Postpartum Lifestyle Behaviors among Women with Hypertensive Disorders of Pregnancy: Data from the HUNT Study.

Hypertensive disorders of pregnancy (HDP) are associated with an increased risk of cardiovascular disease later in life. Clinical guidelines for postpartum follow-up after HDP often recommend lifestyle counseling to reduce this risk. However, knowledge about lifestyle behaviors and perceptions among women with a history of HDP is limited. We linked data from the fourth survey of the population-based Trøndelag Health Study (HUNT4) with data from the Medical Birth Registry of Norway. The associations between HDP and postpartum lifestyle behaviors and perceptions were examined using multivariable logistic regression. In a secondary analysis, HUNT4 participants with a recent history of pre-eclampsia were compared with women with a recent history of pre-eclampsia participating in a postpartum pilot intervention study. Lifestyle behaviors and perceptions were self-reported and included diet (intake frequency of fruits, vegetables, meat, fish, and sugar-sweetened beverages), alcohol intake, physical activity, sleep, smoking, lifestyle satisfaction, and the importance of a healthy lifestyle. Among 7551 parous HUNT4 participants, 610 had a history of HDP. We found no differences in lifestyle behaviors between women with and without a history of HDP. However, women with HDP had higher odds of being unsatisfied with their lifestyle. Women with pre-eclampsia participating in a postpartum lifestyle intervention study tended to have a healthier lifestyle at baseline than women participating in HUNT4. Future studies should explore how lifestyle intervention programs could be adapted to the needs of women who have experienced HDP or other pregnancy complications that are associated with an increased risk of CVD.

The validity of self-reported number of teeth and edentulousness among Norwegian older adults, the HUNT Study.

BACKGROUND: Number of teeth is an established indicator of oral health and is commonly self-reported in epidemiological studies due to the costly and labor-intensive nature of clinical examinations. Although previous studies have found self-reported number of teeth to be a reasonably accurate measure, its accuracy among older adults ≥ 70 years is less explored. The aim of this study was to assess the validity of self-reported number of teeth and edentulousness in older adults and to investigate factors that may affect the accuracy of self-reports. METHODS: This study included two different samples of older adults ≥ 70 years drawn from the fourth wave of the Trøndelag Health Study (the HUNT Study), Norway. Sample 1 (n = 586) was used to evaluate the validity of self-reported number of teeth and sample 2 (n = 518) was used to evaluate self-reported edentulousness. Information on number of teeth and background variables (education, smoking, cognitive function, and self-perceived general and oral health) were self-reported in questionnaires, while clinical oral health examinations assessed number of teeth, number of teeth restored or replaced by fixed prosthodontics and edentulousness. Spearman and Pearson correlation coefficients, Bland-Altman plot, chi-square test and kappa statistics were used to assess the agreement between self-reported and clinically recorded number of teeth. RESULTS: The mean difference between self-reported and clinically recorded number of teeth was low (- 0.22 teeth), and more than 70% of the participants reported their number of teeth within an error of two teeth. Correlations between self-reports and clinical examinations were high for the total sample (0.86 (Spearman) and 0.91 (Pearson)). However, a lower correlation was found among participants with dementia (0.74 (Spearman) and 0.85 (Pearson)), participants having ≥ 20 teeth (0.76 (Spearman) and 0.67 (Pearson)), and participants with ≥ 5 teeth restored or replaced by fixed prosthodontics (0.75 (Spearman) and 0.77 (Pearson)). Self-reports of having teeth or being edentulous were correct in 96.3% of the cases (kappa value 0.93, p value < 0.001). CONCLUSIONS: Among older Norwegian adults, self-reported number of teeth agreed closely with clinical tooth counts and nearly all the edentulous participants correctly reported having no teeth.

Coffee inhibits nuclear factor-kappa B in prostate cancer cells and xenografts.

Chronic inflammation contributes to prostate cancer and the transcription factor Nuclear Factor-kappa B (NF-κB) is constitutively active in most such cancers. We examine the effects of coffee on NF-κB and on the regulation of selected genes in human-derived prostate cancer cells (PC3) and in PC3 xenografts in athymic nude mice. PC3 cells stably transduced with an NF-κB-luciferase reporter were used both in vitro and for xenografts. NF-κB activity was measured by reporter assays, DNA binding and in vivo imaging. Gene expression was measured in PC3 cells, xenografts and tumor microenvironment by low-density arrays. Western blotting of activated caspases was used to quantify apoptosis. Coffee inhibited TNFα-induced NF-κB activity and DNA-binding in PC3 cells. Furthermore, coffee increased apoptosis and modulated expression of a number of inflammation- and cancer-related genes in TNFα-treated PC3 cells. In vivo imaging revealed a 31% lower NF-κB-luciferase activation in the xenografts of the mice receiving 5% coffee compared to control mice. Interestingly, we observed major changes in gene expression in the PC3 cells in xenografts as compared to PC3 cells in vitro. In PC3 xenografts, genes related to inflammation, apoptosis and cytoprotection were down-regulated in mice receiving coffee, and coffee also affected the gene expression in the xenograft microenvironment. Our data demonstrate that coffee inhibits NF-κB activity in PC3 cells in vitro and in xenografts. Furthermore, coffee modulates transcription of genes related to prostate cancer and inflammation. Our results are the first to suggest mechanistic links between coffee consumption and prostate cancer in an experimental mouse model.

Tomato paste alters NF-κB and cancer-related mRNA expression in prostate cancer cells, xenografts, and xenograft microenvironment.

Tomatoes may protect against prostate cancer development, possibly through targeting signaling pathways such as nuclear factor-κB (NF-κB). We investigated whether tomato paste could modulate NF-κB activity and cancer-related gene expression in human derived prostate cancer cells (PC3) and PC3 xenografts. PC3-cells were stably transduced with an NF-κB-luciferase construct, and treated with tomato extracts or vehicle control. Nude mice bearing PC3 xenografts were fed a Western-like diet with or without 10% tomato paste for 6.5 wk. The tomato diet significantly inhibited TNFα stimulated NF-κB activity in cultured PC3 cells, and modulated the expression of genes associated with inflammation, apoptosis, and cancer progression. Accumulation of lycopene occurred in liver, xenografts, and serum of mice fed tomato diet. Tomato paste in the diet did not affect tumor size in mice; however, there was a trend toward inhibition of NF-κB activity in the xenografts. The effect of tomato on gene expression was most prominent in the xenograft microenvironment, where among others NFKB2, STAT3, and STAT6 showed higher expression levels after tomato treatment. Our findings support biological activity of tomatoes in cancer-related inflammation.

Coffee, broccoli and spices are strong inducers of electrophile response element-dependent transcription in vitro and in vivo - studies in electrophile response element transgenic mice.

SCOPE: Cytoprotective gene products, e.g. phase II - and antioxidant enzymes, are important in cellular redox homeostasis. A common feature of these genes is binding sites for transcription factor nuclear factor erythroid-2-related factor 2 (Nrf2), named electrophile response elements (EpREs) within their promoters. METHODS AND RESULTS: To identify dietary bioactive compounds and foods with Nrf2/EpRE inducing properties in an intact organism, we utilized transgenic mice encoding luciferase under control of EpRE from the thioredoxin promoter. We found that 18 of 31 phytochemicals and 10 of 14 dietary plant extracts induced EpRE activity in liver HepG2 cells. Surprisingly, some dietary plant extracts showed profound inducing capability as compared to pure compounds indicating combinatorial effects of compounds found in whole foods. Furthermore, intraperitoneal injections of carnosol, curcumin and tert benzohydroquinine induced EpRE-dependent promoter activity in transgenic mice. In further experiments with curcumin, we found highly induced EpRE activity in intestine, liver, kidney and spleen. Finally, a combination extract made of coffee, thyme, broccoli, rosemary, turmeric and red onion fed orally, induced EpRE mediated luciferase in lung and adipose tissue. CONCLUSION: These results show that plant-based foods contain compounds that can be absorbed and induce the antioxidant defence in a living organism in an organ-specific manner.

Extract of oregano, coffee, thyme, clove, and walnuts inhibits NF-kappaB in monocytes and in transgenic reporter mice.

The transcription factor NF-kappaB is a promising target for chemoprevention. Several dietary plants are efficient inhibitors of NF-kappaB activation in vitro and could act synergistically on the NF-kappaB signaling pathway. In this study, we tested whether dietary plant extracts could inhibit NF-kappaB activation in a synergistic manner in vitro. Second, we investigated the potency of the same dietary plant extracts in the inhibition of NF-kappaB activation in vivo. A combined extract of clove, oregano, thyme, walnuts, and coffee synergistically inhibited lipopolysaccaride (LPS)-induced NF-kappaB activation in a monocytic cell line, compared with the sum of effects from the single extracts. Transgenic NF-kappaB luciferase reporter mice were given a single dose of the combined extract and subsequently challenged with LPS. NF-kappaB activation was monitored by in vivo imaging for 6 hours. In addition, NF-kappaB activity in organs and the expression of immune-related genes in liver were investigated. Based on the area under the curve, the extract decreased whole body LPS-induced NF-kappaB activity the first 6 hours by 35% compared with control mice. Organ-specific NF-kappaB activation was inhibited in intestine, liver, testis, and epididymis of the mice receiving the combination extract. In addition, dietary plants reduced the expression of genes related to inflammation, cell migration, and proliferation in liver. This study shows that dietary plants may be potent modulators of NF-kappaB signaling both in vitro and in vivo, and thus support further investigation of consumption of these plant foods as part of a healthy diet or as a mode of chemoprevention.