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Keywords = FFQ Norfolk food questionnaire

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38 pages, 3544 KiB  
Article
Combined Approach: FFQ, DII, Anthropometric, Biochemical and DNA Damage Parameters in Obese with BMI ≥ 35 kg m−2
by Mirta Milić, Ivan Ožvald, Katarina Matković, Hrvoje Radašević, Maja Nikolić, Dragan Božičević, Lidija Duh, Martina Matovinović and Martina Bituh
Nutrients 2023, 15(4), 899; https://doi.org/10.3390/nu15040899 - 10 Feb 2023
Cited by 1 | Viewed by 2988
Abstract
Although obesity with its comorbidities is linked with higher cancer risk, the data on genome stability in the obese/severely obese are scarce. This is the first study with three DNA damage assessment assays (Fpg-modified and alkaline comet assays and micronucleus cytome assay) performed [...] Read more.
Although obesity with its comorbidities is linked with higher cancer risk, the data on genome stability in the obese/severely obese are scarce. This is the first study with three DNA damage assessment assays (Fpg-modified and alkaline comet assays and micronucleus cytome assay) performed on a severely obese population (n = 53) where the results were compared with daily intake of food groups, nutrient intake, dietary inflammatory index (DII), and anthropometric and biochemical parameters usually measured in obese individuals. Results demonstrated the association between DNA damage levels and a decrease in cell proliferation with anthropometric measurements and the severity of obese status, together with elevated levels of urates, inorganic phosphates, chlorides, and hs troponin I levels. DII was connected with oxidative DNA damage, while BMI and basal metabolic rate (BMR) were associated with a decrease in cell proliferation and DNA damage creation. Measured daily BMR and calculated daily energy intake from the food frequency questionnaire (FFQ) demonstrated no significant difference (1792.80 vs. 1869.86 kcal day−1 mean values). Groups with higher DNA damage than expected (tail intensity in comet assay >9% and >12.4%, micronucleus frequency >13), consumed daily, weekly, and monthly more often some type of food groups, but differences did not show a clear influence on the elevated DNA damage levels. Combination of all three DNA damage assays demonstrated that some type of damage can start earlier in the obese individual lifespan, such as nuclear buds and nucleoplasmic bridges, then comes decrease in cell proliferation and then elevated micronucleus frequencies, and that primary DNA damage is not maybe crucial in the overweight, but in severely obese. Biochemically changed parameters pointed out that obesity can have an impact on changes in blood cell counts and division and also on genomic instability. Assays were able to demonstrate groups of sensitive individuals that should be further monitored for genomic instability and cancer prevention, especially when obesity is already connected with comorbidities, 13 different cancers, and a higher mortality risk with 7–10 disease-free years loss. In the future, both DNA damage and biochemical parameters should be combined with anthropometric ones for further obese monitoring, better insight into biological changes in the severely obese, and a more individual approach in therapy and treatment. Patients should also get a proper education about the foodstuff with pro- and anti-inflammatory effect. Full article
(This article belongs to the Section Nutrition and Public Health)
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Graphical abstract

Graphical abstract
Full article ">Figure 1
<p>Spearman correlations of MN—micronuclei, NB—nuclear buds, NPB—nucleoplasmic bridges and apoptosis in micronucleus <span class="html-italic">cytome</span> assay with inflammatory food index DII.</p>
Full article ">Figure 1 Cont.
<p>Spearman correlations of MN—micronuclei, NB—nuclear buds, NPB—nucleoplasmic bridges and apoptosis in micronucleus <span class="html-italic">cytome</span> assay with inflammatory food index DII.</p>
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<p>Spearman correlations of TI (%DNA in comet tail) in comet assay (no significant correlation) and Fpg comet assay with inflammatory food index DII.</p>
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<p>Calculated dietary inflammatory index (DII) on the individual level for all 53 individuals included in the study.</p>
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<p>Individual DNA damage for micronucleus <span class="html-italic">cytome</span> assay parameters: MN-micronucleus with a reference range up to 12.5 per 1000 binucleated BN cells; NB—nuclear buds with a reference range up to 5 per 1000 BN; NPB—nucleoplasmic bridges with reference range up to 10 per 1000 BN cells in a healthy human population.</p>
Full article ">Figure 5
<p>Individual DNA damage for Fpg and alkaline comet assay TI parameters. For Net Fpg TI, there is no reference value for oxidative damage; the mean value for the entire group was 6%. We demonstrated before that alive and healthy individuals have up to 9% of TI, cancer-free up to 12.4%, cancer cases 17.7%, and deceased 18%. The highest value in this study group was below 18% (tail intensity).</p>
Full article ">Figure 6
<p>Significant differences in biochemical parameters among groups with higher or lower DNA damage parameters in both comet and micronucleus <span class="html-italic">cytome</span> assay, Mann–Whitney U test, <span class="html-italic">p</span> ≤ 0.05.</p>
Full article ">Figure 6 Cont.
<p>Significant differences in biochemical parameters among groups with higher or lower DNA damage parameters in both comet and micronucleus <span class="html-italic">cytome</span> assay, Mann–Whitney U test, <span class="html-italic">p</span> ≤ 0.05.</p>
Full article ">Figure 7
<p>Stepwise regression model for DNA damage prediction of tail intensity (TI, %) values in alkaline comet and Fpg comet assay for obese group of people with BMI ≥ 35 kg m<sup>−2</sup> based on the biochemical and anthropometric parameters used in the study. Values are categorized by coefficient estimates for TI value prediction, while <span class="html-italic">p</span> values reflect the importance of each variable for model prediction. Negative values have negative correlation (red) and positive values have positive correlation with TI (blue) *—<span class="html-italic">p</span>-value &lt; 0.05, **—<span class="html-italic">p</span>-value &lt; 0.01, ***—<span class="html-italic">p</span>-value &lt; 0.001.</p>
Full article ">Figure 8
<p>Stepwise regression model for DNA damage prediction of micronucleus (MN), nuclear bud (NB) and nucleoplasmic bridge (NPB) frequency in MN <span class="html-italic">cytome</span> assay for obese group of people with BMI ≥35 kg m<sup>−2</sup> based on the biochemical and anthropometric parameters used in the study. Values are categorized by coefficient estimates for DNA damage prediction, while <span class="html-italic">p</span> values are responding to the importance of each variable for model prediction. Negative values have negative correlation (red) and positive values have positive correlation with TI (blue) *—<span class="html-italic">p</span>-value &lt; 0.05, **—<span class="html-italic">p</span>-value &lt; 0.01, ***—<span class="html-italic">p</span>-value &lt; 0.001.</p>
Full article ">
18 pages, 700 KiB  
Article
Diet in Scleroderma: Is There a Need for Intervention?
by Alexandra Maria Burlui, Anca Cardoneanu, Luana Andreea Macovei, Ciprian Rezus, Lucian Vasile Boiculese, Mariana Graur and Elena Rezus
Diagnostics 2021, 11(11), 2118; https://doi.org/10.3390/diagnostics11112118 - 15 Nov 2021
Cited by 9 | Viewed by 3656
Abstract
Systemic sclerosis (SSc) patients exhibit a plethora of risk factors for nutritional decline, including the presence of chronic inflammation and the progressive nature of disease-related multisystem involvement. The prevalence and consequences of nutritional decline in scleroderma are frequently underestimated, its management currently remaining [...] Read more.
Systemic sclerosis (SSc) patients exhibit a plethora of risk factors for nutritional decline, including the presence of chronic inflammation and the progressive nature of disease-related multisystem involvement. The prevalence and consequences of nutritional decline in scleroderma are frequently underestimated, its management currently remaining a subject of debate. The main objective of the present study was to perform a detailed assessment of scleroderma patients’ diet as well as their eating habits and to describe the relationships with weight loss and malnutrition risk in the absence of professional nutritional counseling. Methods: We used a translated and validated version of the EPIC-Norfolk FFQ (European Prospective Investigation into Cancer and Nutrition Norfolk Food Frequency Questionnaire) to evaluate the patients’ diet and MUST (Malnutrition Universal Screening Tool) to investigate the risk of malnutrition. Disease activity was estimated using the EUSTAR-AI (European Scleroderma Trials and Research group Activity Index). Results: We included 69 patients with SSc, of which 42 underwent a detailed dietary assessment. Dietary factors were connected to body composition and digestive symptoms. We found high sodium intake and frequent suboptimal energy consumption in our study group, including patients with cardiopulmonary involvement. Liver transaminases were inversely correlated with the consumption of nuts and seeds. Malnutrition and weight loss were significantly associated with pulmonary hypertension, heart failure, albumin levels, and the extent of skin fibrosis, but not advanced age. Although the patients with EUSTAR-AI ≥ 2.5 were more frequently included in the moderate and high malnutrition risk categories, these results did not reach statistical significance. Conclusions: Currently, there is an unmet need for longitudinal and interventional research focusing on the long-term significance, ramifications, and management of nutritional impairment in SSc patients with various clinical manifestations. Our results indicate that scleroderma patients could benefit from personalized nutritional counseling in an interdisciplinary setting. Full article
(This article belongs to the Special Issue Advances in Identification and Management of Systemic Sclerosis)
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Figure 1

Figure 1
<p>Flow diagram of the inclusion and exclusion processes leading up to the final study group.</p>
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<p>Macronutrient energy contributions with respect to malnutrition risk (MUST).</p>
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