Originally published January 29 2014
Cadmium could have adverse effects on brain development, reducing neurogenesis
by L.J. Devon, Staff Writer
(NaturalNews) The EPA publicly states that cadmium toxicity through inhalation and oral exposure can cause developmental effects, such as low fetal weight, skeletal malformations, interference with fetal metabolism and impaired neurological development.
Researchers from the California Institute of Technology in Pasadena, CA, have found further molecular evidence showing how cadmium effects brain development and growth.
Major sources of cadmium According to the EPA, cadmium primarily enters the environment through the burning of oil and coal and the incineration of municipal waste. In the US, it is often obtained as a byproduct from the smelting of lead, copper and zinc ores. In manufacturing, cadmium is used in batteries, metal plating, pigments and plastics.
Smokers directly inhale cadmium into the lungs. Lab tests reveal that the bodies of smokers routinely contain twice as much cadmium than nonsmokers. Cadmium is a threat to everyone's food supply as well, especially in crops on which phosphate fertilizers were applied or in food connected to farms that use sewage sludge. The public can now see various cadmium levels in food products, available now at Labs.NaturalNews.com.
The most devastating effects of cadmium are on the kidneys and lungs. Chronic inhalation can create a buildup of cadmium in the kidneys, leading to kidney stone formation, proteinuria, decreased kidney filtration and even kidney disease. Smokers can burden themselves with cadmium and be more susceptible to bronchiolitis or emphysema.
How cadmium effects brain development of embryosWomen exposed to cadmium during pregnancy are at a higher risk of giving birth to children with low motor and perceptual abilities. Links have been made connecting cadmium body burden in young children to impaired school achievement. Researchers from Pasadena sought to study the molecular and cellular basis for these developmental setbacks in children exposed to cadmium.
In their study they investigated cadmium's role in causing neurological deficits during early embryonic stages in zebra fish. They examined the induction of neurogenesis, the regionalization of the neural tube, pattern formation, cell fate determination and also the survival of proneural genes.
In their research they found that zebra fish embryos developed a smaller head when given cadmium early on in the womb. Unclear boundaries were formed between the brain subdivisions of the embryonic fish, particularly in the mid-hindbrain region.
The normal anterior-to-posterior regionalization of the embryos was defected. This was altered due to cadmium's effect on the commitment of neural progenitor cells.
Furthermore, the researchers observed significant reductions in gene expression, particularly the proneuronal genes. Ngn1 genes were adversely arranged in cell clusters. Zash1a gene expression was less in the developing optic tectum, and the expression of zash1b was less in the telencephalon and tectum regions.
In the facial sensory ganglia region, embryos burdened with cadmium showed fewer differentiated neurons and glia because of reductions in the expression of the gene zn-12. The neurons also had lower transcription levels of specific genes, ngn1 and neuroD.
Throughout their research, a common theme of reduced neuron formation occurred, suggesting that cadmium-induced neurotoxicity is caused by impaired neurogenesis. Neurogenesis, which is the birth of neurons generally during prenatal growth, is essential for brain development. Impaired neurogenesis continually reduced neuronal differentiation and axonogenesis throughout zebra fish embryonic development.
In this study, the researchers attributed cadmium to a reduction in brain development, showing how gene expression can be reduced, ultimately affecting the growth and learning abilities of young life.
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