Autism is on the rise and scientists are narrowing down some potential causes of autism as they research this developmental condition. According to numbers published by the Center for Disease Control (CDC) in 2018, approximately 1 in 59 children are diagnosed with autism. This statistic represents a 15% increase in autism prevalence as compared to numbers from 2016.
While boys are 4 times more likely to be diagnosed as compared to girls, there is progress in identifying the condition in females, who do not always fit the stereotypical picture of autism that boys may.
Autism is identified by three key components of behavior:
While we do not know specifically what causes autism, science has helped to narrow down some of the risk factors, both genetic and environmental (non-genetic). Autism tends to run in families, and there are risk factors such as parental age, space between pregnancies, and some pregnancy/birth complications.
There is no evidence that vaccines cause autism. Scientists are trying to narrow down some of the genetic and environmental-based risk factors, including the involvement in zinc and copper.
Zinc is a mineral and one that we need in trace amounts in our bodies. Our bodies do not store zinc, so we must consume small amounts of it periodically, as it is essential to our health. We ingest zinc by mouth, via foods we eat and supplement that we take.
Zinc is generally found in foods like meats, fish and poultry. Some people choose to take zinc supplements as an immune booster, for treatment of common ailments, to relieve eye disease states, combat fertility issues and to relieve symptoms of some psychiatric disorders, among many other reasons.
There is new information that links zinc deficiency to autism. There is no clear evidence that zinc deficiency causes autism. Researchers refer to a mechanistic link between the two, although it seems difficult to explain in everyday terms.
Below is some vocabulary to familiarize yourself with before reading through the next piece that details this link.
Published last year in a journal called Frontiers in Molecular Science, researchers reported their experiments, detailing the mechanism of zinc-Shank-mediated AMPAR maturation in developing synapses.
The senior author, Dr. Sally Kim of Stanford University School of Medicine in California, explained the team's findings:
"Autism is associated with specific variants of genes involved in the formation, maturation, and stabilization of synapses during early development. Our findings link zinc levels in neurons — via interactions with the proteins encoded by these genes — to the development of autism."
So, their study involved rats and mice. Rats and mice have genetic, biological and behavioral traits that closely resemble humans. Symptoms of human conditions can often be mimicked in rodents.
At the cellular level of developing rat neurons, they found that Shank 2 and Shank 3 proteins seemed to accumulate at the synapses between neurons and could be accelerated by adding additional zinc to the equation.
The zinc can bind to the Shank 2 and Shank 3 proteins after that, and impact the next cellular synapse as the “message” or communication between cells continues. AMPARs are impacted once the zinc binds to the Shank proteins, and maturation can happen more quickly as the cellular communication continues through neurons.
Basically, zinc can shape the properties of the developing neuronal synapses through Shank proteins. This link can impact the genetic coding of DNA and is influential in those genes that are responsible for identifying autism.
Their findings suggest that lack of zinc during the early cellular development in infancy could contribute to the development of autism, in years later.
This mechanical link at the very basic cellular level involves compromised maturation of the synapses and formation of neuron circuits. Although the science isn’t there yet, the understanding of this link between zinc and Shank proteins could potentially lead to better diagnosis, treatment, and prevention of autism down the road.
In another 2018 study published in in the same Frontiers in Molecular Science journal, researchers in Germany and New Zealand worked together to study the effect of zinc supplementation on the behavior in rodents. These mice genetically had the same SHANK-3 associated genetic mutations (modified DNA to mimic autism spectrum disorders) and exhibited “autistic” behaviors.
They were given dietary zinc supplements and evaluated for their rodent behaviors, like grooming, anxiety, and socialization. Over time, some of the symptomatic behaviors were reversed, as were the genetic cellular synaptic activity.
In this study, they reported improvement in autistic-like repetitive behaviors, anxiety-related behaviors, as well as social deficits. While they specifically looked at the synaptic function and plasticity of neurons and cells, these corresponded to the reversal of those autistic-like behaviors.
In a 2019 Belgian publication of Acta Neurologica Belgica, researchers studied the effects of zinc supplementation in children ages 3-8 (a small study of 30 children). The pediatric subjects with autism were given zinc supplementation over 12 weeks and evaluated before and afterwards based on their scores of the Childhood Autism Rating Scale (CARS) and the serum level of metallothionein 1 (MT-1A, these proteins rich in cysteine are primarily found at the cellular level in the membranes of the Golgi apparatus, they are important for regulating zinc and copper levels).
The study showed an increased in cognitive-motor performance after supplementation for 12 weeks, an increase in serum metallothionein 1 concentration, as well as lowered levels of copper circulating through the body.
While this information is promising, it is so specific. Hopefully, it will lead to more research that is applicable to determine zinc as a potential treatment option for autism spectrum disorders down the road.
Science isn’t ready to commit to this one.
In reviewing the literature that details this genetic connection of zinc and autism, the authors make it clear that there isn’t enough data to support taking additional zinc.
There have been no controlled research studies done on pregnant women or babies around taking zinc supplements and the genetic outcomes of autism risk.
In fact, taking zinc supplements during pregnancy could be more harmful than helpful, and at this time is not advised by the medical community.
The genetic research around zinc in the 2018 Frontiers in Molecular Science study pointed to a potential zinc deficiency at the cellular (or neuron) level. These studies were done on mice with genetic mutations similar to individuals with autism, but they are still rodents.
The preliminary study on a small group of humans with ASD in the 2019 journal Acta Neurologica Belgica revealed some interesting improvements with zinc supplementation in children, but it's hard to make a leap at this point about its impact on autism in general, without further extensive testing.
This zinc deficiency does not automatically suggest a dietary issue and taking supplements instead could also impact gut absorption. Even gut absorption can be an individual thing, different for each person.
One of the risks in the consumption of too much zinc is that it decreases the amount of copper absorption in the body, which can result in anemia and bone weakening. Science isn’t ready to connect a zinc deficiency in the gut to a zinc deficiency in the cells to the point that they recommend supplementation for pregnant women or babies.
Science has been trying to narrow the risk factors for autism for a long time. As the numbers of autism diagnoses increase, so do the specifics of the genetic findings that researchers are making.
This new scientific finding is so specific and mechanistic at the cellular level, it can be difficult for most of us to understand.
There is a link between zinc deficiency at the cellular level and rate of communication between developing neurons to code the genes responsible for autism development.
There is some promise to further research zinc supplementation for a potential reversal of autism symptoms.
The basic takeaway is that scientists can narrow their focus on zinc involvement and start to uncover the meaning behind zinc deficiency to guide future research.
It's important to understand as consumers, parents, and professionals that guide parents; that zinc deficiency at the cellular or neuronal level does not translate to nutritional deficiency of zinc. At this time, taking zinc supplements is not recommended to decrease the risk of developing autism, nor for symptom relief of autistic-like behaviors.
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