Papers of the Month
By Nancy Lamontagne
Eating fish linked to better sleep and higher IQ in children
An NIEHS-funded study found that children who ate fish at least once a week slept better and had higher IQ scores than those who consumed fish less frequently or not at all. Other studies linked improved intelligence and better sleep with consumption of omega-3s — the fatty acids found in many types of fish. This study is one of the first to show that sleep may be the link between fish consumption and improved long-term brain function in children.
The new study is based on data from 541 children in China, from 9 to 11 years of age. The children completed a questionnaire about their fish consumption and took an IQ test. Their parents answered questions about sleep quality using a standardized questionnaire. The analysis controlled for factors such as parental education, occupation, and marital status, as well as the number of children in the home.
The researchers found that children who reported eating fish weekly scored 4.8 points higher on the IQ exam than those who seldom or never consumed fish. Those whose meals sometimes included fish scored 3.3 points higher. The study suggested that frequent fish consumption may improve sleep quality, which, in turn, leads to better long-term cognitive outcomes.
Citation: Liu J, Cui Y, Li L, Wu L, Hanlon A, Pinto-Martin J, Raine A, Hibbeln JR. 2017. The mediating role of sleep in the fish consumption - cognitive functioning relationship: a cohort study. Sci Rep 7(1):17961.
Air pollution linked with premature death in elderly
An NIEHS grantee and colleagues reported that short-term exposure to fine particulate air pollution and ozone was associated with a higher risk of premature death among older adults in the U.S. The new findings complement those from an earlier study that linked premature death with long-term exposure to the same pollutants.
For the new study, the researchers examined mortality data for everyone in the U.S. who was enrolled in Medicare from 2000 to 2012. The investigators assessed daily air pollution exposures using models that estimated levels of particulate matter less than 2.5 micrometers in size (PM2.5) and ozone for most of the U.S., including unmonitored areas.
By linking the deaths that occurred between 2000 and 2012 with air pollution data, the researchers found that for every 10 micrograms per cubic meter daily increase in PM2.5 and 10 parts per billion daily increase in warm-season ozone, the daily mortality rate increased by 1.05 percent and 0.51 percent, respectively. The data analysis also revealed that some populations were affected differently. Death rates linked with increased PM2.5 were higher for women, non-whites, and people who qualified for Medicaid. The increased risk of death occurred at PM2.5 and ozone levels below national air quality standards, suggesting that the standards may need to be reevaluated.
Citation: Di Q, Dai L, Wang Y, Zanobetti A, Choirat C, Schwartz JD, Dominici F. 2017. Association of short-term exposure to air pollution with mortality in older adults. JAMA 318(24):2446–2456.
RNA binding proteins and Alzheimer’s disease
Results from a new mouse study, funded in part by NIEHS, showed that RNA-binding proteins likely play a key role in the development of Alzheimer’s disease. The new findings reveal potential new therapeutic targets for the disease.
The brains of people with Alzheimer’s disease exhibit neurofibrillary tangles, or abnormal accumulations of the protein tau. The tangles are thought to injure neurons in a way that may lead to dementia. Using cultured cells, the researchers previously showed that reducing levels of an RNA-binding protein known as T-cell intracellular antigen 1 (TIA1) led to decreased tau accumulation. RNA-binding proteins help form the RNA-protein complexes that are important for DNA replication and regulating gene expression and RNA metabolism.
Building on the previous work, the researchers studied mice that modeled Alzheimer’s disease by accumulating tau in the brain. In these mice, reducing levels of TIA1 protected against neurodegeneration and prolonged survival although neurofibrillary tangles still increased. The team observed that reducing TIA1 decreased the amount of small tau clumps and increased the proportion of large tau clumps that generated neurofibrillary tangles and were less toxic. The study provided evidence that TIA1 plays a key role in mediating the toxicity of tau and suggest that RNA-binding proteins direct the pathway of tau aggregation and the neurodegeneration that follows. The new findings open many new therapeutic targets for exploration.
Citation: Apicco DJ, Ash PEA, Maziuk B, LeBlang C, Medalla M, Al Abdullatif A, Ferragud A, Botelho E, Ballance HI, Dhawan U, Boudeau S, Cruz AL, Kashy D, Wong A, Goldberg LR, Yazdani N, Zhang C, Ung CY, Tripodis Y, Kanaan NM, Ikezu T, Cottone P, Leszyk J, Li H, Luebke J, Bryant CD, Wolozin B. 2018. Reducing the RNA binding protein TIA1 protects against tau-mediated neurodegeneration in vivo. Nat Neurosci 21(1):72–80.
Obesogen shows transgenerational effects
In a new study, NIEHS grantees showed that early exposure to tributyltin (TBT) in mice can increase fat storage in their unexposed descendants. The new findings suggest that obesity involves more than a simple imbalance in calories taken in and those used.
TBT, an anti-fouling agent that is also formed during production of the plastic polyvinyl chloride, has been classified as an obesogen because it disrupts normal development and fat metabolism. The researchers used mice to find out if early life exposure to TBT could alter metabolism in a way that predisposed exposed mice and their descendants to store more fat. Female mice were exposed to TBT throughout pregnancy and lactation. Unexposed male descendants born three generations later were more prone to obesity when the fat in their diet was increased. The team found that the ancestral TBT exposure induced global changes in DNA methylation and altered expression of genes involved in metabolism. Further analyses suggested that ancestral TBT exposure induced changes in how DNA was packaged and that these changes could be passed onto offspring.
According to the researchers, the results point to a need to further study how obesogens may influence epigenetic changes that contribute to obesity in people.
Citation: Chamorro-Garcia R, Diaz-Castillo C, Shoucri BM, Kach H, Leavitt R, Shioda T, Blumberg B. 2017. Ancestral perinatal obesogen exposure results in a transgenerational thrifty phenotype in mice. Nat Commun 8(1):2012.