Category Archives: Biology

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.

Lack of replication no surprise when we’re studying really complex problems

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

For another nice take on this topic see Paul Knoepfler’s blog post here.

One of the sacred (can I say sacred in reference to something scientific?) tenets of the scientific method is reproducibility.  If something is real and measurable, if it’s a fact of the material world, then the expectation is that the result should be reproducible by another experimenter using the same methods as described in the original report.  One of the most well known (among physicists anyway) examples of irreproducible data is the Valentine’s Day Magnetic Monopole detected by Blas Cabrera back in 1982.  Great experimental data.  Never repeated, and therefore viewed as insufficient proof for the existence of a magnetic monopole.

So it’s troubling that in the past few years there have been numerous stories about the lack of reproducibility for different scientific experiments.  In biomedical science the number of  reports on the difficulty of reproducing results has gotten so great that the NIH has begun thinking about how to confirm and require reproducibility of some kinds of experimental results.  Just a few days ago another field, that of psychological priming, saw the publication of an article that the effects of “high-performance priming,” could not be reproduced.  This is another field undergoing serious questioning about whether/why results don’t reproduce, with commentary from such luminaries as Daniel Kahneman. Continue reading →

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 →

How do you take a cheetah’s temperature?

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

The answer, of course, is very carefully (ba-dum-bum!).

Okay, having gotten that horrible joke out of the way, it seems like people are really interested in cheetahs and how they hunt.  I’ve written about monitoring cheetah hunting behaviors before and the implications that technology has for future data gathering and analysis (see here, here and here).  The most recent addition to what seems to be a growing canon of testing and abolishing cheetah hunting myths was published recently in Biology Letters (abstract only; rest behind a paywall.  But see here for a more extensive summary of the paper).  In this work, the researchers report using temperature sensors to test the hypothesis that cheetahs are unsuccessful in some of their hunts because they overheat.

This seems like such a nice, neat story.  That’s probably one reason why it’s taken so long to actually test it.  The story goes something like:  Cheetahs are the fastest land mammals.  Everyone heats up when they run.  If cheetahs run the fastest, they must heat up the most.  Therefore, heat is the gating factor for Cheetah hunting.  Stories are so appealing!  But that appeal, in satisfying our sense of order, can keep us from looking under the hood and asking questions.

Luckily for us, these researchers did.  Robin Hetem and colleagues found that cheetah temperature did not increase substantially during hunts, whether successful or not.  Oddly, temperature did increase after the hunt was over, and furthermore increased more for the cheetahs that were successful.  The study authors speculate that the reason was heightened awareness to scavengers who might want to steal the cheetah’s prey.

This study highlights the value of remote sensing and our rapidly increasing ability to both monitor and store data continuously, and thereby test our notions of the world.  Data of itself isn’t good or bad, but boy is it useful.