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      Food insecurity during pregnancy leads to stress, disordered eating and greater postpartum weight among overweight women

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          Abstract

          Objective

          We sought to understand the influence of food insecurity on women's stress, disordered eating, dietary fat intake and weight during the postpartum period. Design and Methods: We estimated the association between marginal food security and food insecurity—measured during pregnancy and postpartum—and stress, disordered eating, dietary fat intake and weight at 3 and 12 months postpartum using multivariate linear regression, controlling for demographic and socioeconomic characteristics and health behaviors. We assessed effect modification between level of food insecurity and prepregnancy weight status, hypothesizing a stronger association would be found among women who started pregnancy overweight or obese.

          Results

          Food insecurity status during pregnancy was strongly associated with higher levels of stress, disordered eating, and dietary fat intake at 3 and 12 months postpartum; during the postpartum period it was associated with these measures at 12 month postpartum. A significant interaction was found between level of food insecurity and prepregnancy weight status; food insecurity was associated with greater weight and BMI at 12 months only among overweight/obese women.

          Conclusions

          In order to return to one's prepregnancy weight, overweight and obese women who face household food insecurity may need multipronged assistance that addresses not only having enough high quality food, but include stress reduction and eating behavior interventions.

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          Most cited references19

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          Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome.

          The relationship between stress and obesity remains elusive. In response to stress, some people lose weight, whereas others gain. Here we report that stress exaggerates diet-induced obesity through a peripheral mechanism in the abdominal white adipose tissue that is mediated by neuropeptide Y (NPY). Stressors such as exposure to cold or aggression lead to the release of NPY from sympathetic nerves, which in turn upregulates NPY and its Y2 receptors (NPY2R) in a glucocorticoid-dependent manner in the abdominal fat. This positive feedback response by NPY leads to the growth of abdominal fat. Release of NPY and activation of NPY2R stimulates fat angiogenesis, macrophage infiltration, and the proliferation and differentiation of new adipocytes, resulting in abdominal obesity and a metabolic syndrome-like condition. NPY, like stress, stimulates mouse and human fat growth, whereas pharmacological inhibition or fat-targeted knockdown of NPY2R is anti-angiogenic and anti-adipogenic, while reducing abdominal obesity and metabolic abnormalities. Thus, manipulations of NPY2R activity within fat tissue offer new ways to remodel fat and treat obesity and metabolic syndrome.
            • Record: found
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            The eating attitudes test: psychometric features and clinical correlates.

            Psychometric and clinical correlates of the Eating Attitudes Test (EAT) are described for a large sample of female anorexia nervosa (N = 160) and female comparison (N = 140) subjects. An abbreviated 26-item version of the EAT (EAT-26) is proposed, based on a factor analysis of the original scale (EAT-40). The EAT-26 is highly correlated with the EAT-40 (r = 0.98) and the three factors form subscales which are meaningfully related to bulimia, weight, body-image variables and psychological symptoms. Whereas there are no differences between bulimic and restricter anorexia nervosa patients on the total EAT-26 and EAT-40 scores, these groups do indicate significant differences on EAT-26 factors. Norms for the anorexia nervosa and female comparison subjects are presented for the EAT-26, EAT-40 and the EAT-26 factors. It is concluded that the EAT-26 is a reliable, valid and economical instrument which may be useful as an objective measure of the symptoms of anorexia nervosa.
              • Record: found
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              Obesity and the food environment: dietary energy density and diet costs.

              The highest rates of obesity in the United States occur among population groups with the highest poverty rates and the least education. The impact of socioeconomic variables on obesity may be mediated, in part, by the low cost of energy-dense foods. The observed inverse relationship between energy density of foods, defined as available energy per unit weight (kilocalories per gram or megajoules per kilogram), and energy cost (dollars per kilocalorie or dollars per megajoule) means that diets based on refined grains, added sugars, and added fats are more affordable than the recommended diets based on lean meats, fish, fresh vegetables, and fruit. Taste and convenience of added sugars and added fats can also skew food choices in the direction of prepared and prepackaged foods. Paradoxically, attempting to reduce diet costs may lead to the selection of energy-dense foods, increased energy intakes, and overweight. The present energy-cost framework provides an economic explanation for the observed links between obesity and the food environment, with diet cost as the principal intervening variable. If higher food costs represent both a real and perceived barrier to dietary change, especially for lower-income families, then the ability to adopt healthier diets may have less to do with psychosocial factors, self-efficacy, or readiness to change than with household economic resources and the food environment. Continuing to recommend costly diets to low-income families as a public health measure can only generate frustration and culpability among the poor and less-well educated. Obesity in America is, to a large extent, an economic issue.

                Author and article information

                Contributors
                Journal
                101264860
                32902
                Obesity (Silver Spring)
                Obesity (Silver Spring)
                Obesity (Silver Spring, Md.)
                1930-7381
                1930-739X
                4 March 2015
                09 May 2015
                June 2015
                13 June 2019
                : 23
                : 6
                : 1303-1311
                Affiliations
                Division of Community Health and Human Development, School of Public Health, University of California, Berkeley
                National Center for Environmental Assessment, U.S. Environmental Protection Agency, 109 T.W. Alexander Drive, Research Triangle Park, NC 27711 USA
                Department of Epidemiology and Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC 27599
                Author notes
                Corresponding Author: Barbara A. Laraia, Ph.D., M.P.H. RD, Associate Professor, Chair, Public Health Nutrition, School of Public Health, 207-B University Hall, #7360, University of California, Berkeley, Berkeley, CA 94720-7360, blaraia@ 123456berkeley.edu , Tel: (510) 643-7896, Fax: (510) 643-6426
                Article
                NIHMS665855
                10.1002/oby.21075
                6563905
                25959858
                21bac9d4-5ff1-453a-b04a-6a4cdfead8ef

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                Categories
                Article

                Medicine
                food insecurity,pregnancy,weight gain,stress,eating behavior
                Medicine
                food insecurity, pregnancy, weight gain, stress, eating behavior

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