The fall and rise of the LEGO Kingdom: A review of “Brick by Brick”

All opinions are my own and do not necessarily reflect those of Novo Nordisk.

When people ask me what I did growing up, they expect me to say “surf.” I know this because when I tell them what I did for fun their next question is always, “What, you didn’t surf?” I didn’t. Still haven’t learned. Instead I did a lot of the things boys all over the US did. I watched TV. I hung out at the mall and at fast food restaurants. And I played with LEGO.

The brick fundamentally hasn’t changed since I was a kid. My son has a bunch and the basic essence is still snapping things together with that satisfying “click,” and the gradual accretion of form and function from individual, generic elements. Kind of like how life evolves, you know? And yet at the same time LEGO has undergone great changes in packaging, themes, toy categories, and target audiences. Today it’s one of the most respected and recognized toy brands in the world. But something I hadn’t realized until reading “Brick by Brick” by David Robertson and Bill Breen is how close LEGO actually came to crashing and burning in the 90s and early aughts, before recovering to once again become a commercial powerhouse.

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Maternal versus paternal effects on autism

All opinions my own and do not necessarily reflect those of Novo Nordisk

A report just out in JAMA Pediatrics (behind a paywall, but you can see the abstract at the link) reports the intriguing finding (by the way, just for the record, in blogging I’m finding it hard to find synonyms for “interesting.”  Please bear with me) that the recurrence risk for siblings of children with autism is seen even with half-siblings, albeit at a lower rate.  And more intriguing, the risk for sequential half-siblings is higher when the siblings share a mother than when they share a father.

This strikes a chord to me because it is consistent with other recent research I’ve described before, in which the presence of maternal autoantibodies to certain sets of neural proteins was predictive for development of autism.  As the abstract for the current work says, “the significant recurrence risk in maternal half-siblings may support the role of factors associated with pregnancy and the maternal intrauterine environment in ASDs.”  Whether maternal autoantibodies are associated with recurrence risk in this cohort is unknown.  The earlier study was at UC Davis; this one is from Denmark.  I’m generally of the mind that autism is an extremely complex collection of related syndromes, with many different contributing factors (but not vaccines!), so I think it’s best to just do the experiment and test for autoantibodies in the mothers of recurrent siblings.

And the nice thing about a country like Denmark is that this is probably feasible.  Unlike some other nations with extremely fragmented and incomplete health care systems (*cough*United States*cough*), Denmark has very good, integrated medical records.  Denmark also has very high standards for ethics and consent.  So finding a reasonable cohort of mothers and recontacting them may allow a test of whether an association to autoantibodies can be found here as well.  All towards figuring things out, all good.

I wrote to the authors of the study to ask about their work and how it might relate to the autoantibody studies and received the following email response from Dr. Diana E. Schendel of the CDC, via Therese Grønborg:

“Since our paper supports a role for maternal intrauterine effects in ASD, in addition to familial factors, our results are consistent with findings such as the (sic) UC Davis of maternal-derived factors that put the fetus at risk for ASD in pregnancy. One of the pregnancy related factors investigated in ASD etiology concerns abnormal immune system function – perhaps in the mother or perhaps in the fetus – that could impact brain development.

It is important to note that ASD has many potential causes and our study supports the notion of many etiologic pathways – both through family history and prenatal fetal  environments.”

This is a great statement as it jibes with my own views on diseases like autism–that we’re still very early in our understanding of what creates the presentation of a complex phenotype like autistic behavior, and that we need to keep looking and certainly not expecting simple explanations.  Finding explanations is not going to lead directly to new drugs, but greater understanding and a more personalized and nuanced view of each child’s challenges will help maximize their chances of finding success in life.