and provided with a HF for 7 days. Fasted pre- and post serum samples were measured for markers of inflammation (C-reactive protein (CRP), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1)), oxygen radical absorbance capacity (ORAC), and glucose, whereas urine was measured for oxidative stress (8-epi-prostaglandin-F(2alpha) (8-epi)). HF resulted in significant reductions in weight (-3.2%), glucose (-18.7%), and MCP-1 (-15%) (all P<0.01), with no difference between groups. There was a trend for a differential effect between groups for CRP as it decreased 32% in the AS group but increased 50% for P (P=0.076). Inverse correlations were noted between initial values and changes in several inflammatory and oxidative stress markers, including CRP (r= -0.501), 8-epi (r= -0.863), and ORAC (r= -0.546) (all P<0.05). It was concluded that weight loss on a short-term HF caused reduction of some but not all markers of inflammation. A role for oxidative stress in causing inflammation was not confirmed; however, longer term diet-controlled studies are necessary to further explore the trend for a differential response in CRP with antioxidant supplementation.

Rankin JW, Andreae MC, Oliver Chen CY, O'Keefe SF. · Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA 24061-0430, USA. · Diabetes Obes Metab. · Pubmed #18355330 No free full text.

Abstract: AIM: Oxidative stress can initiate increased inflammation that elevates risk for cardiovascular disease. The objective of this study was to determine the effects of daily consumption of raisins on markers of oxidative stress, inflammation and endothelial activation in response to an acute high-fat meal in overweight individuals. METHODS: Seventeen overweight men and women consumed 90 g raisins or isocaloric placebo (264 kcal/day) for 14 days in a randomized, crossover design while following a low-flavonoid diet. The oxidative [urinary 8-iso-prostaglandin-F(2alpha) (8-epi PGF(2alpha)) and serum oxygen radical absorbance capacity (ORAC)], inflammatory (serum C-reactive protein and interleukin-6), endothelial (serum soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1, sVCAM-1) and metabolic [free fatty acids (FFAs), triacylglycerol, glucose and insulin] response to four high-fat (53%) meals was tested pre- and postintervention. RESULTS: Urinary 8-epi PGF(2alpha) decreased (-22%) and fasting ORAC increased (+3%) after both interventions combined. Fasting protein-free ORAC was modestly (+3.5%) higher during the raisin than the placebo intervention. Neither the meals nor the raisins consistently induced fasted markers of inflammation or endothelial dysfunction. Gender influenced postprandial metabolic responses in that males responded with higher serum FFAs, sVCAM-1 and glucose compared with females. CONCLUSIONS: Serum antioxidant capacity was modestly increased by daily raisin consumption, but this did not alter fasted or postprandial inflammatory response in these relatively healthy but overweight individuals. Providing all food in regular pattern reduced measures of oxidative stress.

Rankin JW, Turpyn AD. · Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA 24061-0430, USA. · J Am Coll Nutr. · Pubmed #17536128 links to  free full text

Abstract: OBJECTIVE: Chronic inflammation is associated with elevated risk of heart disease and may be linked to oxidative stress in obesity. Our objective was to evaluate the effect of weight loss diet composition (low carbohydrate, high fat, LC or high carbohydrate, low fat, HC) on inflammation and to determine whether this was related to oxidative stress. METHODS: Twenty nine overweight women, BMI 32.1 +/- 5.4 kg/m(2), were randomly assigned to a self-selected LC or HC diet for 4 wks. Weekly group sessions and diet record collections helped enhance compliance. Body weight, markers of inflammation (serum interleukin-6, IL-6; C-reactive protein, CRP) oxidative stress (urinary 8-epi-prostaglandin F2alpha, 8-epi) and fasting blood glucose and free fatty acids were measured weekly. RESULTS: The diets were similar in caloric intake (1357 kcal/d LC vs. 1361 HC, p=0.94), but differed in macronutrients (58, 12, 30 and 24, 59, 18 for percent of energy as fat, carbohydrate, and protein for LC and HC, respectively). Although LC lost more weight (3.8 +/- 1.2 kg LC vs. 2.6 +/- 1.7 HC, p=0.04), CRP increased 25%; this factor was reduced 43% in HC (p=0.02). For both groups, glucose decreased with weight loss (85.4 vs. 82.1 mg/dl for baseline and wk 4, p<0.01), while IL-6 increased (1.39 to 1.62 pg/mL, p=0.04). Urinary 8-epi varied differently over time between groups (p<0.05) with no consistent pattern. CONCLUSION: Diet composition of the weight loss diet influenced a key marker of inflammation in that LC increased while HC reduced serum CRP but evidence did not support that this was related to oxidative stress.