That's not for lack of trying, of course.
Practically every time we turn around, there's a new study that explores a possible cause, link or even risk factor that might ultimately lead to an autism diagnosis. It's enough to make a person's head spin, especially when, as the case was this year, practically every new month brought a possible-but-not-quite answer. Here's a look at everything science has linked to autism in 2015:
A slew of studies examined the levels of vitamin D in newborns who would later go on to be diagnosed with ASD, but one study published in Molecular Autism in January of 2015 summed up the findings of a small Swedish study. Researchers examined only 58 sibling pairs, but they maintain that in the pairs where one sibling had autism, that sibling had significantly lower levels of vitamin D than their neurotypical brother or sister had.
Journal of the American Medical Association (JAMA) Pediatrics released a study the very next month, February 2015, that drew a line between a higher rate of autism spectrum disorders as well as developmental delays in babies born to mothers who experienced pre-eclampsia or other instances of "faulty placentation." Again, it was a relatively small study with a pool of just over 1,000 subjects, 350 of whom were neurotypically developing children between 2008 and 2011. The study's authors posited an association between restricted placental blood flow and compromised fetal neurodevelopment.
Or, perhaps more accurately, a person's ability to metabolize and rid their bloodstream of it. A study published in Autism Research examined the BPA levels in a group of 98 children and determined that children who were developing typically had lower levels of the plasticizer in their urine.
A study published in the April edition of International Journal of Epidemiology drew a link between the epigenetic DNA — that is, DNA that is affected by but not changed as a consequence of environmental factors — in a father's sperm and risk factors for autism. Again, the study was pretty small (it included samples from only 44 men), but it found that when a man had multiple corresponding or absent DNA markers for neural development, his child was more likely to meet a number of the criteria on the Autism Observation Scale for Infants, or AOSI.
Right on cue, the very next month — May 2015 — brought a new possible culprit with it: the epigenetic DNA present in a mother's DNA. Another study, conducted by multiple researchers and presented at the 2015 International Meeting for Autism Research, examined the methylation process (you can think of methylation as an on/off switch for genetic markers; it's a process that tells them when and where to be active or not) in the DNA of 44 mothers and found that, just like with a father's DNA, a mother's epigenetic DNA potentially affected her child's score on the AOSI.
In contrast to the other studies this year, the study exploring parental age was huge: Published in Molecular Psychiatry, it linked up health registries across multiple countries and, all told, included more than 5 million children, about 30,000 of whom fell somewhere on the autism spectrum. What it found is that, compared to children born to a 20-something mother, kids born to teen moms were 18 percent more likely to be diagnosed with autism, while kids born to moms in their 40s were 15 percent more likely.
When it came to dads, as opposed to children fathered by men in their 20s, those fathered by men in their 40s were 28 percent more likely to be diagnosed with autism, and that number rose to 55 percent when children were fathered by men in their 50s.
Another study published by JAMA in May 2015 explored a possible link between autism and gestational diabetes. When all variables were adjusted for, the study reflected that, compared to the overall national average of 1 in 100 children born with autism, in mother-child pairs where the mother had gestational diabetes, that average rose to about 1 in 80.
A study published in the Journal of Autism and Developmental Disorders in September looked at blood samples from nearly 600,000 women and examined the levels of three pregnancy hormones: estriol, hCG and alpha-fetoprotein. After adjusting for other ASD risk factors, researchers say that women with especially low levels of estriol gave birth to babies with a higher risk for autism. What's more is that hCG levels in either the top or bottom 10 percent of study participants corresponded with a higher risk of autism for baby boys.
Then in October, at Neuroscience '15, the annual meeting of the Society for Neuroscience, researchers at the Feinstein Institute presented findings that linked certain maternal antibodies to an increase in autism, particularly among baby boys. Essentially a certain immune protein that helps protect mothers against illness or infection was able to cross the brain-blood barrier in early-stage fetal development and bind to fetal brain cells, interfering with their structure.
In mice, researchers were able to locate the gene marker responsible for this particular protein and delete it, which opens up a potential course of early action in autism treatment options.
At that same conference, researchers from the Washington University School of Medicine presented their small study of 134 children, 76 of whom were born at least 10 weeks preterm. Scientists have posited for some time that preterm births increase a child's risk of an ASD or ADHD diagnosis, and this particular study focused on a possible reason for that.
All the subjects were given MRIs — full-term babies on their first and second days of life, and preterm babies on the first and second days following their due date. The researchers found that the scans of the preterm infants' brains showed weaker brain networking in the parts of the brain responsible for attention, communication and emotion.
The next month, we were back to talking about environmental factors again, this time in the context of epigenetic markers and, again, methylation. A study published in Environmental Research found that genes are affected but not altered by environmental factors that a mother was potentially exposed to during her pregnancy. In this case, they looked at mothers who smoked and found that there were epigenetic markers for that behavior in their childrens' blood even five years later. The hope is that by examining epigenetic markers in autistic children, researchers may be able to determine if they were exposed to certain environmental factors that may have put them at risk for ASD with any degree of commonality.
In early December, a Swedish study published in Molecular Psychology posited a potential link between PCOS and autism. Some scientists have previously theorized that there is a direct link between androgens — male sex hormones — and autism, and this study would seem to support that. Women with PCOS often have higher levels of androgen and can pass them to their fetus across the placenta. This was a large study, examining nearly 250,000 people over the course of 23 years. They found that autism in children born to women with PCOS was 59 percent more prevalent.
A new study in JAMA Pediatrics in December suggested that using antidepressants during pregnancy might also be a potential culprit. Children of mothers who treated their depression during the second and third trimesters were at an increased risk — 87 percent — of developing autism. Despite that large-sounding number, the actual percentage of children diagnosed in the study group was very low. For instance, in the group with the largest number of diagnoses, children of women who took prenatal SSRIs (the most common form of antidepressants), the percentage of children diagnosed was still just 1.4 percent.
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