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Environmental Research Jan 2021Environmental (and occupational) exposure to neurotoxic substances is a worldwide problem that can affect children's neurodevelopment (ND). In Latin American and... (Review)
Review
Environmental (and occupational) exposure to neurotoxic substances is a worldwide problem that can affect children's neurodevelopment (ND). In Latin American and Caribbean (LAC) countries there are over 300 million children living under the threat of neurodevelopmental delays due to toxic environmental exposure. Large industrial centers, intense mining and agricultural activities, along with changing complex ecosystems constitute a mosaic that drives contamination of air, water and the food chain. Neurotoxic contaminants such as pesticides (organochlorines, organophosphates, carbamates, pyrethroids, neonicotinoids, and manganese fungicides), chemicals of industrial use (phthalates), and metals (Hg, Pb, Al, As, F, Cd, Mo, Mn) are at the center of environmental exposure studies. Exposure to neurotoxic substances singly or in combination with other compounds or socioeconomic stressors (maternal education, socio-economic and nutritional status) intertwined with occupational and para-occupational exposure can affect ND (motor, cognition, behavior) of children. Significant negative effects of pesticides and neurotoxic elements on ND were found in all studied countries, affecting especially the less-privileged children from laboring families. Studies showed that exposures to the neurotoxicants in human milk are secondary to their more lasting effects during prenatal exposure. This review integrates exposure (prenatal and breastfeeding), metabolism, and ND effects of neurotoxicants. It highlights the overwhelming evidence showing that current levels of exposures are hazardous and detrimental to children's ND in LAC countries. The evidence indicates that a reduction in neurotoxicant exposure is essential to protect children's ND. Therefore, it is urgent to adopt policies and actions that prevent and remediate region-specific children's ND issues.
Topics: Caribbean Region; Child; Ecosystem; Environmental Exposure; Female; Humans; Latin America; Milk, Human; Pregnancy
PubMed: 32941839
DOI: 10.1016/j.envres.2020.110199 -
The Journal of Infectious Diseases Nov 2023Poor sleep health is an underrecognized health challenge, especially for people with human immunodeficiency virus (HIV). Gut microbiota related to sleep are...
BACKGROUND
Poor sleep health is an underrecognized health challenge, especially for people with human immunodeficiency virus (HIV). Gut microbiota related to sleep are underinvestigated.
METHODS
The IDOze microbiota substudy included 190 women (114 with HIV and 76 without HIV). Wrist actigraphy measured total sleep duration, sleep efficiency, number of wake bouts, wake after sleep onset, fragmentation index, and sleep timing. 16S rRNA gene sequencing identified gut microbial genera. Analysis of compositions of microbiomes with bias correction was used to investigate cross-sectional associations between gut microbiota and sleep. Abundances of sleep-related gut microbial genera were compared between women with and without HIV.
RESULTS
Enrichment of 7 short-chain fatty acid-producing genera (eg, Butyricimonas, Roseburia, and Blautia) was associated with lower fragmentation index. Enrichment of 9 genera (eg, Dorea) was associated with lower sleep efficiency and/or more wake after sleep onset. Enrichment of proinflammatory Acidaminococcus was associated with late sleep midpoint and offset time. These associations were largely consistent regardless of HIV status. The abundance of Butyricimonas was lower among women with HIV compared to those without HIV.
CONCLUSIONS
Seventeen genera were identified to be associated with sleep continuity or timing. Butyricimonas, a potentially beneficial genus associated with sleep continuity, was less abundant among women with HIV.
Topics: Humans; Female; Gastrointestinal Microbiome; RNA, Ribosomal, 16S; Cross-Sectional Studies; HIV Infections; Sleep; HIV
PubMed: 37650624
DOI: 10.1093/infdis/jiad371 -
European Journal of Nuclear Medicine... Apr 2023Radioactive iodine (I) therapy is a conventional post-surgery treatment widely used for papillary thyroid carcinoma (PTC). Since I is orally administered, we hypothesize...
PURPOSE
Radioactive iodine (I) therapy is a conventional post-surgery treatment widely used for papillary thyroid carcinoma (PTC). Since I is orally administered, we hypothesize that it may affect gut microbiome. This study aims to investigate alterations of intestinal microbiome caused by I therapy in PTC patients and explore its association with response to I therapy.
METHODS
Fecal samples of 60 PTC patients pre- and post-I therapy were collected to characterize the I therapy-induced gut microbiota alterations using 16S rRNA gene sequencing. According to the inclusion criteria, sequence data of 40 out of the 60 patients, divided into excellent response (ER) group and non-excellent response (NER) group, were recruited to investigate the possible connection between gut microbiota and response to I therapy. Multivariate binary logistic regression was employed to construct a predictive model for response to I therapy.
RESULTS
Microbial richness, diversity, and composition were tremendously altered by I therapy. A significant decline of Firmicutes to Bacteroides (F/B) ratio was observed post-I therapy. I therapy also led to changes of gut microbiome-related metabolic pathways. Discrepancies in β diversity were found between ER and NER groups both pre- and post-I therapy. Furthermore, a predictive model for response to I therapy with a p value of 0.003 and an overall percentage correct of 80.0% was established, with three variables including lymph node metastasis, relative abundance of g_Bifidobacterium and g_Dorea. Among them, g_Dorea was identified to be an in independent predictor of response to I therapy (p = 0.04).
CONCLUSION
For the first time, the present study demonstrates the gut microbial dysbiosis caused by I therapy in post-surgery PTC patients and reveals a previously undefined role of gut microbiome as predictor for I ablation response. G_Dorea and g_Bifidobacterium may be potential targets for clinical intervention to improve response to I in post-operative PTC patients.
TRIAL REGISTRATION
ChiCTR2100048000. Registered 28 June 2021.
Topics: Humans; Gastrointestinal Microbiome; Iodine Radioisotopes; Thyroid Cancer, Papillary; RNA, Ribosomal, 16S; Thyroid Neoplasms
PubMed: 36512067
DOI: 10.1007/s00259-022-06072-5 -
Environmental Research Sep 2020Aluminum and mercury are environmentally ubiquitous. Individually they are both neurotoxic elements with shared neuro-pathogenic pathways: oxidative stress, altered... (Review)
Review
Aluminum and mercury are environmentally ubiquitous. Individually they are both neurotoxic elements with shared neuro-pathogenic pathways: oxidative stress, altered neurotransmission, and disruption of the neuroendocrine and immune systems. In the infant, Al and Hg differ in type of exposure, absorption, distribution (brain access), and metabolism. In environmentally associated exposure (breast milk and infant formulas) their co-occurrences fluctuate randomly, but in Thimerosal-containing vaccines (TCVs) they occur combined in a proprietary ratio; in these cases, low-doses of Thimerosal-ethylmercury (EtHg) and adjuvant-Al present the most widespread binary mixture in less developed countries. Although experimental studies at low doses of the binary Hg and Al mixture are rare, when studied individually they have been shown to affect neurological outcomes negatively. In invitro systems, comparative neurotoxicity between Al and Hg varies in relation to the measured parameters but seems less for Al than for Hg. While neurotoxicity of environmental Hg (mainly fish methyl-Hg, MeHg) is associated with neurobehavioral outcomes in children, environmental Al is not associated, except in certain clinical conditions. Therefore, the issues of their neurotoxic effects (singly or combined) are discussed. In the infant (up to six months) the organic-Hg and Al body burdens from a full TCV schedule are estimated to reach levels higher than that originating from breastfeeding or from high aluminum soy-based formulas. Despite worldwide exposure to both Al and Hg (inorganic Hg, MeHg, and Thimerosal/EtHg), our knowledge on this combined exposure is insufficient to predict their combined neurotoxic effects (and with other co-occurring neurotoxicants).
Topics: Aluminum; Animals; Body Burden; Child; Female; Humans; Infant; Mercury; Methylmercury Compounds; Milk, Human; Neurotoxicity Syndromes; Thimerosal; Vaccines
PubMed: 32544722
DOI: 10.1016/j.envres.2020.109734 -
Exposure to mercury during the first six months via human milk and vaccines: modifying risk factors.American Journal of Perinatology Aug 2007Breastfeeding is the best natural protection infants have against morbidity and mortality, and the development of safe and effective vaccines has made it possible to... (Review)
Review
Breastfeeding is the best natural protection infants have against morbidity and mortality, and the development of safe and effective vaccines has made it possible to immunize children against infectious disease. Both of these mechanisms for ensuring good health in children may be compromised by contact with mercury (Hg). Maternal exposure to environmental Hg during pregnancy can predispose nursing children to neurodevelopmental disorders. Despite the World Health Organization assurance that thimerosal-preserved vaccines are safe to use in infants, the United States, the European Union, and dozens of other countries have eliminated thimerosal as a vaccine preservative and stopped the immunization of children with such vaccines. Because of the increase in environmental pollution and the need to produce cheap and safe vaccines, there is a need to address the uncertainty of vaccine-ethylmercury risk of toxicity and Hg exposure during breastfeeding.
Topics: Breast Feeding; Central Nervous System; Dose-Response Relationship, Drug; Ethylmercury Compounds; Female; Humans; Infant; Infant, Newborn; Infant, Premature; Maternal Exposure; Mercury; Milk, Human; Preservatives, Pharmaceutical; Risk Factors; Thimerosal; Vaccines
PubMed: 17564957
DOI: 10.1055/s-2007-982074 -
Frontiers in Aging Neuroscience 2023Gut-brain axis might play an important role in cognitive impairments by various diseases including Alzheimer's disease (AD).
BACKGROUND
Gut-brain axis might play an important role in cognitive impairments by various diseases including Alzheimer's disease (AD).
OBJECTIVE
To investigate the differences in gut microbial composition, intestinal barrier function, and systemic inflammation in patients with AD or mild cognitive impairment (MCI), and normal control (NC) cases.
METHODS
A total of 118 subjects (45 AD, 38 MCI, and 35 NC) were recruited. Cognitive function was assessed using Mini-Mental State Examination (MMSE), and Montreal Cognitive Assessment Scale (MoCA). Functional ability was assessed using Activity of Daily Living Scale (ADL). The composition of gut microbiome was examined by 16S rRNA high-throughput sequencing. Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) was used to predict functional transfer of gut microbiota. Gut barrier dysfunction was evaluated by measuring the levels of diamine oxidase (DAO), D-lactic acid (DA), and endotoxin (ET). The serum high-sensitivity C-reactive protein (hs-CRP) level was used to indicate systemic inflammation.
RESULTS
Compared with normal controls, patients with cognitive impairments (AD and MCI) had lower abundance of and higher levels of DAO, DA, and ET. Kyoto Encyclopedia of Genes and Genomes (KEGG) results showed that the pathways related to glycan biosynthesis and metabolism increased in MCI patients, while the ones related to membrane transport decreased. The abundance of and was negatively correlated with the content of ET, and positively correlated with the scores of MMSE and MoCA. The hs-CRP levels were similar among the three groups. A significant negative correlation was observed between the severity of gut barrier dysfunction and cognitive function.
CONCLUSION
Cognitive impairments might be associated with gut microbial dysbiosis and intestinal barrier dysfunction.
PubMed: 37350810
DOI: 10.3389/fnagi.2023.1174599 -
Diabetes Dec 2023Prediabetes is a metabolic condition associated with gut microbiome composition, although mechanisms remain elusive. We searched for fecal metabolites, a readout of gut...
UNLABELLED
Prediabetes is a metabolic condition associated with gut microbiome composition, although mechanisms remain elusive. We searched for fecal metabolites, a readout of gut microbiome function, associated with impaired fasting glucose (IFG) in 142 individuals with IFG and 1,105 healthy individuals from the UK Adult Twin Registry (TwinsUK). We used the Cooperative Health Research in the Region of Augsburg (KORA) cohort (318 IFG individuals, 689 healthy individuals) to replicate our findings. We linearly combined eight IFG-positively associated metabolites (1-methylxantine, nicotinate, glucuronate, uridine, cholesterol, serine, caffeine, and protoporphyrin IX) into an IFG-metabolite score, which was significantly associated with higher odds ratios (ORs) for IFG (TwinsUK: OR 3.9 [95% CI 3.02-5.02], P < 0.0001, KORA: OR 1.3 [95% CI 1.16-1.52], P < 0.0001) and incident type 2 diabetes (T2D; TwinsUK: hazard ratio 4 [95% CI 1.97-8], P = 0.0002). Although these are host-produced metabolites, we found that the gut microbiome is strongly associated with their fecal levels (area under the curve >70%). Abundances of Faecalibacillus intestinalis, Dorea formicigenerans, Ruminococcus torques, and Dorea sp. AF24-7LB were positively associated with IFG, and such associations were partially mediated by 1-methylxanthine and nicotinate (variance accounted for mean 14.4% [SD 5.1], P < 0.05). Our results suggest that the gut microbiome is linked to prediabetes not only via the production of microbial metabolites but also by affecting intestinal absorption/excretion of host-produced metabolites and xenobiotics, which are correlated with the risk of IFG. Fecal metabolites enable modeling of another mechanism of gut microbiome effect on prediabetes and T2D onset.
ARTICLE HIGHLIGHTS
Prediabetes is a metabolic condition associated with gut microbiome composition, although mechanisms remain elusive. We investigated whether there is a fecal metabolite signature of impaired fasting glucose (IFG) and the possible underlying mechanisms of action. We identified a fecal metabolite signature of IFG associated with prevalent IFG in two independent cohorts and incident type 2 diabetes in a subanalysis. Although the signature consists of metabolites of nonmicrobial origin, it is strongly correlated with gut microbiome composition. Fecal metabolites enable modeling of another mechanism of gut microbiome effect on prediabetes by affecting intestinal absorption or excretion of host compounds and xenobiotics.
Topics: Adult; Humans; Prediabetic State; Diabetes Mellitus, Type 2; Niacin; Fasting; Glucose; Blood Glucose
PubMed: 37699401
DOI: 10.2337/db23-0170 -
Advances in Neurotoxicology 2018The toxicology of mercury (Hg) is of concern since this metal is ubiquitously distributed in the environment, and living organisms are routinely exposed to Hg at low to...
The toxicology of mercury (Hg) is of concern since this metal is ubiquitously distributed in the environment, and living organisms are routinely exposed to Hg at low to high levels. The toxic effects of Hg are well studied and it is known that they may differ depending on the Hg chemical species. In this chapter, we emphasize the neurotoxic effects of Hg during brain development. The immature brain is more susceptible to Hg exposure, since all the Hg chemical forms, not only the organic ones, can harm it. The possible consequences of Hg exposure during the early stages of development, the additive effects with other co-occurring neurotoxicants, and the known mechanisms of action and targets will be addressed in this chapter.
PubMed: 32346667
DOI: 10.1016/bs.ant.2018.03.005 -
Journal of Personalized Medicine Dec 2020Obesity is a major risk factor for developing gallstone disease (GSD). Previous studies have shown that obesity is associated with an elevated ratio in the gut... (Review)
Review
Obesity is a major risk factor for developing gallstone disease (GSD). Previous studies have shown that obesity is associated with an elevated ratio in the gut microbiota. These findings suggest that the development of GSD may be related to gut dysbiosis. This review presents and summarizes the recent findings of studies on the gut microbiota in patients with GSD. Most of the studies on the gut microbiota in patients with GSD have shown a significant increase in the phyla (Lactobacillaceae family, genera , , , , , , and ), ( genus), , (genera , , and ) and a significant decrease in the phyla (family , and genera , , , , ), (genera , , , and ), ( genus), and ( genus). The influence of GSD on microbial diversity is not clear. Some studies report that GSD reduces microbial diversity in the bile, whereas others suggest the increase in microbial diversity in the bile of patients with GSD. The phyla (especially family ) and ( genus) are most commonly detected in the bile of patients with GSD. On the other hand, the composition of bile microbiota in patients with GSD shows considerable inter-individual variability. The impact of GSD on the / ratio is unclear and reports are contradictory. For this reason, it should be stated that the results of reviewed studies do not allow for drawing unequivocal conclusions regarding the relationship between GSD and the / ratio in the microbiota.
PubMed: 33375615
DOI: 10.3390/jpm11010013 -
Clinical Nutrition (Edinburgh, Scotland) Jun 2006Mercury and lead are toxic metals widely spread in the environment with bio-accumulative features that raises public health concerns. Both metals are equally dispersed... (Review)
Review
Mercury and lead are toxic metals widely spread in the environment with bio-accumulative features that raises public health concerns. Both metals are equally dispersed in the human food chain but exposure and risk of toxicity during early human development are modulated by the diet and nutritional status. Understanding how Hg and Pb occur and interact with nutrients is fundamental to establish guidelines for diminishing exposure and the risk of toxicity. The risk of fetal and infant exposure to Hg can be influenced by maternal amalgam filling (inorganic Hg) and fish consumption (monomethyl Hg), whereas the risk of exposure to Pb is complex: maternal absorption depends on nutrient interactions (Ca and P); and maternal body Pb accumulation responds to all factors known to interact with bone and calcium metabolism. Maternal exposure to Hg and Pb is more important during fetal development than during breastfeeding. Moreover, these metals (especially Pb) are frequently higher in infant formulas which do not carry the nutritional and psychological advantages and protection of breastfeeding. Infant's reference dose is lower for Hg than for Pb, but risk of Pb contamination for fetuses and infant (breast- or formula-fed) is higher and lasts longer than Hg. Breastfeeding is essential to complete infant development. Interruption or suppression of breast-feeding with cow's milk-based formulas is not an option to environmental pollution.
Topics: Breast Feeding; Calcium, Dietary; Diet; Environmental Exposure; Female; Fetal Development; Humans; Infant Formula; Infant, Newborn; Lead; Maternal-Fetal Exchange; Mercury; Nutritional Status; Pregnancy
PubMed: 16307830
DOI: 10.1016/j.clnu.2005.10.007