Combined Approach: FFQ, DII, Anthropometric, Biochemical and DNA Damage Parameters in Obese with BMI ≥ 35 kg m−2

Author:

Milić Mirta1ORCID,Ožvald Ivan23,Matković Katarina1ORCID,Radašević Hrvoje4,Nikolić Maja1,Božičević Dragan2,Duh Lidija2,Matovinović Martina5,Bituh Martina6ORCID

Affiliation:

1. Mutagenesis Unit, Institute for Medical Research and Occupational Health (IMROH), 10001 Zagreb, Croatia

2. Special Hospital for Extended Treatment of Duga Resa, 47250 Duga Resa, Croatia

3. Neuropsychiatric Hospital dr. Ivan Barbot of Popovača, 44317 Popovača, Croatia

4. Andrija Štampar Teaching Institute of Public Health, 10000 Zagreb, Croatia

5. Department of Internal Medicine, University Hospital Centre Zagreb, 10000 Zagreb, Croatia

6. Laboratory for Food Chemistry and Biochemistry, Faculty of Food Technology and Biotechnology, University of Zagreb, 10000 Zagreb, Croatia

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 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.

Funder

Special Hospital for Extended Treatment of Duga Resa

Institute for Medical Research and Occupational Health

Publisher

MDPI AG

Subject

Food Science,Nutrition and Dietetics

Reference74 articles.

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