The University of Sydney caps doctoral theses at 80,000 words (excluding references). The theory is that external reviewers don’t want to read more than that (true!). One can apply to the Dean to increase the word limit to 100,000, which is what I did. But my doctoral thesis, as initially written, was closer to 140,000 words. So I had to cut three chapters that I really liked — the political economy of theories of genetic causation, how evidence-based medicine was captured by Big Pharma, and the history of the regulation of mercury.
I believe that some of the information in those excised chapters would be useful to policymakers in Washington, D.C. trying to figure out how to deal with the epidemics of chronic disease in children. So today I am sharing my original (slightly updated), never-before-seen, chapter 6, which challenges the entire paradigm of genetic determinism in disease causation.
I. Introduction
In the first chapter, I showed that the rise in autism prevalence is primarily a story of environmental triggers (with some smaller percentage due to diagnostic expansion and genetics). The story of how genetic theories became the dominant narrative in the autism debate thus needs to be explained. The hegemony of genetic theories of disease causation comes at a tremendous cost to society because they crowd out more promising alternatives. This problem is particularly acute in connection with autism, where genetic research swallows up the vast majority of research funding — and has for more than twenty years. So, one of the keys to effectively addressing the autism epidemic will be to demonstrate the flaws in the genetic approach to disease causation and replace it with a more comprehensive ontology that has better explanatory power.
To put this debate in context, I want to recap the genetic argument in connection with autism as I have presented it thus far. In the 1990s, it was routine for scientists, doctors, and policymakers to assure worried parents that autism was genetic. To the extent that anyone ventured a guess, the explanation was that autism was 90% genetic, 10% environmental. Then the state of California commissioned 16 of the top geneticists in the country (Hallmayer et al. 2011) to study birth records of all twins born in the state between 1987 and 2004. Hallmayer et al. (2011) concluded that at most, genetics explains 38% of the autism epidemic, and they pointed out twice that this was likely an overestimate. Blaxill (2011) argues that the eventual consensus will be 90% environmental, 10% genetic. And in chapter 5, I showed a model from Ioannidis, (2005b, p. 700) that suggests that only 1/10th of 1% of “discovery oriented exploratory research studies” (which include nutrition and genetic studies with massive numbers of competing variables) are replicable.
And yet, a disproportionate share of federal research money in connection with autism is going to study genetic theories of disease causation. In 2013, the Interagency Autism Coordinating Committee spent $308 million on autism research across all federal agencies and private funders participating in research (IACC, 2013a). This is a shockingly low amount to spend on research given estimates that autism is currently costing the US $268 billion a year (Leigh and Du, 2015).
When one drills down into how the IACC spent the $308 million, it is largely focused on genetic research (especially if one examines the funding in the funding category “What Caused This To Happen And Can This Be Prevented?”) (IACC, 2013b). This is in spite of the fact that several groups of leading doctors and scientists including Gilbert and Miller (2009), Landrigan, Lambertini, and Birnbaum (2012), the American College of Obstetricians and Gynecologists (2013), and Bennett et al. (2016) have all concluded that autism and other neurodevelopment disorders are likely caused by environmental triggers.
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