Twins Research Suggests Connection Between Low Birth Weight and Autism
Recent research identified a correlation between autism and low birth weight by surveying thousands of pairs of Swedish twins, where one of the pair had autism. Northwestern University psychologist Molly Losh, who studies communications sciences and diseases, is the lead researcher of the study and published the findings recently in Psychological Medicine.
What are the implications of the research and what future autism research is planned? Losh answers these questions and talks about the findings. She said that since her research only tested twins, the results don't necessarily apply to single births.
What did you find in the study where you looked at twins where one has autism and one doesn't?
We found that lower birth weight was a strong predictor of autism.
Why did you decide to focus on low birth weight as a risk factor for autism?
We really don’t know a whole lot about the different environmental factors that could influence autism. The majority of my work focuses on documenting genetically meaningful features in people with autism and their relatives for use in genetic studies. But I think the further the field gets along in identifying susceptibility genes, the more we’re recognizing that it’s likely that at least in a handful of cases, these genes are going to be interacting with environmental risk factors to produce the symptoms of autism. And so just looking at the literature, lower birth weight had been identified in earlier studies and so I thought that would be a good candidate to look at in this really large cohort available in the Swedish Twin Registry.
What’s the benefit of using twins in a scientific study?
Monozygotic twins share virtually all of their genetic material, and so differences between them can be isolated to non-genetic factors, such as weight.
Was there any part of the process of the study that was challenging?
It’s definitely challenging to do an international collaboration. It’s a lot easier to talk about findings and make progress on work if you’re able to meet in person. So we overcame that challenge, I went to Sweden a few times and we met in the States a few times. I think they are just an incredible group of epidemiologists and biostatisticians and scientists just in general, so I was really lucky to get to work with them. I was new to twin studies so I guess that was a challenge for me, and I learned a lot about them from Dr. Lichtenstein’s group.
What was it like to work with the Swedish Twin Registry?
The Swedish Twin Registry has been conducting longitudinal population-based studies of risks to disease for decades. And so my role was just a very small part of one of the studies that they have going on. So it was a great opportunity to get to work with them. The data that they have are just so incredibly valuable and that they make them available to researchers outside the Karolinska Institutet is really a wonderful thing, it’s very generous.
Did the results of the study surprise you?
I guess I was surprised by the strength of the findings in this select group of discordant twins [meaning one has autism and one doesn't]. Those are very strong results.
How has the study been received?
I think it’s been received very well. There is a lot of interest in the causes of autism in general and the possible non-genetic causes of autism in particular. Now that we’ve pinpointed one possible such cause, I think there seems to be some excitement about having a new target for further investigation.
Is Dr. Lichtenstein doing any follow up on the study?
This work was part of a broader study the Child and Adolescent Twin Study of Sweden that continues, yes. So they are doing additional work with these families and have a number of other papers out analyzing other factors. They didn’t just focus on autism in the study.
What projects are you working on next?
My other projects are family study projects where we’re trying to identify genetically meaningful features in individuals with autism and their family members for use in genetic studies. We’re also doing cross-population studies of the same nature, focusing on comparing features in family members of people with autism to those of family members of people with Fragile X syndrome to understand where there might be overlap that could be tied to particular genes, or lead us to features that are tied to particular genes, and then eventually we’ll be doing molecular genetic analyses to actually see whether there is genetic variation related with the sort of behavioral and neuropsychological variation that we’re seeing running in families.
Is there anything you’d like to add?
I think it’s encouraging that the field of autism in general seems to be really embracing this idea of the importance of looking at both genetic and non-genetic factors and how they might interact in the causes of autism. There’s a lot of incredible work going on and I think that it’s reason for optimism.
How did you become interested in studying autism?
I was always interested in issues with brain and language and then, early on, as a student I had an opportunity to volunteer in a lab with a graduate student on her project where she was looking at language development in kids with autism, and I got really interested in that and so pursued doctoral work looking at language and social cognition and autism in other populations.
Could you describe your education background?
I have a Ph.D. in developmental psychology and post-doctoral training in autism and psychiatric genetics.
Is the work you do now primarily focused on autism or do you do research in other areas as well?
We’re primarily focused on autism but I’m also doing projects that include populations that are related to autism, so other neurodevelopmental disabilities like Fragile X syndrome.
What is Fragile X syndrome?
Fragile X syndrome is a single gene disorder. It’s the most common inherited cause of intellectual disability, and it’s also the most common monogenetic condition associated with autism. So, about half of all people with Fragile X also meet diagnostic criteria for autism, and that suggests that the gene that plays a role in Fragile X might play some sort of role in autism as well.
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