RESUMO
While weight gain is common following migration to a new country and Mexican Americans have a disparate prevalence of overweight and obesity. In particular, Mexican American women have one of the world's highest rates of Metabolic Syndrome (MetS), characterized by abdominal obesity, insulin resistance, hypertension, and dyslipidemia, all of which increase the risk for atherosclerotic cardiovascular disease (CVD). Although the etiology of this dilemma is not well understood, using the framework of allostatic load (AL), we posit that exposure to multiple physiologic, psychosocial and environmental stressors over the course of the lifespan may contribute to an increased risk of MetS among indigenous Mexican immigrant women. Two such frequently overlooked stressors are: 1) a history of childhood growth stunting (CGS) and 2) dietary changes post migration that result in decreased diversity of the gut microbiome (dysbiosis). To date, little is known about how migration experiences differentially affect the relationship between CGS and MetS in adulthood. The purpose of this theoretical article is to present a proposed model of how early life stressors (ELS), specifically CGS, may interact with insalubrious aspects of the immigration experience to promote an increased risk for MetS among indigenous Mexican immigrant women. This model may be used in a bi-national effort to guide intervention efforts to decrease CGS in Mexico and to prevent, monitor or delay the components of MetS post migration in the US.
Assuntos
Disbiose/epidemiologia , Disbiose/fisiopatologia , Emigrantes e Imigrantes/estatística & dados numéricos , Transtornos do Crescimento/fisiopatologia , Povos Indígenas/estatística & dados numéricos , Síndrome Metabólica/epidemiologia , Síndrome Metabólica/fisiopatologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Feminino , Humanos , México/epidemiologia , Pessoa de Meia-Idade , Prevalência , Estados Unidos/epidemiologiaRESUMO
Periodontal disease (PD) comprises a group of diseases involving inflammatory aspects of the host and dysbiotic events that affect periodontal tissues and could have systemic implications. Diverse factors and comorbidities have been closely associated with PD such as diabetes, obesity, aging, hypertension, and so on; although, underlying mechanisms or causal associations have not been established completely. Interestingly, these same factors have been widely associated with progression or severe coronavirus disease 2019 (COVID-19), an illness caused by coronavirus SARS-CoV-2. Since inflammatory and dysbiotic factors as well as comorbidities affect systemic health, it is possible that periodontal status indicates the risk of complication of COVID-19. However, assessment of oral health history including periodontal status in COVID-19 patients has not been reported. Knowing PD is associated with severe COVID-19 could help identify risk groups and establish pertinent recommendations.
Assuntos
COVID-19/epidemiologia , Pandemias , Doenças Periodontais/epidemiologia , Fatores Etários , Artrite Reumatoide/epidemiologia , Doenças Cardiovasculares/epidemiologia , Comorbidade , Diabetes Mellitus/epidemiologia , Progressão da Doença , Suscetibilidade a Doenças , Disbiose/epidemiologia , Feminino , Infecções por HIV/epidemiologia , Humanos , Hepatopatias/epidemiologia , Masculino , Neoplasias/epidemiologia , Obesidade/epidemiologia , Doenças Periodontais/microbiologia , Gravidez , Complicações Infecciosas na Gravidez/epidemiologia , Transtornos Respiratórios/epidemiologia , Fatores de Risco , Fatores Sexuais , Fumar/epidemiologiaRESUMO
BACKGROUND: Asthma is the most prevalent chronic disease of childhood. Recently, we identified a critical window early in the life of both mice and Canadian infants during which gut microbial changes (dysbiosis) affect asthma development. Given geographic differences in human gut microbiota worldwide, we studied the effects of gut microbial dysbiosis on atopic wheeze in a population living in a distinct developing world environment. OBJECTIVE: We sought to determine whether microbial alterations in early infancy are associated with the development of atopic wheeze in a nonindustrialized setting. METHODS: We conducted a case-control study nested within a birth cohort from rural Ecuador in which we identified 27 children with atopic wheeze and 70 healthy control subjects at 5 years of age. We analyzed bacterial and eukaryotic gut microbiota in stool samples collected at 3 months of age using 16S and 18S sequencing. Bacterial metagenomes were predicted from 16S rRNA data by using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States and categorized by function with Kyoto Encyclopedia of Genes and Genomes ontology. Concentrations of fecal short-chain fatty acids were determined by using gas chromatography. RESULTS: As previously observed in Canadian infants, microbial dysbiosis at 3 months of age was associated with later development of atopic wheeze. However, the dysbiosis in Ecuadorian babies involved different bacterial taxa, was more pronounced, and also involved several fungal taxa. Predicted metagenomic analysis emphasized significant dysbiosis-associated differences in genes involved in carbohydrate and taurine metabolism. Levels of the fecal short-chain fatty acids acetate and caproate were reduced and increased, respectively, in the 3-month stool samples of children who went on to have atopic wheeze. CONCLUSIONS: Our findings support the importance of fungal and bacterial microbiota during the first 100 days of life on the development of atopic wheeze and provide additional support for considering modulation of the gut microbiome as a primary asthma prevention strategy.
Assuntos
Bactérias/genética , Disbiose/epidemiologia , Fezes/microbiologia , Fungos/fisiologia , Microbioma Gastrointestinal/genética , Hipersensibilidade Imediata/epidemiologia , Metabolismo dos Carboidratos , Estudos de Casos e Controles , Pré-Escolar , Estudos de Coortes , Equador/epidemiologia , Humanos , Lactente , RNA Ribossômico 16S/genética , Sons Respiratórios , População Rural , Taurina/metabolismoRESUMO
Sorghum is the fifth most produced cereal in the world and is a source of nutrients and bioactive compounds for the human diet. We summarize the recent findings concerning the nutrients and bioactive compounds of sorghum and its potential impact on human health, analyzing the limitations and positive points of the studies and proposing directions for future research. Sorghum is basically composed of starch, which is more slowly digested than that of other cereals, has low digestibility proteins and unsaturated lipids, and is a source of some minerals and vitamins. Furthermore, most sorghum varieties are rich in phenolic compounds, especially 3-deoxyanthocyanidins and tannins. The results obtained in vitro and in animals have shown that phenolics compounds and fat soluble compounds (polycosanols) isolated from sorghum benefit the gut microbiota and parameters related to obesity, oxidative stress, inflammation, diabetes, dyslipidemia, cancer, and hypertension. The effects of whole sorghum and its fractions on human health need to be evaluated. In conclusion, sorghum is a source of nutrients and bioactive compounds, especially 3-deoxyanthocyanidins, tannins, and polycosanols, which beneficially modulate, in vitro and in animals, parameters related to noncommunicable diseases. Studies should be conducted to evaluate the effects of different processing on protein and starch digestibility of sorghum as well as on the profile and bioavailability of its bioactive compounds, especially 3-deoxyanthocyanidins and tannins. Furthermore, the benefits resulting from the interaction of bioactive compounds in sorghum and human microbiota should be studied.
Assuntos
Produtos Agrícolas/química , Medicina Baseada em Evidências , Alimento Funcional/análise , Saúde Global , Sementes/química , Sorghum/química , Animais , Produtos Agrícolas/crescimento & desenvolvimento , Produtos Agrícolas/metabolismo , Digestão , Disbiose/epidemiologia , Disbiose/prevenção & controle , Dislipidemias/epidemiologia , Dislipidemias/prevenção & controle , Manipulação de Alimentos , Humanos , Hipertensão/epidemiologia , Hipertensão/prevenção & controle , Neoplasias/epidemiologia , Neoplasias/prevenção & controle , Valor Nutritivo , Estresse Oxidativo , Risco , Sementes/crescimento & desenvolvimento , Sementes/metabolismo , Sorghum/crescimento & desenvolvimento , Sorghum/metabolismo , Especificidade da EspécieRESUMO
Emerging evidence suggests that gut microbiota is critical in the maintenance of physiological homeostasis. This study was designed to test the hypothesis that dysbiosis in gut microbiota is associated with hypertension because genetic, environmental, and dietary factors profoundly influence both gut microbiota and blood pressure. Bacterial DNA from fecal samples of 2 rat models of hypertension and a small cohort of patients was used for bacterial genomic analysis. We observed a significant decrease in microbial richness, diversity, and evenness in the spontaneously hypertensive rat, in addition to an increased Firmicutes/Bacteroidetes ratio. These changes were accompanied by decreases in acetate- and butyrate-producing bacteria. In addition, the microbiota of a small cohort of human hypertensive patients was found to follow a similar dysbiotic pattern, as it was less rich and diverse than that of control subjects. Similar changes in gut microbiota were observed in the chronic angiotensin II infusion rat model, most notably decreased microbial richness and an increased Firmicutes/Bacteroidetes ratio. In this model, we evaluated the efficacy of oral minocycline in restoring gut microbiota. In addition to attenuating high blood pressure, minocycline was able to rebalance the dysbiotic hypertension gut microbiota by reducing the Firmicutes/Bacteroidetes ratio. These observations demonstrate that high blood pressure is associated with gut microbiota dysbiosis, both in animal and human hypertension. They suggest that dietary intervention to correct gut microbiota could be an innovative nutritional therapeutic strategy for hypertension.