Category Archives: Public Health

Internet access is a public (and private) health issue

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

If the Founding Fathers had lived today, they would surely have included internet access as one of our inalienable rights.  No, scratch that, because if they had lived today they would have used Google Docs to crowdsource the Declaration and the result would probably have been much more generic and middle of the road than it actually is.  Also, the Declaration would also have been limited it to about 500 words so readers wouldn’t get bored and surf somewhere else, and it would have had embedded GIFs. Preferably animated.

Still, the ability to access the internet and everything that comes with that is, if not a right, an incredible advantage.  So I was stunned when I read in the Seattle Times the other day that a significant fraction of people in the US–about twenty percent–have little to no internet connection, although those numbers have recently begun to creep up, presumably due to smartphone uptake.   But of course, being a good Seattlelite with a liberal bent, my next reaction was to say, well, let’s not rush to judgement or conclusions.  Maybe those people just don’t want the internet.  Not that there’s anything wrong with that…

Except the article goes on to say that while seniors generally did not feel they were missing anything, the majority of other respondents did feel they were missing something important and were being left behind because of their limited access.  So it’s not a life decision; it’s a question of cost, access and education. Continue reading →

Maternal versus paternal effects on autism

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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.

What does the Hela genome agreement imply for consent and genome data usage?

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

A fair amount of reporting (for example here, here and here) has gone into the recent news that the NIH and the descendants of Henrietta Lacks have reached an agreement about the conditions under which the genome sequence of the HeLa cell line will be shared.  The basic parameters are that researchers wanting access to the data will need to apply for permission, the application committee will include members of the Lacks family, any publications will acknowledge the contribution of the Henrietta Lacks, and future genome sequences will be submitted to dbGAP.

This is a generally welcome development, and in no small part due to the work of Rebecca Skloot.  Her book, The Immortal Life of Henrietta Lacks provided the impetus to the current developments by popularizing the story of Ms. Lacks and the cell line derived from her tissues.  However, this agreement also can be seen as a precedent of sorts, and the future implications for the ethics of consent, genetic information sharing and genomic research are unclear.

Whose genome is it, anyway?

In Pasco Phronesis, David Bruggeman penned a post on some of the possible implications.  He discusses one of the key elements of genetic consent that I generally haven’t seen elaborated on much in the current literature: familial consent and exposure.   To what extent do those who share part of a sequenced genome have a say in the granting and rescinding of consent for the usage of genetic information?   Continue reading →

Finding an Alka Seltzer for the oceans

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All opinions are my own and do not necessarily reflect those of Novo Nordisk
Some time ago I wrote an article for Real Change (reposted here) about research being done at the University of Washington to understand the effects of ocean acidification due to rising atmospheric carbon dioxide levels.  The rising pH of the oceans is another one in my list of things we don’t worry enough about with climate change but really should.  Like the bees.  It’s such a seemingly tiny, subtle thing.  The measured decrease in pH of maybe 0.1 units is due to ocean waters absorbing atmospheric CO2 and the resulting conversion of some of that to carbonic acid.  Seems small but it’s really a big deal.
Scientists have documented apparent effects of ocean acidity on coral reefs and oysters, among other organisms (abstracts from links; articles behind paywalls), and while oyster farmers can try to add antacids to their spawning beds, the oceans as a whole are a bit large for a local solution.  Which is why I was excited to see the Paul Allen Family Foundation post the current submissions to their Ocean Challenge (HT @deirdrelockwood).
Let me provide a disclaimer that I have not read most of these proposals in depth.  However, scanning through the titles and sampling a few in greater detail, it’s clear that the Ocean Challenge has prompted a number of groups to come up with ideas about how to try and monitor, test, and mitigate the effects of ocean acidification, at least at the local level and in some cases on a grander scale.  The proposals are available online for public comment, and finalists selected in September.
There are a couple of things to really like about this.   All the proposal summaries are devoid of names and affiliations, which may lead to more unbiased evaluations by public commentators.  This is something that’s been debated for years with respect to other granting agencies like the NIH.  Another great thing is that this is open–anyone can apply and everyone’s ideas are out there for others to learn from, debate, and expand upon.  I’m a fan of open source science, and transparency, and this feels like it’s in that vein.  And last, this is really a big problem.  Not to say government agencies aren’t funding and studying this, but as we’ve seen with other private non-profit foundations like the Gates Foundation, there is a third way beyond government and private industry to try and effect policy and make changes.  I hope for success from this effort.  Because I would really miss oysters.

More developments in autism prediction

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

A recent publication about efforts to find early indicators for autism recently came out in the journal Brain and reports an intriguing observation about brain size.  The researchers sought to identify whether Magnetic Resonance Imaging (MRI) of the brains of infants and very young children could help to predict which children would go on to develop autism.  Like many pilot studies of this sort, the experiment was done simply by looking.  The researchers identified a cohort of newborn siblings of autistic children and also a control cohort without that risk factor and began taking MRI images of their brains at the age of between 6-9 months, and again at 12-15 months and 18-24 months.  Prior research has shown that having a sibling with autism greatly increases the probability that a child will also develop autism, so in this situation the expectation was that some of the sibling group would develop autism and researchers would retrospectively be able to look at the data collected during the study and identify MRI features that correlated with development of disease, should any exist.

The impetus behind this is that previous research has not shown any definitive behavioral clues in infants (6 months or younger) that predict the development of autism.  However, the earlier a child is diagnosed, the earlier behavioral interventions can be applied to help that child and his or her family cope with future challenges. Continue reading →