A sporadic journal on biology and biology education, including (but certainly not limited to) their social, philosophical, ideological, economic and political aspects and the evaluation of curricular efficacy.
As I am working on updating the Biofundamentals course (and turning the web notes into a book), I find myself reading and rereading a number of great books. Mostly so that I do not forget, I will list them here. On the off chance anyone cares, I have linked them to reviews.
Neither faculty or "Students do not shed their
constitutional rights...at the schoolhouse gate." Tinker v. Des Moines
Independent Community School District, 393 U.S. 503 (1969).
Having read Professor Hayward’s now notorious October 2013
it is clear he takes delight in rattling cages. Nevertheless, some of the issues
raised could serve as interesting jumping off points for discussion. For
example, I have always objected to being lumped together with other Caucasians
when it comes to ethnic identity. But assuming that he maintains an atmosphere
of civility, it is difficult to understand how it is even imaginable that his
comments rise to the level of “hate speech”. That said, I would love to listen
to the debate that might ensue if students were asked to critically consider the Loretta sketch from Monty Python’s
Life of Brian [http://youtu.be/sFBOQzSk14c]. One wonders whether this video (or
even showing this video in class) is a form of hate speech?
But really, that is not the issue here, rather there are two
issues: the defense of academic freedom and the importance of training our
students to learn to defend their positions, and critique the positions of
others, based on empirical evidence and rigorous and logical argument.
Why does this matter?Primarily because as faculty we are called upon to present and analyze a
wide range of potentially disconcerting (and perhaps even threatening) facts,
phenomena, and their implications. A short list, off the top of my head, includes
the evolutionary bases and outcomes of sexual selection and the various forms
of social organization,
the dynamics of immunity and the social outcomes arising from the refusal to
vaccinate children (which could be seen as a form of child abuse), the origin
of the universe and the elements of life, not to mention evolutionary
mechanisms in general (which could offend a range of more literalist religious
groups), the generation, costs and benefits of genetically modified organisms
(including, in the future, humans), as well as the implications of social
policy in the context of feeding the world’s population, the ramifications,
positive, negative, economic and sociopolitical of climate change. Given the
importance of social biology in species as deeply socialized as humans, one
might even imagine a discussion of the origins of customs ranging from “honor”
killings to the personal and political subjugation of women or the origins of
slavery and its modern variants (which could be seen as “disrespecting” certain
cultures.)What will the position of the
BFA be if faculty are publicly denounced by a group of devout students
demanding retraction or the punishment of the faculty member?
It is in this
context that Paul Chinowsky’s remarks (presumably made as chair of the BFA
rather than as an individual faculty member) - assuming that they have been
accurately reported (“If any (other) faculty member said this, we would
find ourselves in a dean’s
office or possibly on suspension for writing this. ... The question is, are we
going to allow this or condone this from someone in our own faculty?” ),
seem, at least to me, to be overtly threatening, and certainly not
dispassionately supportive of faculty who hold potentially unpopular or
this an appropriate role or position for a BFA chair
to take, given that this a chair rather than a CEO position. Am I to be marched
to the Dean’s office (perhaps even by the BFA chair) or
not allowed to teach until my views become consistent with the current
orthodoxy, or rather the orthodoxy imposed by a vocal subgroup of the student
body?I suggest that these are extremely
serious questions that strike at the heart of faculty freedom, and the
viability of intelectual life on
campus, and I am shocked that they have been addressed in such a cavalier
manner — when speaking for the BFA (and the faculty at large) a more
circumspect and supportive stance would seem appropriate.
 Pity for example the poor slime mold
that becomes part of the stalk rather than a spore cell, and so sacrifices
itself for the good of the community.Of
course we probably should also talk about the internal and external mechanisms
involved in the suppression of social cheating, but that is another course.
Recently, I came across a sticker advocating "restoring the balance" by bringing back the wolf. Great idea, I thought, but perhaps not daring enough. What about following the lead of those who refuse to vaccinate their children! Given the complete absence of empirical evidence that vaccination increases the odds of autism or other diseases, one must conclude that these brave souls are working to restore the balance in their own small way. We can help them by bringing back smallpox, plague, and other potentially lethal (but currently avoidable) diseases. What right do we have to drive viruses like polio to extinction? To be perfectly consistent, however, we might also want to refuse expensive medical care to those unvaccinated children who fall ill. Of course children rarely make their own decisions about vaccination (and perhaps water and waste treatment plants as well), but it seems reasonable that they share the costs of their parents semi-religious beliefs. While we are at it, we might also outlaw antibiotics, as this would lead to a dramatic increase in avoidable deaths, another balancing move. After all, in a balanced system viruses and bacteria have as much of a right to infect us as we have avoid infection.
Another day, another PR barrage centered on a scientific paper and a real danger that people will be tempted to treat a serious human disease with untried, ineffective, and potentially harmful “cures.” The paper, published in the prestigious magazine Cell, reports that some autism-like symptoms in mice, generated by treating pregnant animals with a compound that mimics viral infection, can be ameliorated by treating their offspring with the bacteria Bacterioides fragilis (1). Rob Knight, a major player in the “American Gut” project, claims that, “The broader potential of this research is obviously an analogous probiotic that could treat subsets of individuals with autism spectrum disorder.”(2) This is a truly remarkable claim given the multiple inherent and substantial limitations of the original study.
So what are these limitations and why do they lead to significant doubts about whether their “promise” is either misguided or likely to be fulfilled? The first and most obvious issue is whether mice, no matter how experimentally manipulated, can actually be autistic or, better put, whether the symptoms such manipulated mice display are related in any useful way to developing an understanding of autism or the more general “autism spectrum disorder” (ASD) in humans, yet alone alleviate the symptoms displayed by people diagnosed with ASD.
Let us begin with what autism is currently defined to be. According to the National Institute of Neurological Disorders and Stroke, “The hallmark feature of ASD is impaired social interaction.”(3) Because people are so deeply and inherently social, ASD is a serious condition. That said, it remains unclear whether ASD is one or a number of distinct diseases that produce similar symptoms.
Mice, and in fact the vast majority of animals, are very, very much less social than humans, and in so far as they are social, they are social in dramatically different ways. Moreover, mice often differ quite dramatically from humans in their responses to various physiological insults and how diseases arise and progress. Unless carefully taken into account, these differences can make observations in mice more or less irrelevant to humans. This has been revealed most recently in the course of comparative studies on sepsis, the life threatening consequence of a wide-spread bacterial infection, where “… researchers report evidence that the mouse has been totally misleading as a model system to investigate at least three major killers – sepsis, burns, and trauma. As a result, years and billions of dollars have been wasted following false leads, they say.” (Kolata, 2013).
Let us consider the mouse as a model for autism/ASD used in the Cell study. The investigators used an inbred line called C57BL/6N. To induce autism/ASD-like symptoms, pregnant mice were injected on embryonic day 12.5 (birth occurs between 19-21 days) with the compound poly(I:C); this treatment mimics an acute viral infection. Administration of this compound hyper-stimulates the mother’s immune system, leading to a condition known as “maternal immune activation” (MIA) associated with elevated levels of inflammatory factors in the maternal blood, placenta, and amniotic fluid. These changes have dramatic effects on fetal development and the affected offspring often display behaviors seemingly analogous to some of those displayed by people with ASD. Of course, since mice never display the types of social behaviors that normal people do, whether the symptoms mice from MIA mothers display are relevant to individuals diagnosed with ASD is speculative at best.
What the authors of the Cell paper focused on were changes in the behavior of the gut, that is primarily changes in cellular behavior affecting the gut’s permeability in MIA-derived mice and the possibility of repairing these behaviors through treatment of afflicted mice with bacteria. There have been some reports that humans with autism/ASD have gastrointestinal abnormalities, but the data is unclear. A small study, published in the British Medical Journal, found no relationship between an ASD diagnosis and gastrointestinal symptoms (4) while a larger study by the Autism Microbiome Consortium reported “significant enrichment of bowel symptoms and disorders in patients with ASD (11.74% vs. 4.5%, p<0.0001 by chi-square test)”, perhaps not a completely unexpected result from a project centered on the relationship between autism and gut bacteria, but these authors note that their conclusions “may well be affected by the limitations of our study,” which relate to the specific population of patients examined. Here it is worth noting that only a minority (~12%) of individuals with ASD appeared to display gastrointestinal symptoms.
The authors of the Cell paper pursued the hypothesis that autistic/ASD-like symptoms displayed by mice might well arise directly from the defects in their gastrointestinal tract associated with MIA treatment. They found changes in the relative abundance of intestinal microbes between normal and MIA mice. We know that the interaction between intestinal microbes and gut is critical for the normal “development, maintenance, and repair of the intestinal epithelium.” Following on they tested whether feeding mice B. fragilis, a microbe also found in humans and previously shown to ameliorate experimental colitis, could influence the effects of MIA. Their observation was a striking yes. This treatment also corrected some, but not all of the autism/ASD-linked behavioral effects found in MIA offspring mice. Most interestingly, however, from the perspective of the defining social aspects of autism and ASD, “they (the B. fragilis treated MIA mice) retain deficits in sociability and social preference” (emphasis added). Now given that autism/ASD is primarily a disease of social interactions, together with the rather dramatic differences between human and mouse immune systems brought to our attention by the sepsis studies, these observations suggest that this study’s results may well not be relevant to ASD. Moreover, from a practical perspective “B. fragilis, which accounts for only 0.5% of the human colonic flora, is the most commonly isolated anaerobic pathogen due, in part, to its potent virulence factors. Species of the genus Bacteroides have the most antibiotic resistance mechanisms and the highest resistance rates of all anaerobic pathogens. Clinically, Bacteroides species have exhibited increasing resistance to many antibiotics.” (6) This suggests that the use of B. fragilis as a “probiotic” treatment in humans might be actively dangerous.
Based on the lack of compelling evidence i) that mice really can, in any meaningful sense, be made to be autistic, ii) that there are substantial differences between mice and humans, particularly with respect to their immune systems, which is critical to these studies, and iii) that treatment of mice with B. fragilis fails to reverse the social symptoms of MIA mice, one might well have expected that objective, disinterested scientists would refrain from excessive hyperbole until more relevant and DEFINITIVE data is available. This would not be of great concern if confined to the scientific community but the danger is that such sanguine interpretations in the public press will lead parents or caretakers of people with ASD to “medicate” affected children with unproven, ineffective, and potentially hazardous “probiotic” treatments. This concern is not a theoretical one when one considers how ubiquitous self-medication is in our society. Any trip to the grocery store or Costco will reveal the widespread availability of dietary supplements including probiotics and other “alternative” medicines that claimed to prevent or treat a wide array of disorders, real or imagined, including gastrointestinal ailments. In the absence of a sober evaluation of the soundness of the observations made in mice and, more importantly, their relevance to humans, the essential question is whether it is socially irresponsible not to include clear and appropriate caveats directed to a scientifically-naïve population who may rightly assume the experiments described represent established fact and therefore, give license to self-directed probiotic treatment of affected individuals, or included in diets of unaffected children as a prophylactic measure.