Objective Explore the factors that could explain the differences of fatality rates among indigenous groups with COVID-19 diagnosis compared to the rest of the population in Mexico. Study design We analyzed the public data of COVID-19 surveillance, of the Mexican Ministry of Health, to estimate COVID-19 fatality rates by ethnicity. Methods We explored associated factors using Cox proportional hazards models stratified by outpatient and hospital management at diagnosis; analysis was conducted in three scenarios: national level, states with 89% of indigenous population, and South Pacific region. Results 412,017 COVID-19 cases were included, with 1.1% of indigenous population. Crude fatality rate per 1,000 person-weeks was 64.8% higher among indigenous than in non-indigenous (29.97 vs. 18.18, respectively), and it increased more than twice within outpatients (5.99 vs. 2.64). Cox analysis revealed that indigenous with outpatient management had higher fatality rate compared to non-indigenous outpatients; at national level (HR 1.63 95% CI 1.34-1.98), within the subgroup of 13 states (HR 1.66 95% CI 1.33-2.07), and South Pacific region (HR 2.35 95% CI 1.49-3.69). Factors associated with higher fatality rates among non-indigenous and indigenous outpatients were age, sex and comorbidities. Conclusions COVID-19 fatality is higher among indigenous populations, particularly within cases managed as outpatients.
Epidemiological studies have reported that the Mexican population is highly susceptible to dyslipidemia. The MARC1, ADCY5, and BCO1 genes have recently been involved in lipidic abnormalities. This study aimed to analyze the association of single nucleotide polymorphisms (SNPs) rs2642438, rs56371916, and rs6564851 on MARC1, ADCY5, and BCO1 genes, respectively, with the lipid profile in a cohort of Mexican adults. We included 1900 Mexican adults from the Health Workers Cohort Study. Demographic and clinical data were collected through a structured questionnaire and standardized procedures. Genotyping was performed using a predesigned TaqMan assay. A genetic risk score (GRS) was created on the basis of the three genetic variants. Associations analysis was estimated using linear and logistic regression. Our results showed that rs2642438-A and rs6564851-A alleles had a risk association for hypertriglyceridemia (OR = 1.57, p = 0.013; and OR = 1.33, p = 0.031, respectively), and rs56371916-C allele a trend for low HDL-c (OR = 1.27, p = 0.060) only in men. The GRS revealed a significant association for hypertriglyceridemia (OR = 2.23, p = 0.022). These findings provide evidence of an aggregate effect of the MARC1, ADCY5, and BCO1 variants on the risk of hypertriglyceridemia in Mexican men. This knowledge could represent a tool for identifying at-risk males who might benefit from early interventions and avoid secondary metabolic traits.
Background: Inconsistent epidemiological evidence between uric acid (UA) and bone mineral density (BMD) has been observed. Therefore, we evaluated the association between UA and BMD in Mexican adults. Methods: This analysis was conducted on 1423 participants from the Health Workers Cohort Study. We explored cross-sectional associations using linear regression and longitudinal associations using fixed-effects linear regression by sex and age groups (<45 and ≥45 years). Results: In females <45 years old, the cross-sectional analysis showed that UA levels were positively associated with total hip BMD. However, in the longitudinal analysis, we observed a negative association with the femoral neck and lumbar spine BMD. In contrast, in males <45 years old, we found an increase in total hip and femoral neck BMD in the groups with high levels of UA in the longitudinal association. On the other hand, in females ≥45 years old, we observed a longitudinal association between UA and loss of BMD at different sites. We did not observe an association between UA levels and BMD in males ≥45 years old. Conclusions: Our results suggest higher serum UA levels are associated with low BMD at different skeletal sites in Mexican females. Further studies are needed to delineate the underlying mechanisms behind this observation.
Previous studies have reported that the SIDT2 and ABCA1 genes are involved in lipid metabolism. We aimed to analyze the association—the gene x gene interaction between rs17120425 and rs1784042 on SIDT2 and rs9282541 on ABCA1 and their diet interaction on the HDL-c serum levels—in a cohort of 1982 Mexican adults from the Health Workers Cohort Study. Demographic and clinical data were collected through a structured questionnaire and standardized procedures. Genotyping was performed using a predesigned TaqMan assay. The associations and interactions of interest were estimated using linear and logistic regression. Carriers of the rs17120425-A and rs1784042-A alleles had slightly higher blood HDL-c levels compared to the non-carriers. In contrast, rs9282541-A was associated with low blood HDL-c levels (OR = 1.34, p = 0.013). The rs1784042 x rs9282541 interaction was associated with high blood HDL-c levels (p = 3.4 × 10−4). Premenopausal women who carried at least one rs17120425-A allele and consumed high dietary fat, protein, monounsaturated, or polyunsaturated fatty acids levels had higher HDL-c levels than the non-carriers. These results support the association between the genetic variants on SIDT2 and ABCA1 with HDL-c levels and suggest gene–gene and gene–diet interactions over HDL-c concentrations in Mexican adults. Our findings could be a platform for developing clinical and dietary strategies for improving the health of the Mexican population.
Osteoporosis is characterized by a decline in bone mineral density (BMD) and increased fracture risk. Free radicals and antioxidant systems play a central role in bone remodeling. This study was conducted to illustrate the role of oxidative-stress-related genes in BMD and osteoporosis. A systematic review was performed following the PRISMA guidelines. The search was computed in PubMed, Web of Sciences, Scopus, EBSCO, and BVS from inception to November 1st, 2022. The risk of bias was evaluated using the Joanna Briggs Institute Critical Appraisal Checklist tool. A total of 427 potentially eligible articles exploring this search question were detected. After removing duplicates (n = 112) and excluding irrelevant manuscripts based on screenings of their titles and abstracts (n = 317), 19 articles were selected for full-text review. Finally, 14 original articles were included in this systematic review after we applied the exclusion and inclusion criteria. Data analyzed in this systematic review indicated that oxidative-stress-related genetic polymorphisms are associated with BMD at different skeletal sites in diverse populations, influencing the risk of osteoporosis or osteoporotic fracture. However, it is necessary to look deep into their association with bone metabolism to determine if the findings can be translated into the clinical management of osteoporosis and its progression.
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