Abstract INTRODUCTION Anemia is a public health problem worldwide and is most prevalent in preschool children, for whom it is the most frequent cause of nutritional deficits. In turn, iron deficiency is the main cause of anemia, affecting 43% of children globally. Previous studies in Cuba show rates of iron deficiency in preschool children between 38.6% and 57.6%, higher in infants (71.2% to 81.1%). WHO recommends using serum ferritin as an indicator of iron deficiency accompanied by acute (C-reactive protein) and chronic (α1-acid glycoprotein) inflammation biomarkers. OBJECTIVE Assess how inflammation affects measuring and reporting of iron-deficiency anemia rates in Cuban preschool children. METHODS Data were obtained from serum samples contained in the National Anemia and Iron Deficiency Survey, and included presumably healthy preschool Cuban children (aged 6–59 months). Serum samples were collected from 1375 children from randomly selected provinces in 4 regions of the country from 2014 through 2018. We examined the association between ferritin and two inflammatory biomarkers: C-reactive protein and α1-acid glycoprotein. Individual inflammation-adjusted ferritin concentrations were calculated using four approaches: 1) a higher ferritin cut-off point (<30 g/L); 2) exclusion of subjects showing inflammation (C-reactive protein >5 mg/L or α1-acid glycoprotein >1 g/L); 3) mathematical correction factor based on C-reactive protein or α1-acid glycoprotein; and 4) correction by regression with the method proposed by the Biomarkers Reflecting Inflammation and Nutritional Determinants of Anemia Group. We estimated confidence intervals of differences between unadjusted prevalence and prevalence adjusted for inflammation by each method. RESULTS The proportion of children with inflammation according to C-reactive protein concentrations >5 mg/L was lower (11.1%, 153/1375) than the proportion measured according to the concentrations of α1-acid glycoprotein, at >1 g/L (30.8%, 424/1375). The percentage of children with high concentrations of at least one of the aforementioned biomarkers was 32.7% (450/1375). Thus, each correction method increased the observed prevalence of iron deficiency compared to unadjusted estimates (23%, 316/1375). This increase was more pronounced when using the internal regression correction method (based only on C-reactive protein) or the method based on a higher cut-off point. Adjustment using all four methods changed estimated iron deficiency prevalence, increasing it from 0.1% to 8.8%, compared to unadjusted values. CONCLUSION One-third of preschool children had biomarkers indicating elevated inflammation levels. Without adjusting for inflammation, iron deficiency prevalence was underestimated. The significant disparity between unadjusted and inflammation-adjusted ferritin when using some approaches highlights the importance of selecting the right approach for accurate, corrected measurement. The internal regression correction approach is appropriate for epidemiological studies because it takes into account inflammation severity. However, other models should be explored that account for inflammation and also provide better adjusted ferritin concentrations.

ABSTRACT INTRODUCTION Age-related cognitive disorders, including Alzheimer disease, are among the main causes of disability and dependence in older adults worldwide. High blood homocysteine levels (hyperhomocysteinemia) are a risk factor for diseases whose metabolism involves different B vitamins. Antioxidant vitamins provide a protective effect by mitigating oxidative stress generated by these diseases. Epidemiological studies have presented varying results on the relationships between blood levels of these vitamins and such cognitive disorders. OBJECTIVE Evaluate the association of vitamin and homocysteine levels with mild cognitive impairment and Alzheimer disease in a group of Cuban older adults. METHODS A cross-sectional study was conducted in Havana, Cuba, of 424 persons aged ≥65 years: 43 with Alzheimer disease, 131 with mild cognitive impairment, and 250 with no signs of cognitive impairment. Dementia was diagnosed using criteria of the International 10/66 Dementia Research Group and Diagnostic and Statistical Manual of Mental Disorders (DSM IV), and mild cognitive impairment was diagnosed using Petersen’s criteria. Blood levels of vitamins (thiamine, B-2, folate, B-12, C and A) and homocysteine were measured by standard procedures. Analysis of variance for continuous variables and percentage comparison tests for dichotomous variables were used to compare groups. RESULTS Persons with Alzheimer disease presented significantly lower levels of vitamins B-2, C and A than healthy participants (p <0.05). Homocysteine levels were significantly higher in those with Alzheimer disease and mild cognitive impairment than in participants with no cognitive impairment (p <0.05). Statistically, levels of thiamine, folic acid, and vitamin B-12 were not significantly different across groups. Compared with those without cognitive impairment, prevalence rates (PR) in the Alzheimer group were significantly higher for hyperhomocysteinemia (PR = 3.26; 1.84–5.80) and deficiency of all B vitamins: thiamine (PR = 1.89; 1.04–3.43), B-2 (PR = 2.85; 1.54–5.26), folate (PR = 3.02; 1.53–5.95), B-12 (PR = 2.21; 1.17–4.19), vitamin C (PR = 3.88; 2.12–7.10) and A (PR = 5.47; 3.26–9.17). In mild cognitive impairment, prevalence rates were significantly higher for hyperhomocysteinemia (PR = 1.42; 1.08–1.87), vitamin B-2 deficiency (PR = 1.70; 1.24–2.32) and vitamin A deficiency (PR =1.88; 1.05–3.38). CONCLUSIONS Hyperhomocysteinemia and various vitamin deficiencies are related to Alzheimer disease and mild cognitive impairment. Longitudinal studies are needed to further elucidate the relationship between different nutritional biomarkers and dementia. A better understanding of this relationship could provide a basis for therapeutic and preventive strategies.