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      Long-Term Change in both Dietary Insulinemic and Inflammatory Potential Is Associated with Weight Gain in Adult Women and Men

      1 , 2 , 3 , 3 , 3 , 4 , 1 , 2 , 3 , 5
      The Journal of Nutrition
      Oxford University Press (OUP)

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          ABSTRACT

          Background

          The influence of long-term dietary patterns on weight gain and the underlying potential biological mechanisms are not fully understood.

          Objective

          We prospectively examined the association of changes in 2 empirical hypothesis-oriented dietary patterns (insulinemic and inflammatory) and weight gain over 24 y at 4-y intervals.

          Methods

          We followed 54,397 women in the Nurses’ Health Study and 33,043 men in the Health Professionals Follow-Up Study (1986–2010), and computed the empirical dietary index for hyperinsulinemia (EDIH) and empirical dietary inflammatory pattern (EDIP) scores from food frequency questionnaires administered every 4 y. Both scores are weighted sums of 18 food groups, which characterize dietary insulinemic or inflammatory potential based on plasma levels of insulin response or inflammatory biomarkers. We used multivariable-adjusted linear regression to examine 4-y changes in the dietary scores and weight change within the same period.

          Results

          The mean baseline body mass index (BMI, in kg/m2) was 25.4. Compared with participants who made minimal dietary changes (quintile 3) over 6 4-y periods; participants who changed their diets toward lower insulinemic or inflammatory potential (quintile 1) gained significantly less weight (in kilograms per 4 y) independent of total energy intake, BMI, physical activity, and smoking status: EDIH: −0.65 (95% CI: −0.73, −0.57), EDIP: −0.29 (−0.37, −0.21) among women; and EDIH: −0.60 (−0.71, −0.49), EDIP: −0.19 (−0.27, −0.07) among men. In contrast, those who changed their diets toward higher insulinemic or inflammatory potential (quintile 5) gained significantly more weight: EDIH: 0.43 (0.36, 0.51), EDIP: 0.15 (0.07, 0.23) among women; and EDIH: 0.49 (0.38, 0.59), EDIP: 0.22 (0.11, 0.33) among men (P-trend < 0.0001 for all comparisons). Associations were stronger among individuals who were overweight or obese, younger, less physically active, and had never smoked.

          Conclusions

          High dietary insulinemic and inflammatory potential is associated with substantial long-term weight gain in adult men and women independent of total energy intake. Dietary patterns with low insulinemic and inflammatory potential may aid in weight gain prevention.

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          Most cited references27

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          Validity of a Dietary Questionnaire Assessed by Comparison With Multiple Weighed Dietary Records or 24-Hour Recalls

          The authors evaluated the validity of a 152-item semiquantitative food frequency questionnaire (SFFQ) by comparing it with two 7-day dietary records (7DDRs) or up to 4 automated self-administered 24-hour recalls (ASA24s) over a 1-year period in the women's Lifestyle Validation Study (2010–2012), conducted among subgroups of the Nurses’ Health Studies. Intakes of energy and 44 nutrients were assessed using the 3 methods among 632 US women. Compared with the 7DDRs, SFFQ responses tended to underestimate sodium intake but overestimate intakes of energy, macronutrients, and several nutrients in fruits and vegetables, such as carotenoids. Spearman correlation coefficients between energy-adjusted intakes from 7DDRs and the SFFQ completed at the end of the data-collection period ranged from 0.36 for lauric acid to 0.77 for alcohol (mean r  = 0.53). Correlations of the end-period SFFQ were weaker when ASA24s were used as the comparison method (mean r  = 0.43). After adjustment for within-person variation in the comparison method, the correlations of the final SFFQ were similar with 7DDRs (mean r  = 0.63) and ASA24s (mean r  = 0.62). These data indicate that this SFFQ provided reasonably valid estimates for intakes of a wide variety of dietary variables and that use of multiple 24-hour recalls or 7DDRs as a comparison method provided similar conclusions if day-to-day variation was taken into account.
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            Inflammatory pathways and insulin action.

            Obesity and type 2 diabetes are associated with a state of abnormal inflammatory response. While this correlation has also been recognized in the clinical setting, its molecular basis and physiological significance are not yet fully understood. Studies in recent years have provided important insights into this curious phenomenon. The state of chronic inflammation typical of obesity and type 2 diabetes occurs at metabolically relevant sites, such as the liver, muscle, and most interestingly, adipose tissues. The biological relevance of the activation of inflammatory pathways became evident upon the demonstration that interference with these pathways improve or alleviate insulin resistance. The abnormal production of tumor necrosis factor alpha (TNF-alpha) in obesity is a paradigm for the metabolic significance of this inflammatory response. When TNF-alpha activity is blocked in obesity, either biochemically or genetically, the result is improved insulin sensitivity. Studies have since focused on the identification of additional inflammatory mediators critical in metabolic control and on understanding the molecular mechanisms by which inflammatory pathways are coupled to metabolic control. Recent years have seen a critical progress in this respect by the identification of several downstream mediators and signaling pathways, which provide the crosstalk between inflammatory and metabolic signaling. These include the discovery of c-Jun N-terminal kinase (JNK) and I kappa beta kinase (I kappa K) as critical regulators of insulin action activated by TNF-alpha and other inflammatory and stress signals, and the identification of potential targets. Here, the role of the JNK pathway in insulin receptor signaling, the impact of blocking this pathway in obesity and the mechanisms underlying JNK-induced insulin resistance will be discussed.
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              Development and Validation of an Empirical Dietary Inflammatory Index.

              Knowledge on specific biological pathways mediating disease occurrence (e.g., inflammation) may be utilized to construct hypotheses-driven dietary patterns that take advantage of current evidence on disease-related hypotheses and the statistical methods of a posteriori patterns.
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                Author and article information

                Journal
                The Journal of Nutrition
                Oxford University Press (OUP)
                0022-3166
                1541-6100
                May 2019
                May 01 2019
                April 20 2019
                May 2019
                May 01 2019
                April 20 2019
                : 149
                : 5
                : 804-815
                Affiliations
                [1 ]Division of Medical Oncology, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, OH
                [2 ]The Ohio State University Comprehensive Cancer Center—Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Columbus, OH
                [3 ]Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA
                [4 ]Department of Nutrition, Simmons University, Boston, MA
                [5 ]Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA
                Article
                10.1093/jn/nxy319
                6499102
                31004153
                5faa0cbf-5582-406b-82b7-daaf09b81722
                © 2019

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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