Inverse association between intelligence quotient and urinary retinol binding protein in Chinese school-age children with low blood lead levels

AlphaCog

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Jan 28, 2014
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Highlights
• Urinary RBP is identified as a new factor associated with children IQ.
• Urinary RBP might act as effect biomarker of Mn, Cd and Se exposure.
• Low concentration of lead have a negative impact on children’s IQ.

Abstract
Objectives: Examine the relationship between blood lead concentration and children’s intelligence quotient (IQ) in Chinese children 8–12 years old. Participants and methods: This is a cross-sectional study, and participants included 446 children from three primary schools in Jiangsu, China. We collected environmental and genetic information from questionnaires. Blood lead (Pb), manganese (Mn), cadmium (Cd) and selenium (Se) concentrations were measured using inductively coupled plasma mass spectrometry (ICP-MS). IQ was assessed using the Combined Raven’s Test and then converted to a standard IQ score according to Chinese children’s norm. Morning urine samples were collected to measure retinol binding protein (RBP). Results: The average blood lead concentration was 33.13 μg L−1 (geometric mean), and the blood lead concentration (BoxCox transform) was inversely and significantly associated with IQ (r = −0.11, p = 0.02). The geometric mean of blood Mn, Cd and Se was 7.02 μg L−1, 0.18 μg L−1 and 94.77 μg L−1, respectively. Blood Mn, Cd and Se showed no association with IQ, but all of them associated with urinary RBP. Urinary RBP was identified as a new factor associated with IQ (β = −6.49, p = 0.011). Conclusions: Urinary RBP was recognized as a new indicated factor associated with children’s IQ. Mn, Cd and Se exposure might affect urinary RBP concentration and further IQ. Findings also support that blood lead concentrations in 8–12 years old children, even <44 μg L−1, have a negative association with IQ.
 

Overton

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Great find! Would be interesting to see if the plot is linear for all RBP levels or if it's an S Curve type effect, where lower amount shows a different association than higher RBP amounts.
 
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AlphaCog

AlphaCog

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Link between vitamin A and learning abilities established by team led by Salk researchers​

La Jolla, CA – Forget something lately? If so, perhaps you should try an extra helping of sweet potatoes or other vitamin A-rich foods on the holiday table.

Researchers at the Salk Institute for Biological Studies have discovered that vitamin A promotes learning, and they have provided the first evidence that the vitamin affects brain cell activity in a region linked to learning and memory.

The results, published in the current issue of the journal Neuron, underscores concerns about the consequences of vitamin A deficiency, estimated to affect 190 million children worldwide.

“We have long known that vitamin A is needed for proper development of the nervous system in a growing embryo,” said Ronald Evans, Salk professor and senior author of the study. “This is the first evidence that vitamin A is needed for brain function during life.”

Vitamin A has a variety of beneficial properties?in particular, its role in vision has been appreciated for many years. The vitamin exerts these effects by attaching to specific molecules called receptors that reside within cells, detect the vitamin’s presence, and help it to control complex genetic networks.

There is a family of receptors for vitamin A, and different combinations of family members are active in different tissues in the body. Investigators in Evans’ laboratory noticed that two of these receptors, named RARbeta and RXRgamma, were active in only a small number of cells, “and some of those cells happened to be in parts of the brain that had been implicated as important in learning and memory,” explained Ming-Yi Chiang, first author on the study. “This finding prompted us to think that these two receptors might affect the ability to learn.”

Chiang and her colleagues made “knockout” mice that lacked genes for the two brain-specific receptors. The brains of the mice appeared to be normal in structure, indicating that the lack of the receptors did not affect embryonic development of the brain. The mice developed normally but performed much more poorly than ordinary mice in standard intelligence tests.

“Since the wiring in these mice appeared to be normal, we decided to look at whether the cells were working properly,” said Evans.

To do this, they teamed up with investigators in two other Salk laboratories, headed by Professors Fred Gage and Charles Stevens. The Stevens group examined the ability of brain cells from the “knockout” mice to undergo a process widely believed to be critical for learning.

During learning, brain cells communicate with one another across small gaps called synapses. When an electrical impulse has traveled the length of a brain cell and reached the tip, a chemical messenger shoots across the gap and triggers an impulse in an adjacent cell. “Like runners in a relay,” said Stevens, “pathways of brain cells generate our thoughts and memories.”

But in a race, not all batons are passed equally well, and communication across synapses can also vary. In fact, learning is accompanied by well-defined changes in the efficiency with which messages cross synapses. “It’s as if the brain fine-tunes those pathways involved in learning a particular task or fact,” says Stevens.

The investigators found that brain cells from the hippocampus of the knockout mice, the brain region known to be important in learning and memory, do not have this ability to modify their synapses. “Therefore, we have an unexpected link between a common but essential nutrient, the capacity to learn, and the cellular circuits in the brain that control learning,” says Evans. “Together, the evidence suggests that vitamin A is a type of molecular key that unlocks one of the most powerful functions of the human brain.”

Salk co-investigators include Dinah Misner, Gerd Kemperman, Thomas Schikorski, and Professor Fred Gage. Evans and Stevens are Howard Hughes Medical Institute investigators. Evans is also March of Dimes Chair in Molecular Developmental Biology. The study was done in collaboration with Vincent Giguére at McGill University in Montreal and Henry M. Sucov at the University of Southern California School of Medicine.

The work was supported by the G. Harold and Leila Y. Mathers Foundation, the Robert Glenn Rapp Foundation and the National Institutes of Health.

The Salk Institute for Biological Studies, located in La Jolla, Calif., is an independent nonprofit institution dedicated to fundamental discoveries in the life sciences, the improvement of human health and conditions, and the training of future generations of researchers. The Institute was founded in 1960 by Jonas Salk, MD, with a gift of land from the City of San Diego and the financial support of the March of Dimes Birth Defects Foundation.
 
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AlphaCog

AlphaCog

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Significance of vitamin A to brain function, behavior and learning​

Abstract
Retinoid acid, the bioactive metabolite of vitamin A, is a potent signaling molecule in the brains of growing and adult animals, regulates numerous gene products, and modulates neurogenesis, neuronal survival and synaptic plasticity. Vitamin A deficiency (VAD) is a global health problem, yet our knowledge of its effects on behavior and learning is still emerging. Here we review studies that have implicated retinoids in learning and memory deficits of post-embryonic and adult rodent and songbird models. Dietary vitamin A supplementation improves learning and memory in VAD rodents and can ameliorate cognitive declines associated with normal aging. Songbird studies examine the effects of retinoid signaling on vocal/auditory learning and are uniquely suited to study the behavioral effects of VAD because the neural circuitry of the song system is discrete and well understood. Similar to human speech acquisition, avian vocal learning proceeds in well-defined stages of template acquisition, rendition and maturation. Local blockade of retinoic acid production in the brain or excess dietary retinoic acid results in the failure of song maturation, yet does not affect prior song acquisition. Together these results yield significant insights into the role of vitamin A in maintaining neuronal plasticity and cognitive function in adulthood.
 
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