Article

Effect of Weight Loss and Lifestyle Changes on Vascular Inflammatory Markers in Obese Women: A Randomized Trial

Center for Obesity Management, Department of Geriatrics and Metabolic Diseases, Second University of Naples, Naples, Italy.
JAMA The Journal of the American Medical Association (Impact Factor: 30.39). 04/2003; 289(14):1799-804. DOI: 10.1001/jama.289.14.1799
Source: PubMed

ABSTRACT Obesity is an independent risk factor for cardiovascular disease, which may be mediated by increased secretion of proinflammatory cytokines by adipose tissue.
To determine the effect of a program of changes in lifestyle designed to obtain a sustained reduction of body weight on markers of systemic vascular inflammation and insulin resistance.
Randomized single-blind trial conducted from February 1999 to February 2002 at a university hospital in Italy.
One hundred twenty premenopausal obese women (body mass index > or =30) aged 20 to 46 years without diabetes, hypertension, or hyperlipidemia.
The 60 women randomly assigned to the intervention group received detailed advice about how to achieve a reduction of weight of 10% or more through a low-energy Mediterranean-style diet and increased physical activity. The control group (n = 60) was given general information about healthy food choices and exercise.
Lipid and glucose intake; blood pressure; homeostatic model assessment of insulin sensitivity; and circulating levels of interleukin 6 (IL-6), interleukin 18 (IL-18), C-reactive protein (CRP), and adiponectin.
After 2 years, women in the intervention group consumed more foods rich in complex carbohydrates (9% corrected difference; P<.001), monounsaturated fat (2%; P =.009), and fiber (7 g/d; P<.001); had a lower ratio of omega-6 to omega-3 fatty acids (-5; P<.001); and had lower energy (-310 kcal/d; P<.001), saturated fat (-3.5%; P =.007), and cholesterol intake (-92 mg/d; P<.001) than controls. Body mass index decreased more in the intervention group than in controls (-4.2; P<.001), as did serum concentrations of IL-6 (-1.1 pg/mL; P =.009), IL-18 (-57 pg/mL; P =.02), and CRP (-1.6 mg/L; P =.008), while adiponectin levels increased significantly (2.2 microg/mL; P =.01). In multivariate analyses, changes in free fatty acids (P =.008), IL-6 (P =.02), and adiponectin (P =.007) levels were independently associated with changes in insulin sensitivity.
In this study, a multidisciplinary program aimed to reduce body weight in obese women through lifestyle changes was associated with a reduction in markers of vascular inflammation and insulin resistance.

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    • "Recently, low-grade inflammation has been recognized as an integral part of the development and progression of atherosclerosis (Hansson, 2005). On the other hand, research suggests that the levels of local and systemic inflammation can be reduced by different lifestyles and pharmacological interventions including drugs, weight loss, smoking cessation or exercise (Esposito et al., 2003; Petersen et al., 1995). "
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    ABSTRACT: Little is known about the inflammatory effects of resistance exercise in healthy and even less in diseased individuals such as cardiac patients. The purpose of this study was to examine the acute pro- and anti-inflammatory responses during resistance exercise (RE) in patients with coronary artery disease. Eight low risk patients completed two acute RE protocols at low (50% of 1 RM; 2x18 rps) and moderate intensity (75% of 1 RM; 3x8 rps) in random order. Both protocols included six exercises and had the same total load volume. Blood samples were obtained before, immediately after and 60 minutes after each protocol for the determination of lactate, TNFα, INF-γ, IL-6, IL-10, TGF-β1, and hsCRP concentrations. IL-6 and IL-10 levels increased (p < 0.05) immediately after both RE protocols with no differences between protocols. INF-γ was significantly lower (p < 0.05) 60 min after the low intensity protocol, whereas TGF-β1 increased (p < 0.05) immediately after the low intensity protocol. There were no differences in TNF-& and hs-CRP after both RE protocols or between protocols. The above data indicate that acute resistance exercise performed at low to moderate intensity in low risk, trained CAD patients is safe and does not exacerbate the inflammation associated with their disease. Key pointsAcute resistance exercise is safe without exacerbating inflammation in patients with CAD.Both exercise intensities (50 and 75% of 1 RM) elicit desirable pro-and anti-inflammatory responses.With both exercise intensities (50 and 75% of 1 RM) acceptable clinical hemodynamic alterations were observed.
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    • "Australia 56 0.56 NA 30.1 <30% TF, <10% SF moderate intensity, 30 min/S, most days/wk 12 Bo et al. 2007 [31] Italy 56 0.58 MS 30.0 reduced TF and SF intake moderate intensity (i. e. brisk walking), ~150 min/wk 13 Arciero et al. 2006 [32] USA 43 0.48 NA 27.8 high protein (40%) and low fat (20%) diet resistance and cardiovascular training, 20 min/S, 4–6 S/wk 14 Brekke et al. 2005 [33] Sweden 42 0.37 NA 26.1 <30% TF intake, <10% SF intake walking or more intensive exercise, 30 min/S, 4–5 S/wk 15 Watkins et al. 2003 [34] USA 50 0.50 NA 33.7 500 kcal/d restriction, <20% TF cycle ergometry and jogging, or walking, ~60 min/S, 3–4 S/wk 16 Lindstrom et al. 2003 [35] Finland 55 0.66 IGT 31.3 200 kcal/d restriction, <30% TF, <10% SF endurance exercise & resistance training, >30 min/S 17 Esposito et al. 2003 [36] Italy 35 1.00 NA 34.5 1400 kcal/d, 55% carbohydrate, 30% TF, <10% SF aerobic exercise (walking and swimming) 18 Mensink et al. 2003 [37] Netherlands 56 0.43 IGT 29.5 >55% carbohydrate, <30% TF, <10% SF moderate physical activity, >30 min/S, 5 S/wk 19 McAuley et al. 2002 [38] New Zealand 46 0.71 IR 34.5 400 kcal/d restriction, 27% TF, 9% SF Moderate exercise plus resistance training, >20 min/S, 5 S/wk 20 Miller et al. 2002 [39] USA 54 0.62 NA 33.7 500 kcal/d restriction, 27% TF, 6% SF aerobic (brisk walking and biking), 30–45 min/S, 3 S/wk 21 Reseland et al. 2001 [40] Norway 45 0.00 MS 27.5 400 kcal/d restriction, <30% TF endurance exercise, 1 h/S, 3 S/wk 22 Oldroyd et al. 2001 [41] UK 58 0.40 IGT 30.2 <30% TF intake, ~50% carbohydrate aerobic exercise, 20–30 min/S, 2–3 S/wk 23 Kuller et al. 2001 [42] USA 47 1.00 NA 25.0 Calorie restriction upto 1300 kcal, 25% TF, 7% SF increasing physical activity to 1250 kcal expended weekly 24 Ornish et al. 1998 [43] USA 60 0.09 NA 26.9 10%-fat vegetarian diet moderate-intensity aerobic, 1 h/S, 5 S/wk 25 Stefanick et al. 1998 (female) [16] USA 57 1.00 NA 25.6 <30% TF intake, <7% SF intake aerobic (jogging and brisk walking), 60 min/S, 3 S/wk 26 Stefanick et al. 1998 (male) [16] USA 48 1.00 NA 27.8 <30% TF intake, <7% SF intake aerobic (jogging and brisk walking), 60 min/S, 3 S/wk variance τ 2 . If τ 2 = 0, homogeneity is implied among true effects across individual studies such that μ=θ. "
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    ABSTRACT: Background and aims Fasting insulin (FI), fasting glucose (FG), systolic blood pressure (SBP), high density lipoproteins (HDL), triacylglycerides (TAG), and body mass index (BMI) are well-known risk factors for type 2 diabetes. Reliable estimates of lifestyle intervention effects on these factors allow diabetes risk to be predicted accurately. The present meta-analyses were conducted to quantitatively summarize effects of diet and exercise intervention programs on FI, FG, SBP, HDL, TAG and BMI in adults without diabetes. Materials and methods MEDLINE and EMBASE were searched to find studies involving diet plus exercise interventions. Studies were required to use adults not diagnosed with type 2 diabetes, involve both dietary and exercise counseling, and include changes in diabetes risk factors as outcome measures. Data from 18, 24, 23, 30, 29 and 29 studies were used for the analyses of FI, FG, SBP, HDL, TAG and BMI, respectively. About 60% of the studies included exclusively overweight or obese adults. Mean age and BMI of participants at baseline were 48 years and 30.1 kg/m2. Heterogeneity of intervention effects was first estimated using random-effect models and explained further with mixed-effects models. Results Adults receiving diet and exercise education for approximately one year experienced significant (P <0.001) reductions in FI (-2.56 ± 0.58 mU/L), FG (-0.18 ± 0.04 mmol/L), SBP (-2.77 ± 0.56 mm Hg), TAG (-0.258 ± 0.037 mmol/L) and BMI (-1.61 ± 0.13 kg/m2). These risk factor changes were related to a mean calorie intake reduction of 273 kcal/d, a mean total fat intake reduction of 6.3%, and 40 minutes of moderate intensity aerobic exercise four times a week. Lifestyle intervention did not have an impact on HDL. More than 99% of total variability in the intervention effects was due to heterogeneity. Variability in calorie and fat intake restrictions, exercise type and duration, length of the intervention period, and the presence or absence of glucose, insulin, or lipid abnormalities explained 23-63% of the heterogeneity. Conclusions Calorie and total fat intake restrictions coupled with moderate intensity aerobic exercises significantly improved diabetes risk factors in healthy normoglycemic adults although normoglycemic adults with glucose, insulin, and lipid abnormalities appear to benefit more.
    Diabetology and Metabolic Syndrome 11/2014; 6(1). DOI:10.1186/1758-5996-6-127 · 2.50 Impact Factor
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    • "Previous studies have shown that caloric restriction and IF reduce levels of circulating pro-inflammatory IL-1β and TNF-α, and increase anti-inflammatory IL-10 levels in animal models and human subjects [83-85]. In the brain, IL-10 may inhibit the development and progression of chronic neurodegenerative diseases. "
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    ABSTRACT: Background Systemic bacterial infections often result in enduring cognitive impairment and are a risk factor for dementia. There are currently no effective treatments for infection-induced cognitive impairment. Previous studies have shown that intermittent fasting (IF) can increase the resistance of neurons to injury and disease by stimulating adaptive cellular stress responses. However, the impact of IF on the cognitive sequelae of systemic and brain inflammation is unknown. Methods Rats on IF for 30 days received 1 mg/kg of lipopolysaccharide (LPS) or saline intravenously. Half of the rats were subjected to behavioral tests and the other half were euthanized two hours after LPS administration and the hippocampus was dissected and frozen for analyses. Results Here, we report that IF ameliorates cognitive deficits in a rat model of sepsis by a mechanism involving NF-κB activation, suppression of the expression of pro-inflammatory cytokines, and enhancement of neurotrophic support. Treatment of rats with LPS resulted in deficits in cognitive performance in the Barnes maze and inhibitory avoidance tests, without changing locomotor activity, that were ameliorated in rats that had been maintained on the IF diet. IF also resulted in reduced levels of mRNAs encoding the LPS receptor TLR4 and inducible nitric oxide synthase (iNOS) in the hippocampus. Moreover, IF prevented LPS-induced elevation of IL-1α, IL-1β and TNF-α levels, and prevented the LPS-induced reduction of BDNF levels in the hippocampus. IF also significantly attenuated LPS-induced elevations of serum IL-1β, IFN-γ, RANTES, TNF-α and IL-6 levels. Conclusions Taken together, our results suggest that IF induces adaptive responses in the brain and periphery that can suppress inflammation and preserve cognitive function in an animal model of systemic bacterial infection.
    Journal of Neuroinflammation 05/2014; 11(1):85. DOI:10.1186/1742-2094-11-85 · 4.90 Impact Factor
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