Chemicals banned decades ago linked to increased autism risk today

According to the research, children born after being exposed to the highest levels of certain compounds of the chemicals, called organochlorine chemicals, during their mother's pregnancy were roughly 80 percent more likely to be diagnosed with autism when compared to individuals with the very lowest levels of these chemicals. That also includes those who were completely unexposed.
Although production of organochlorine chemicals was banned in the United States in 1977, these compounds can remain in the environment and become absorbed in the fat of animals that humans eat, leading to exposure.
With that in mind, Kristen Lyall, ScD, assistant professor in Drexel University's A.J. Drexel Autism Institute, and her collaborators, decided to look at organochlorine chemicals during pregnancy since they can cross through the placenta and affect the fetus' neurodevelopment."


Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems Journal of Child Psychology and Psychiatry

Conduct problems (CP) and attention deficit hyperactivity disorder (ADHD) are often comorbid and have each been linked to ‘unhealthy diet’. Early-life diet also associates with DNA methylation of the insulin-like growth factor 2 gene (IGF2), involved in fetal and neural development. We investigated the degree to which prenatal high-fat and -sugar diet might relate to ADHD symptoms via IGF2 DNA methylation for early-onset persistent (EOP) versus low CP youth.
Methods

Participants were 164 youth with EOP (n = 83) versus low (n = 81) CP drawn from the Avon Longitudinal Study of Parents and Children. We assessed if the interrelationships between high-fat and -sugar diet (prenatal, postnatal), IGF2 methylation (birth and age 7, collected from blood), and ADHD symptoms (age 7–13) differed for EOP versus low CP youth.
Results

Prenatal ‘unhealthy diet’ was positively associated with IGF2 methylation at birth for both the EOP and low CP youth. For EOP only: (a) higher IGF2 methylation predicted ADHD symptoms; and (b) prenatal ‘unhealthy diet’ was associated with higher ADHD symptoms indirectly via higher IGF2 methylation.
Conclusions

Preventing ‘unhealthy diet’ in pregnancy might reduce the risk of ADHD symptoms in EOP youth via lower offspring IGF2 methylation."



'via Blog this'

Prenatal BPA exposure linked to anxiety and depression in boys -- ScienceDaily

Boys exposed prenatally to a common chemical used in plastics may be more likely to develop symptoms of anxiety and depression at age 10-12. The new study by researchers at the Columbia Center for Children's Environmental Health (CCCEH) within the Mailman School of Public Health examined early life exposure to the chemical Bisphenol A (BPA). Results are published in the journal Environmental Research.




Community water fluoridation predicts increase in age-adjusted incidence and prevalence of diabetes in 22 states from 2005 and 2010

Community water fluoridation is considered a significant public health achievement of the 20th century. In this paper, the hypothesis that added water fluoridation has contributed to diabetes incidence and prevalence in the United States was investigated. Panel data from publicly available sources was used with population-averaged models to test the associations of added and natural fluoride on the outcomes at the county level in 22 states in the years 2005 and 2010. The findings suggest that a 1 mg increase in the county mean added fluoride significantly positively predicts a 0.23 per 1,000 person increase in age-adjusted diabetes incidence (P < 0.001) and a 0.17% increase in age-adjusted diabetes prevalence percent (P < 0.001), while natural fluoride concentration is significantly protective. For counties using fluorosilicic acid as the chemical additive, both outcomes were lower: by 0.45 per 1,000 persons (P < 0.001) and 0.33% (P < 0.001), respectively. These findings are adjusted for county-level and time-varying changes in per capita tap water consumption, poverty, year, population density, age-adjusted obesity and physical inactivity and mean number of years since water fluoridation started. Sensitivity analyses revealed robust effects for both types of fluoride. Community water fluoridation is associated with epidemiological outcomes for diabetes."


Cat scratches, not bites, are associated with unipolar depression--cross-sectional study. - PubMed - NCBI

A recent study performed on 1.3 million patients showed a strong association between being bitten by a cat and probability of being diagnosed with depression. Authors suggested that infection with cat parasite Toxoplasma could be the reason for this association.


METHOD:
A cross sectional internet study on a non-clinical population of 5,535 subjects was undertaken.


RESULTS:
The subjects that reported having been bitten by a dog and a cat or scratched by a cat have higher Beck depression score. They were more likely to have visited psychiatrists, psychotherapists and neurologists in past two years, to have been previously diagnosed with depression (but not with bipolar disorder). Multivariate analysis of models with cat biting, cat scratching, toxoplasmosis, the number of cats at home, and the age of subjects as independent variables showed that only cat scratching had positive effect on depression (p = 0.004). Cat biting and toxoplasmosis had no effect on the depression, and the number of cats at home had a negative effect on depression (p = 0.021).

 CONCLUSIONS:
Absence of association between toxoplasmosis and depression and five times stronger association of depression with cat scratching than with cat biting suggests that the pathogen responsible for mood disorders in animals-injured subjects is probably not the protozoon Toxoplasma gondii but another organism; possibly the agent of cat-scratched disease - the bacteria Bartonella henselae."



'via Blog this'

Want to Survive Ebola? Perhaps Malaria Infection Can Help? | GEN News Highlights | GEN


Diet and exercise can reduce protein build-ups linked to Alzheimer's


Extracellular vesicles and viruses: Are they close relatives?

Extracellular vesicles (EVs) released by various cells are small phospholipid membrane-enclosed entities that can carry miRNA. They are now central to research in many fields of biology because they seem to constitute a new system of cell–cell communication. Physical and chemical characteristics of many EVs, as well as their biogenesis pathways, resemble those of retroviruses. Moreover, EVs generated by virus-infected cells can incorporate viral proteins and fragments of viral RNA, being thus indistinguishable from defective (noninfectious) retroviruses. EVs, depending on the proteins and genetic material incorporated in them, play a significant role in viral infection, both facilitating and suppressing it. Deciphering the mechanisms of EV-cell interactions may facilitate the design of EVs that inhibit viral infection and can be used as vehicles for targeted drug delivery."


Is acetaminophen in pregnancy linked to behavioral problems in offspring? - Medical News Today

The findings indicate that children born to women who used of acetaminophen (paracetamol) at 18 and 32 weeks of pregnancy were more likely to have behavioral problems and to be hyperactive. Those whose mothers used acetaminophen at 32 weeks of pregnancy were more likely to have emotional and other challenges.


Pubmed acetaminophen + autism or  acetaminophen + ADHD




Less Salmon, More Plaques? Link Between Omega-3s and Aβ Reinvigorates Fish Oil Debate | ALZFORUM

Omega-3 fatty acids as an intervention for Alzheimer’s disease may not be dead in the water just yet. A new study may reinvigorate interest in the fish oils. Researchers led by Helena Chui at the University of Southern California have used PET and MRI scans to correlate markers of Alzheimer’s disease with blood levels of the essential fatty acid docosahexaenoic acid (DHA). They report that people with the least amount of DHA have the most amyloid and atrophy in brain regions associated with AD. The findings, published August 8 in JAMA Neurology, do not prove that DHA blocks AD pathology, however they do mesh well with animal studies suggesting the fatty acid thwarts Aβ accumulation. “The … study has the potential to rekindle interest in the therapeutic potential of DHA,” wrote Joseph Quinn of Oregon Health & Sciences University in Portland in an editorial that accompanied the paper. Quinn headed a previous DHA clinical trial, but was not involved in the current study.

Unexpected role of interferon-γ in regulating neuronal connectivity and social behaviour : Nature

Immune dysfunction is commonly associated with several neurological and mental disorders. Although the mechanisms by which peripheral immunity may influence neuronal function are largely unknown, recent findings implicate meningeal immunity influencing behaviour, such as spatial learning and memory. Here we show that meningeal immunity is also critical for social behaviour; mice deficient in adaptive immunity exhibit social deficits and hyper-connectivity of fronto-cortical brain regions. Associations between rodent transcriptomes from brain and cellular transcriptomes in response to T-cell-derived cytokines suggest a strong interaction between social behaviour and interferon-γ (IFN-γ)-driven responses. Concordantly, we demonstrate that inhibitory neurons respond to IFN-γ and increase GABAergic (γ-aminobutyric-acid) currents in projection neurons, suggesting that IFN-γ is a molecular link between meningeal immunity and neural circuits recruited for social behaviour. Meta-analysis of the transcriptomes of a range of organisms reveals that rodents, fish, and flies elevate IFN-γ/JAK-STAT-dependent gene signatures in a social context, suggesting that the IFN-γ signalling pathway could mediate a co-evolutionary link between social/aggregation behaviour and an efficient anti-pathogen response. This study implicates adaptive immune dysfunction, in particular IFN-γ, in disorders characterized by social dysfunction and suggests a co-evolutionary link between social behaviour and an anti-pathogen immune response driven by IFN-γ signalling.

Autoantigen cross-reactive environmental antigen can trigger multiple sclerosis-like disease. - PubMed - NCBI

BACKGROUND:

Multiple sclerosis is generally considered an autoimmune disease resulting from interaction between predisposing genes and environmental factors, together allowing immunological self-tolerance to be compromised. The precise nature of the environmental inputs has been elusive, infectious agents having received considerable attention. A recent study generated an algorithm predicting naturally occurring T cell receptor (TCR) ligands from the proteome database. Taking the example of a multiple sclerosis patient-derived anti-myelin TCR, the study identified a number of stimulatory, cross-reactive peptide sequences from environmental and human antigens. Having previously generated a spontaneous multiple sclerosis (MS) model through expression of this TCR, we asked whether any of these could indeed function in vivo to trigger CNS disease by cross-reactive activation.

FINDINGS:

A number of myelin epitope cross-reactive epitopes could stimulate T cell immunity in this MS anti-myelin TCR transgenic model. Two of the most stimulatory of these 'environmental' epitopes, from Dictyostyelium slime mold and from Emiliania huxleyi, were tested for the ability to induce MS-like disease in the transgenics. We found that immunization with cross-reactive peptide from Dictyostyelium slime mold (but not from E. huxleyi) induces severe disease.

CONCLUSIONS:

These specific environmental epitopes are unlikely to be common triggers of MS, but this study suggests that our search for the cross-reactivity triggers of autoimmune activation leading to MS should encompass epitopes not just from the 'infectome' but also from the full environmental 'exposome.'

“Kissing Disease” Virus (Epstein-Barr virus) Promotes Malignant Breast Cancer Development | GEN News Highlights | GEN


Antibiotic-induced perturbations in gut microbial diversity influences neuro-inflammation and amyloidosis in a murine model of Alzheimer’s disease : Scientific Reports

Severe amyloidosis and plaque-localized neuro-inflammation are key pathological features of Alzheimer’s disease (AD). In addition to astrocyte and microglial reactivity, emerging evidence suggests a role of gut microbiota in regulating innate immunity and influencing brain function. Here, we examine the role of the host microbiome in regulating amyloidosis in the APPSWE/PS1ΔE9 mouse model of AD. We show that prolonged shifts in gut microbial composition and diversity induced by long-term broad-spectrum combinatorial antibiotic treatment regime decreases Aβ plaque deposition. We also show that levels of soluble Aβ are elevated and that levels of circulating cytokine and chemokine signatures are altered in this setting. Finally, we observe attenuated plaque-localised glial reactivity in these mice and significantly altered microglial morphology. These findings suggest the gut microbiota community diversity can regulate host innate immunity mechanisms that impact Aβ amyloidosis.

Herpes Simplex Virus Type 1 Neuronal Infection Elicits Cellular and Molecular Mechanisms of Neuroinflammation and Neurodegeneration in in vitro and in vivo Mice Models - IOS Press

Abstract: Herpes simplex virus type 1 (HSV-1) is a neurotropic virus able to establish a persistent latent infection in the host. Herpes simplex encephalitis (HSE) is associated with a high mortality rate and significant neurological, neuropsychological, and neurobehavioral sequelae, which afflict patients for life. Currently, it is unclear whether asymptomatic recurrent reactivations of HSV-1 occur in the central nervous systems in infected people, and if these events could lead to a progressive deterioration of neuronal function. In this context, HSV-1 constitutes an important candidate to be included among the risk factors for the development of Alzheimer’s disease. Our group have demonstrated that HSV-1 triggers neurodegenerative events in in vitro and in vivo induced neuronal infection, evidenced by increase in tau hyperphosphorylation and caspase-3 dependent cleavage of tau protein, resembling what occurs in neurodegenerative diseases. In addition, in an in vivo model, a reactivation episode during asymptomatic latency of HSV-1 infection in mice was accompanied by upregulation of neuroinflammatory markers (toll-like receptor-4, interferon α/β, and p-IRF3). Besides, previous reports have shown that HSV-1 inhibits apoptosis during early infection, but is pro-apoptotic during productive infection. Taking in consideration that the stress sensors AMPK and Sirt1 are involved in neuronal survival and neuroprotection, we hypothesized that HSV-1 could activate the AMPK/Sirt1 axis as a strategy to establish latency through inhibition of apoptosis and restoration of the energy status. Thus, we demonstrated that HSV-1 modulates the AMPK/Sirt1 axis differentially during infection, interfering with pro-apoptotic signaling and regulating mitochondrial biogenesis, pivotal processes in the lifetime of neurons in the central nervous system. In conclusion, our findings support the idea that HSV-1 could contribute to induce neurodegenerative processes in age-associated pathologies such as Alzheimer’s diseasAbstract: Herpes simplex virus type 1 (HSV-1) is a neurotropic virus able to establish a persistent latent infection in the host. Herpes simplex encephalitis (HSE) is associated with a high mortality rate and significant neurological, neuropsychological, and neurobehavioral sequelae, which afflict patients for life. Currently, it is unclear whether asymptomatic recurrent reactivations of HSV-1 occur in the central nervous systems in infected people, and if these events could lead to a progressive deterioration of neuronal function. In this context, HSV-1 constitutes an important candidate to be included among the risk factors for the development of Alzheimer’s disease. Our group have demonstrated that HSV-1 triggers neurodegenerative events in in vitro and in vivo induced neuronal infection, evidenced by increase in tau hyperphosphorylation and caspase-3 dependent cleavage of tau protein, resembling what occurs in neurodegenerative diseases. In addition, in an in vivo model, a reactivation episode during asymptomatic latency of HSV-1 infection in mice was accompanied by upregulation of neuroinflammatory markers (toll-like receptor-4, interferon α/β, and p-IRF3). Besides, previous reports have shown that HSV-1 inhibits apoptosis during early infection, but is pro-apoptotic during productive infection. Taking in consideration that the stress sensors AMPK and Sirt1 are involved in neuronal survival and neuroprotection, we hypothesized that HSV-1 could activate the AMPK/Sirt1 axis as a strategy to establish latency through inhibition of apoptosis and restoration of the energy status. Thus, we demonstrated that HSV-1 modulates the AMPK/Sirt1 axis differentially during infection, interfering with pro-apoptotic signaling and regulating mitochondrial biogenesis, pivotal processes in the lifetime of neurons in the central nervous system. In conclusion, our findings support the idea that HSV-1 could contribute to induce neurodegenerative processes in age-associated pathologies such as Alzheimer’s disease

Bacterial Amyloid and DNA are Important Constituents of Senile Plaques: Further Evidence of the Spirochetal and Biofilm Nature of Senile Plaques.

It has long been known that spirochetes form clumps or micro colonies in vitro and in vivo. Cortical spirochetal colonies in syphilitic dementia were considered as reproductive centers for spirochetes. Historic and recent data demonstrate that senile plaques in Alzheimer's disease (AD) are made up by spirochetes. Spirochetes, including Borrelia burgdorferi, are able to form biofilm in vitro. Senile plaques are also reported to contain elements of biofilm constituents. We expected that AβPP and Aβ (the main components of senile plaques) also occur in pure spirochetal biofilms, and bacterial DNA (an important component of biofilm) is also present in senile plaques. Histochemical, immunohistochemical, and in situ hybridization techniques and the TUNEL assay were used to answer these questions. The results obtained demonstrate that Aβ and DNA are key components of both pure spirochetal biofilms and senile plaques in AD and confirm the biofilm nature of senile plaques. These observations validate previous observations that AβPP and/or an AβPP-like amyloidogenic protein are an integral part of spirochetes, and indicate that bacterial amyloid is a constituent of senile plaques. DNA fragmentation in senile plaques further confirms their bacterial nature and provides biochemical evidence for spirochetal cell death. Spirochetes evade host defenses, locate intracellularly, form more resistant atypical forms and notably biofilms, which contribute to and sustain chronic infection and inflammation and explain the slowly progressive course of dementia in AD. To consider co-infecting microorganisms is equally important, as multi-species biofilms may result in a higher resistance to treatments and a more severe dementia.

Gut Bacteria Consumes Neurochemical (GABA) Linked To Depression

A recently-discovered strain of gut bacteria has been found to consume GABA, a neurochemical found in the brain. The neurotransmitter has a calming effect on the brain, and the bacteria’s reliance on GABA could explain how the microbiome has an effect on mood.
The bacterial species found in the gut – called KLE1738 – was found to grow in culture only when supplemented with GABA molecules. “Nothing made it grow, except GABA,” said Philip Strandwitz, a postdoctoral research associate from Northeastern University in Boston. Strandwitz and his colleagues presented their findings at the annual meeting of the American Society for Microbiology, in June.
This is the first time a bacterial species has been found which uses a neurotransmitter as an energy source. As GABA calms down brain activity by inhibiting signals between nerve cells, the researchers were surprised to find that it’s necessary for some microbial life.

Genetic risk for obesity grew stronger in 'obesogenic' environment

Lending support to the idea that high-calorie diets, sedentariness and other aspects of the contemporary American lifestyle may be driving the obesity epidemic, UC San Francisco researchers have found that people who carry greater genetic risk for obesity were more likely to have a higher body mass index if they were born later in the 20th century.

The study, published Tuesday, July 5 in JAMA, looked at 7,482 white and 1,306 black participants in the U.S. nationwide Health and Retirement Study who were born between 1900 and 1958. Researchers calculated a genetic risk score for each participant, based on whether they had any of 29 genetic variants that are associated with obesity, and looked to see how this score compared with their BMI.
The number of variants each person had did not increase in the population over time, while their effects on people did, pointing to environmental influences. 




Project TENDR: Targeting Environmental Neuro-Developmental Risks. The TENDR Consensus Statement

SUMMARY: Children in America today are at an unacceptably high risk of developing neurodevelopmental disorders that affect the brain and nervous system including autism, attention deficit hyperactivity disorder, intellectual disabilities, and other learning and behavioral disabilities. These are complex disorders with multiple causes—genetic, social, and environmental. The contribution of toxic chemicals to these disorders can be prevented.

APPROACH: Leading scientific and medical experts, along with children’s health advocates, came together in 2015 under the auspices of Project TENDR: Targeting Environmental Neuro-Developmental Risks to issue a call to action to reduce widespread exposures to chemicals that interfere with fetal and children’s brain development. Based on the available scientific evidence, the TENDR authors have identified prime examples of toxic chemicals and pollutants that increase children’s risks for neurodevelopmental disorders. These include chemicals that are used extensively in consumer products and that have become widespread in the environment. Some are chemicals to which children and pregnant women are regularly exposed, and they are detected in the bodies of virtually all Americans in national surveys conducted by the U.S. Centers for Disease Control and Prevention. The vast majority of chemicals in industrial and consumer products undergo almost no testing for developmental neurotoxicity or other health effects.

CONCLUSION: Based on these findings, we assert that the current system in the United States for evaluating scientific evidence and making health-based decisions about environmental chemicals is fundamentally broken. To help reduce the unacceptably high prevalence of neurodevelopmental disorders in our children, we must eliminate or significantly reduce exposures to chemicals that contribute to these conditions. We must adopt a new framework for assessing chemicals that have the potential to disrupt brain development and prevent the use of those that may pose a risk. This consensus statement lays the foundation for developing recommendations to monitor, assess, and reduce exposures to neurotoxic chemicals. These measures are urgently needed if we are to protect healthy brain development so that current and future generations can reach their fullest potential."



Multiple sclerosis patients have a distinct gut microbiota compared to healthy controls. - PubMed - NCBI

Multiple sclerosis (MS) is an immune-mediated disease, the etiology of which involves both genetic and environmental factors. The exact nature of the environmental factors responsible for predisposition to MS remains elusive; however, it's hypothesized that gastrointestinal microbiota might play an important role in pathogenesis of MS. Therefore, this study was designed to investigate whether gut microbiota are altered in MS by comparing the fecal microbiota in relapsing remitting MS (RRMS) (n = 31) patients to that of age- and gender-matched healthy controls (n = 36). Phylotype profiles of the gut microbial populations were generated using hypervariable tag sequencing of the V3-V5 region of the 16S ribosomal RNA gene. Detailed fecal microbiome analyses revealed that MS patients had distinct microbial community profile compared to healthy controls. We observed an increased abundance of Psuedomonas, Mycoplana, Haemophilus, Blautia, and Dorea genera in MS patients, whereas control group showed increased abundance of Parabacteroides, Adlercreutzia and Prevotella genera. Thus our study is consistent with the hypothesis that MS patients have gut microbial dysbiosis and further study is needed to better understand their role in the etiopathogenesis of MS.