Thursday, February 6, 2014

Vaccinate, yes - salt, maybe

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In this week's Science magazine, a study suggests that a buildup of chloride levels in rodent fetuses damages their developing neurons, and prevents a switch that moderates the extreme activity from engaging in newborns, thus triggering autistic behavior. The report focuses on the use of a chloride-lowering drug, bumetanide, that seems to be helpful even after the young have developed autistic symptoms.

Fifty or 60 years ago, doctors used to recommend that women cut out extra salt (sodium chloride) in their diet, to ease the swelling and risk of pre-eclampsia, but lately, doctors have advised women that they should stick to their regular diets during pregnancy - and we know how much salt is in fast food and processed foods. Is it too much? Could it be the trigger?

Anecdotally, my mother kept to a salt-free diet while she was pregnant with me and had no problems with delivery. When my dad returned from Japan, she couldn't keep to the salt restriction, and they had to use forceps to deliver my brother.

Growing up, we all had to be vaccinated, and many of those vaccinations, such as for small pox and polio, were done in school. I cannot recall any autistic kids, although I had several classmates with other mental disabilities.

I didn't have my first taste of McDonald's until I was in my teens. But we probably got plenty of salt from canned goods, sauerkraut, cured ham and sausages.

Although I suspect a link to high salt consumption and autism spectrum disorders, more study needs to be done. I don't have the same wariness of vaccination; the overwhelming good vaccines do outweighs the fear that they may do harm, and so far, scientific studies have not linked them to autism.

Here's the news release on the study:
A drug given to pregnant mice with models of autism prevents autistic behavior in their offspring, a new report shows, and though the drug could not be administered prenatally in humans (there is no way to screen for autism in human fetuses), clinical trials of this drug administered later in development, in young children who have already developed autistic symptoms, are showing progress. The causes of autism spectrum disorder, or ASD, are complex. Prolonged excitation of brain neurons seems partly to blame. Thus, GABA - the main inhibitory neurotransmitter in the brain - has drawn attention; GABA typically excites neurons in the brain of a growing fetus and then quiets them during birth, a switch mediated by oxytocin from the mother, and one that has a protective effect. But in autism, this switch doesn’t happen. The neurons remain excited because chloride - a key signaling molecule - builds to higher concentrations than it should. In the aforementioned clinical trials, a chloride-lowering drug called bumetanide appeared to have restored the GABA switch in children with ASD, reducing the severity of both autism and Asperger syndrome. To better understand if bumetanide affects the cellular processes that underlay the GABA switch in the way they believed it did (by lowering chloride levels), and to determine whether restoring the switch alone could reduce autistic symptoms, Roman Tyzio and colleagues (several of whom had been involved in the trials) studied two rodent models of autism. Oxytocin didn’t signal from mother to baby in the pregnant rodents, the researchers found, and as a result, chloride built to higher concentrations than it should have inside fetal neurons. By injecting the mothers with bumetanide, however, the researchers were able to reduce chloride levels to their appropriate amount - and in turn, to restore the GABA switch. Critically, mouse offspring exposed to this treatment didn’t demonstrate traits of autism. This study provides support for use of bumetanide in ongoing clinical trials in young children who have already developed autistic symptoms. 

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