Intentional weight loss and mortality among initially healthy men and women
ABSTRACT Most prospective observational studies suggest that weight loss increases the risk of premature death among obese individuals. This is surprising because clinical studies show that weight loss generally leads to overall improvements in cardiovascular risk factors. It is sometimes argued that the increased mortality observed with weight loss must depend on confounding or poor study designs. This review was conducted to summarize results from studies on intentional weight loss and mortality among healthy individuals, while carefully considering the designs and problems in these studies. Evaluation criteria with a rating scale were developed. Of the studies evaluated, two found decreased mortality with intentional weight loss, three found increased mortality, and four found no significant associations between intentional weight loss and total mortality. Thus, it is still not possible for health authorities to make secure recommendations on intentional weight loss. More studies designed to specifically address this issue are warranted.
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- "e l s e v i e r . c o m / l o c a t e / y g y n o individuals is now also beginning to emerge . In a recent review Wolin et al. suggested that obesity causes a substantial proportion of all cancers, and emerging evidence suggests that adult weight loss reduces cancer risk . "
ABSTRACT: Obesity is a major risk factor for the development of endometrial cancer (EC). An improved understanding of biologic mechanisms associated with weight loss, including alteration in inflammation, hormonal balance, and cancer antigens expression may lead to the development of effective cancer prevention strategies. The goal of this study was to explore longitudinal biomarker changes in obese women who underwent weight loss intervention, testing the hypothesis biomarker levels can be altered through intentional weight loss. Serum samples from 89 participants with Class II and Class III obesity and 43 non morbidly obese comparisons were obtained in Re-Energize with Nutrition, Exercise and Weight Loss (RENEW) study as previously reported. Twenty-one bead-based xMAP immunoassays were utilized, including cancer-associated antigens, cytokines, chemokines, and hormones. One-way repeated measures ANOVA was used to examine the association between changes in biomarker expression levels over time (baseline, 6 months and 12 months). Linear mixed effects models were used to examine longitudinal relationships between biomarker expression levels. Mean levels of VEGF, soluble E-selectin, GH, adiponectin, IL-6, IL-7, CA-125, and IGFBP-1 significantly differed between time periods. In adjusted mixed linear models, decreasing BMI was significantly associated with lower levels of soluble E-selectin and IL-6 and increases in GH, adiponectin, and IGFBP-1. This is one of the first efforts to explore changes in cancer-associated biomarkers in a cohort of weight loss research participants at high risk for EC development. Our findings demonstrate that changes in the expression of markers can be achieved with weight loss intervention.Gynecologic Oncology 12/2011; 125(1):114-9. DOI:10.1016/j.ygyno.2011.12.439 · 3.69 Impact Factor
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- "os basados en ocho estudios, publicados de 1993 al 2005. Los resultados más importantes son las diferencias en la mortalidad dependiendo del género, de la enfermedad coexistente y de la intencionalidad de la pérdida de peso. En mujeres y en las personas con sobrepeso y diabetes, disminuyó el riesgo de mortalidad por la pérdida de peso intencional. Simonsen y cols. (2008) 25 , realizaron una revision de estudios prospectivos publicados de 1995 al 2005, en la que analizaron la asociación de la pérdida de peso intencional sobre la mortalidad en individuos sanos. Desarrollaron un instrumento para evaluar la calidad metodológica de los estudios, en el cual tomaron en cuenta 10 criterios seleccionados por los"
ABSTRACT: The beneficial effect of intentional weight loss on mortality is controversial. The purpose of this study was to conduct a systematic review and analyze the quality of prospective studies that assess weight loss on mortality. An electronic search at MEDLINE/PubMed, SciELO, and EBSCO data base, of studies with a follow-up of five or more years, published from January, 2000 to October, 2009, was conducted. Quality of the studies was assessed by Simonsen's criteria. Twenty studies were analyzed. At the beginning of the studies, the age of the subjects ranged from 20 to 101 years. Nine studies included those who intended to loose weight. The quality of the studies ranged from 8 to 17 points (out of 20). Weight loss increased the mortality rate in 15 studies and decreased it in 5. Seven of the studies assessing intention to loose weight showed that weight loss increased the mortality rate, whereas in two the mortality rate decreased. In three out of the four studies that assessed weight fluctuation, the mortality rate increased. These results underline the importance of preventing weight increase, as well as the need to avoid gaining or loosing weight more than 4%.Nutricion hospitalaria: organo oficial de la Sociedad Espanola de Nutricion Parenteral y Enteral 10/2010; 25(5):718-24. · 1.25 Impact Factor
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ABSTRACT: The overall objective of this thesis was to study genetic mechanisms of body weight regulation. Two genome-wide approaches to identify chromosomal regions/candidate genes/genetic variants involved in body weight regulation were applied. Saar et al. (2003) presented the first genome-wide linkage scan for early onset obesity and detected suggestive evidence for linkage. In contrast, the first genome-wide association study for early onset obesity presented in Hinney et al. (2007) led to the re-identification of FTO, the currently best supported candidate gene for obesity. Thus, our investigation underlines two things: first, GWAs are in principle suitable to detect genes with small to modest genetic effect sizes, and second, with our relatively small but well defined sample of cases and controls it is possible to detect the same effects which required genotyping of several thousand population based unselected probands for body weight. Moreover, this thesis comprised the examination of three candidate genes for obesity (BDNF, GLUT4 and DGAT). Additionally, we observed that carriers of functionally relevant MC4R mutations are able to reduce their body weight, but that they seem to have difficulties to sustain this weight loss over time. Common obesity is caused by a complex interplay of genetic background and environmental factors. While monogenic forms of obesity are well understood, GWAs now seem to offer the option to detect oligo- and polygenes. As these genes are typically characterized by small to modest genetic effect sizes but are more common they might be more important than monogenes with regard to clinical implications. In sum, this work is part of a puzzle that might lead to evidence-based, personalized medicine which will be based on a solid scientific base by investigating the molecular genetic mechanisms of body weight regulation with regard to confirmed findings in independent large samples and by more carefully addressing methodological flaws.