Wednesday, August 29, 2012

Writing about autism science? 10 things

Word on the street--well, really on a blog from a researcher--is that the writer of the autism/inflammation New York Times op-ed, Moises Velasquez-Manoff, is working on an "annotated" version of the article that will "back up" his claims. Some annotation would have been useful to begin with; as I noted in my analysis of that op-ed, in many instances, discerning the origin of his information was difficult or impossible. I understand that something that appears originally in print can't have hyperlinks to appropriate references, but the writer certainly could have beefed up in-text citations (author names, journal publications), at least avoiding the criticism that the piece was unsatisfactorily sourced. 

Sourcing was not the only issue with that piece, however. Velasquez-Manoff has a book to sell, and that book, like many popular science books, has a narrative that may not necessarily stand up to precise scientific scrutiny, if the NYT piece was an indication (people will be able to determine for themselves on September 4). Indeed, a criticism leveled at many such books is this lack of care in qualifying scientific results and interpreting them with caution and caveats. It's an understandable instinct. Think about the good storytellers you know. How much care do they exercise in avoiding hyperbole or sins of co-mission and omission in telling a "good" story? Some writers of popular science books commit these sins to tell a good story, too. Others do not, yet their work is popular and well received. It is possible to be accurate and cautious and still tell a rousing tale.

The problem with writing about science, though, is that science isn't just a story. It's about facts and open questions, and it's almost never defensible to write as though a door has closed, a box has been checked, or a mystery has been completely solved. We owe it to readers to avoid simplification to the point of a sin of omission and to avoid overinterpreting to the point of hyperbole.

When it comes to writing stories about health and medicine, the stakes climb. With these stories, we're not writing only about scientific findings. What we write is also about people. Many writers seek a narrative hook, a personal story that frames the rest of the piece. I can't even count the number of autism-related stories that open with a (very real) tale of woe featuring an overwhelmed or traumatized parent talking about the grief and horror of having a child with autism. This tactic catches the reader--and happens to be one that the largest autism nonprofit in the United States also employs--successfully tugging at heart and purse strings and attracting mouse clicks. But this tugging and this narrative approach are so frequent in such stories as to be near-cliches, and they do few favors for the autistic people these stories are really about.

The presentation of autism as a monster to battle or a stalker out to destroy your life has repercussions that some autistic adults argue go beyond an unfair and painful characterization of what they believe is Who They Are. News stories about autistic people whose parents and caregivers have murdered them often carry a clear attitude of "autism is so hard, no wonder they got killed." When every news story you read describes autism as a horrific affliction and all of those with it as suffering, when mainstream news organizations persist in focusing only on what parents have to say about autism rather than talking to autistic people, when stories focus on preventing autism--with worms, no less--autistic people, real, living, breathing people, feel pain and get angry and argue that even if they are nonspeaking, they can be perfectly capable of communicating for themselves.

If you are someone who writes about health and medicine and who covers a story related to neurobiology--particularly autism--please consider the following 10 suggestions. They might help you avoid the pitfalls of hyperbole and poor interpretation and causing pain to autistic people.

  1. Interview an autistic person for insight whenever possible. If you need suggestions for leads, feel free to contact me. If you were writing a piece about any other human condition, would you talk only to parents or relatives of people with that condition if the people who have it could communicate for themselves?
  2. If a researcher claims to have "solved" autism, please exercise healthy skepticism and follow up with someone who doesn't have a dog in the hunt. Of all of the neurobiological conditions, autism may be the most variable. It's extremely unlikely that any one research path or group or hypothesis will explain all autism. Don't ride that wave with them.
  3. Don't generalize. Stick with what the findings say, not what the discussion or the conclusions or the authors or the news releases say. Have an ear for when someone is overgeneralizing. Example generalization: "X causes autism." What causes autism has not been established, and the causes themselves--and how they work--are likely going to form a very long list. We are still very early in formulating that list, much less what the items on that list do.
  4. Don't mistake correlation for cause. When a study reports a "link," that term usually means a mathematical relationship: When X was more frequent, autism was more frequent." That doesn't mean that X causes autism. It doesn't even mean that X has anything to do with autism.
  5. Don't overstate the meaning of risk. Risk is a scary word, although we all live with the 100% risk of dying someday, regardless of what other risks we face. When a study result refers to "increased risk," look at the numbers. If they say that the presence of factor X was associated with a relative risk of 2.1, for example, then the population with factor X had twice the autism compared to the group without that factor. If the average risk of having a child with autism in the absence of that factor is 1%, then this particular factor was associated with about a 2% risk. And relative risk applies only for that study--it does not tell you what the actual risk is. 
  6. Keep in mind that even these links don't imply a true causal relationship. They're just math associations. A famous example of how these relationships can end up being misinterpreted is the protein CRP and heart disease. Because of a mathematical association between the presence of this protein and the occurrence of heart disease, researchers thought for a pretty long time that CRP might cause heart disease, and drugs were even targeted to lowering its levels. Turns out, it doesn't cause heart disease, so the drugs were no use. Instead, it's either a side effect of heart disease (reverse causality) or just higher because of some indirect influence. Now, take any recent X factor you've heard is "linked" to or "causes" autism and substitute it and autism into the above story to understand how unpromising correlation can really be.
  7. Be aware of how you write about autism and of the fact that autistic people may read what you're writing. How you describe autism is, for those readers, describing themselves, their very being. Please try to avoid lapsing into the parlance of affliction, suffering, disease, desperation for a cure, war, and despair or comparisons of "low" and "high" function. A good science geek knows that function is often a matter of environment, not a constant measure. Although some autism parents may disagree, one key to making this world a better place for autistic people is for society not to see or treat them as unhearing, nonverbal, illiterate rocking obsessives who don't understand what people are saying about them. Unlike neurodegenerative or fatal diseases, autism is not universally perceived or lived as a negative condition, and it's important to remember that.
  8. If the study in question is about mice, never talk about how the results will lead to a therapy or a cure or write about the mice as though somehow, they are just tiny humans with tails. Mice have misled us before. They are only a way to model what might happen in a mammal sorta kinda related to us. They are not Us, otherwise we'd live in tiny, crowded places, having 10 children at once and ignoring them when they grow fur, and this autism thing wouldn't be an issue.
  9. Don't use phrases like "gene that causes autism" or "gene that is linked to autism" or "faulty gene" or "defective gene." What you really want to say is "gene variant" or "version of the gene." There isn't an "autism" gene; there are gene changes that might be linked to autism.
  10. Also avoid referencing "environmental factors" without providing some specific examples. Those examples should not be "chemicals" or "toxins," which are vague, meaningless, and stupid. Established environmental risk factors for autism include parental age and extreme prematurity. Try those, but handle with care.
Finally, I know deadlines are tight, but never take a paper author's interpretation as The Final Word. Try to find someone not connected with the work and get their comment. Journalism 101, I know, but it's surprising how often articles do not include this kind of balance. By balance, I don't mean "gives the other side." I just mean, "possibly modulates enthusiastic author's overinterpretation or overselling of results and their significance." 


Which is where we got started with this most recent brouhaha in the first place.

Monday, August 27, 2012

Autism, immunity, inflammation, and the New York Times

[Note: An interview that appeared 9/4/12 on Wired's Website of the writer of the op-ed piece I critique here and conducted by an associate of his seems to imply that I am not a scientist and should have "ask(ed) a scientist" before commenting on these issues. For the record: I am, in fact, a scientist, with a PhD in biological sciences and postdoctoral training, both in vertebrate developmental biology and the latter in mammalian developmental genetics (with mice!), areas associated with this discussion. In addition, I have spent 8 years deeply engaged in following, evaluating, and writing about autism-related research.]

The Preamble
On Saturday, the New York Times online ran a piece from its Sunday Review Opinion pages entitled, “An immune disorder at the root of autism.” The piece is packed with overstatements and overinterpretations and lacks much-needed modulation and qualification. More than that, it promises a "preventative" for autism that is, pardon me, off the hook(worm). 

The author is Moises Velasquez-Manoff, who has a book coming up, An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases. Although I understand that someone who has written a book may well have expertise in a specific subject area, a fund of knowledge does not give them carte blanche to bring their bias without scientific counterpoint to the editorial pages of the New York Times. Velasquez-Manoff's  book hits the stands on September 4. 
                                                                                                                    
Velasquez-Manoff's work appears to rely on the “hygiene hypothesis” to explain a host of modern-day ills that are, presumably, on the rise, in part because we’re just not toting around enough parasitic worms (more later). Among these modern-day afflictions, Velasquez-Manoff includes autism. Except that autism, you see, probably isn’t actually on the rise that much or a modern-day affliction. And the hygiene hypothesis itself is controversial** and remains a hypothesis that doesn't necessarily explain all immune dysregulation. I have a hard time taking controversial hypotheses in progress and faux epidemics as an unequivocal rationale for anything.

From the headline to the final paragraphs focused on using parasitic worms to treat or even prevent autism, the science as Velasquez-Manoff presents it is limited at best, and frequently unsourced and unreferenced. Where a source is given or traceable, the conclusions are overstated or cherry-picked. Yet to a lay reader, he writes plausibly and with confidence. The upshot is that anyone without a deeper understanding of immunology or autism could come away from reading this piece thinking that autistic children or pregnant women should immediately be exposed to parasitic worms and rolled around in dung as a cure. Lest you think I exaggerate about what people will do at the slightest hint of efficacy in autism, see here, here, here, here, and here

Squishy science, misrepresentative headlines, and hyperleaps to conclusions are not that unusual in science stories. But articles and editorials about autism require special attention to accuracy. Anyone paying attention likely is aware of the vaccine–autism controversy. Anyone paying a little more attention, particularly someone writing an article about autism, should know that using the words “inflammation” and “autism” or “immune disorder” and “autism” inflames the substantial number of people whose resistance to vaccines because of autism fears has led to outbreaks of pertussis and measles that in turn have led to fatalities. That use requires the support of an extraordinarily well-sourced, fact-based article.

Lest you think I overstate, Velasquez-Manoff’s piece has already made it onto the “mercury in vaccines causes autism” discussion boards, and someone tweetspammed me last night (with three tweets) about vaccines and autism in response to my tweet about this article. I’m sure the party has just begun. Accurate science, however, likely won't be one of the attendees.

The science
First, the headline: “An Immune Disorder at the Root of Autism.” No one knows what causes autism, but every week (or even every day), some new candidate turns up, either as a potential cause or adding to risk, from being the second born to having lungs with symmetrical branching. A big factor, according to most studies, is genetics, often in interaction with environmental factors--not “toxins” like pesticides or air pollution, necessarily, but factors like parental age. The vast majority of autism research focuses on one or other of these factors, sometimes both. Environment in the case of autism seems to primarily mean the womb, according to a good-sized twin study. Of course, the womb is a busy and complex place, so no one quite knows what happens there that might influence the development of autism or how the development of autism affects the womb. Many candidates exist, among them the hypothesis that a maternal infection during pregnancy might set the stage for inflammation that triggers autism. That’s a hypothesis, though, and even a generous interpretation of it doesn’t warrant such an unequivocal and--excuse me--inflammatory headline.

Inflammation and autism, as I noted above, are a touchy pairing. One of the core arguments of those who oppose vaccines because of autism fears--which the vast majority of scientific research has debunked--is that the vaccines trigger some kind of inflammation that brings on autism. Inflammation or dysregulated immunity may play a role in a subset of autism, but the body of research on autism and inflammation is, as yet, rather limited. Not a huge body of work to go on yet, but interesting research directions to follow.**

When a researcher or a writer becomes deeply engaged in a concept, like the idea that autism and inflammation are linked, it can be difficult to step back from that commitment to an idea and handle it with moderation and qualification. It’s also very tempting to take one’s hypotheses and create elaborate scenarios of “if that, then this, then that, then this” and then start to see them as actualities. But scientists and people who write about science should try to take one wary step at a time. One group at CalTech, led by Paul Patterson, which does work with a mouse model of autism, exercises a pretty good level of caution in reporting and interpreting their results, not failing to note that work done in mice is not necessarily an accurate reflection of how things will pan out in people.  

Velasquez-Manoff is not so cautious. First, he appears to describe autism as a “parallel epidemic” with autoimmune diseases, even though a careful review of the literature shows that there likely isn’t an “epidemic” of autism. I'm also having trouble finding any data to confirm an epidemic of autoimmune diseases (he provides no sourcing), although I find that incidence rates in general seem to go up with improvements in diagnostic tools, a scenario that is common with application of new technologies in many diseases and disorders. Without that parallel or even confirmation of either "epidemic," his carefully constructed, fragile “if that, then this” scenario suffers from that point on. 

Even if the parallel were accurate, his argument would suffer in other ways. For example, he takes the work from Patterson’s lab and states, without qualification, that in that model, “Autism results from collateral damage” of maternal infection of the mother mouse as an "unintended consequence of self defense" in pregnancy. Except that mice don’t have autism, which is a human neurobiological construct shaped in part by social and cultural perceptions of what is considered “normal.” I’m pretty sure the lives of mice don’t incorporate these features. I’ve worked with a lot of mice. I know mice. And we, sir, are not mice. The most we can justifiably say is that they may have “autistic-like” behaviors. That’s it.

This example of overstatement is just one of many that litter Velasquez-Manoff’s piece. In fact, the opening of the article is an overstatement. I’ll step over the lede’s reference to autism as an “affliction" (terminology that pains and incenses many autistic people) and go straight to graf two. There, we find what Velasquez-Manoff calls “the short of it.” He claims that a “subset of autism--perhaps one third and very likely more--looks like a type of inflammatory disease. And it begins in the womb.”

I’m guessing the headline writer didn’t make it to the second paragraph. But what has me scratching my head more is how Velasquez-Manoff can say without qualification that autism “looks like” an inflammatory disease that “begins in the womb” when actual autism researchers don’t have any firm idea of what causes autism or what the factors in the womb are. A subset of autism may be immune related, in part because of genetics. The writer doesn’t source his “one third” value, but I think it’s a generous inference from this Italian study. One third does not, however, equate to all cases of autism. Nowhere else in this piece does Velasquez-Manoff remind us of that subset distinction or qualify generalizations about autism, perhaps one of the most idiosyncratic of neurobiological conditions.

Velasquez-Manoff goes on to say that your immune system should work like an “action hero,” leaping into action accurately and without misfires before returning to a “Zen-like calm.” Your immune system is never in a state of Zen-like calm unless maybe you’re living in a sterile room at Plum Island, sanitized to the gills. In addition, your immune system is much more of an unpredictable and ungrateful harpy who will, on occasion, totally overreact to viral invasion and just kill you in the process; see, for example, the Spanish flu or the recent outbreak of H1N1. An action hero, this is not. Your immune system is not your buddy. It’s a cellular gang that follows instructions, even if those instructions result in collateral damage.

After this heroification of your immune system, Velasquez-Manoff goes on to say, without ambiguity, that the immune system fails in its presumed balancing act in “autistic individuals.” Not some autistic people. Not “might fail” or “some researchers hypothesize that it might fail.” No memory of that “one third” notation. Just… it fails in autistic people. Period.

And that’s where he lost me completely, not because I wasn’t following him but because that phrasing alone breaks the promise any science writer owes a reader to be as honest and warts-and-all as needed to ensure accuracy. It is simply indefensible to have written that sentence as though it were scientific gospel. Even the words of his second paragraph (subset, one third) don’t support it. It is not his last instance of this transgression.

No doubt much to your relief if you’ve read this far, I’m not going to parse this opinion piece sentence by sentence. Sourcing and citation are limited throughout. As he did with the Patterson work, the author overstates and leaps to conclusions that are not warranted. I’m just going to hit some points where the scientific leaping outdoes a show jumper on her best day.

Velasquez-Manoff gives a list of some of the factors that have been linked by correlation to autism, including a “mother’s diagnosis of asthma or allergies” in pregnancy. The list could consist of hundreds of factors, genetic and environmental, but he gives us only the handful arguably linked to immunity. He spends time on infection, particularly the finding from a Danish study that a viral infection resulting in hospitalization in the first trimester of pregnancy is linked to increased autism risk in the child. 

Although he says that blaming the autism "epidemic" on infections is "folly," it forms the backdrop of the piece. Infections and other stuff like maternal (of course) autoimmune gene variants, obesity, and metabolic syndrome, he says, lead to inflammation that causes “maternal immune dysregulation.” He calls these "paths" to autism, even though in all cases, they are correlations associated with increased risk, not causes. Indeed, no one has resolved the chicken-egg question of the relationship between the womb and autism: Does the development of autism influence the womb environment or does the womb environment influence the development of autism? 

Then Velasquez-Manoff references another Danish study from last year that he calls “direct evidence of this prenatal imbalance,” saying that amniotic fluid samples from newborns in Denmark who later were diagnosed with autism “looked mildly inflamed.” The thing is, that Danish study largely found very little evidence at all of elevated inflammatory markers investigated in the amniotic fluid in the 331 samples from children later identified as autistic. The one marker they identified as increased was  MCP-1, which, they concluded, “may decipher an etiologic immunologic dysfunction or play rather an indirect role in the pathophysiology of (autism spectrum disorder).” What Velasquez-Manoff doesn’t note is that the Danish researchers did not find elevated levels of any of the markers of inflammation when comparing the entire autism and control cohorts but found these MCP-1 correlations only after breaking down the cohort into groups based on specific autism diagnoses.

The molecule in question is known for its involvement in neurodegenerative diseases. Autism is not neurodegenerative. MCP-1 was identified in one study as elevated in a study of post-mortem autistic brains, but much of that cohort of 11 also had epilepsy. In other words, a correlation and a confounded finding in a small group of post-mortem brains isn’t enough to warrant using the words “direct evidence” of a hypothesized prenatal imbalance as causative in autism. It’s interesting stuff and worth following up, particularly as it relates to a potential subset of autistic people with immune dysregulation. In the interests of intellectual honesty and absence of follow-up as yet, however, we have to leave it at that. 

Velasquez-Manoff then asks, “What has happened to the modern immune system?” and goes on to assert that the concepts underlying the “hygiene hypothesis” also underlie autism and correlations between autism and maternal autoimmune disorders or asthma. An “evolutionary answer,” he says, is that we are no longer sufficiently riddled with parasites and microbes (we actually still have our microbes), so our immune system, twiddling its presumably heroic thumbs, casts its roving eye elsewhere--i.e., on ourselves. See, people who still live with parasites, he says, “don’t suffer from inflammatory diseases as much as we do” (italics mine). “We,” I assume, being the clean people of the western world. No sources given, and that assertion does not dovetail with, for example, what we know about asthma rates in Latin America (really high) versus Western Europe (not so high), although in places where things like leprosy, parasitic worm infections that include river blindness, and nasty bacterial eye infections are high, type 1 diabetes is low. Raise your hand if you're willing to make that tradeoff. And then he says, “Autism also follows this pattern” and “seems to be less prevalent in the developing world.”

After I cleaned up the pieces of my cranium, I suffered through his eliding of the fact that when you’re dealing with intestinal parasites and their friends, you and your government may not really have the time to go around carefully diagnosing developmental disorders. I suffered through his unsourced dismissal of epidemiologists who say as much, and I just about had a coronary when he cited “at least one (unnamed) Western doctor” (the best kind, you know) who had found autism was “nearly nonexistent” in a Cambodian population “rife with parasites and acute infections.” Um… if, as Velasquez-Manoff seems to argue, maternal infection sets the stage for maternal immune dysfunction and presumably autism, how is it that a population rife with acute infections evades autism? He doesn’t ever name the “Western doctor,” but autism does exist in Cambodia [ETA: link references an autism population in that nation--"an additional unserved population in Cambodia was children with disabilities. Children with Down Syndrome, autism, or other disabilities typically led isolated lives"--and describes a specific case; see also PDF linked below, which describes data from an evaluation study in Cambodia. I try to avoid paywalls, but here and here are studies addressing developmental disabilities/mental health in the developing world, including Cambodia, and factors influencing the lack of previous diagnosis], and while we’re at it, here are a few other things Cambodian children must endure because they’ve got this great “evolutionary”-based existence that 'protects' them against autism.

[FYI: Here is a great summary [PDF of PowerPoint] of work going on in “developing” countries to better establish what the rates of autism are. I’m not sure what the rate of parasitic worm infections is in each of these places, but I imagine there’s some overlap.]

Whether he means to or not, Velasquez-Manoff then echoes one of the favorite refrains of the anti-vaccine movement, that back when the world was a beautiful place of dirty, worm-infested children, clean water, 100% breastfeeding, and no television, it was a place where the immune system could do its work peacefully and with presumably Zen-like calm, weeding out the weak among us and leaving behind the strong. Of course, infant mortality was sky high, primarily as a result of diseases against which we vaccinate. And I don’t know about you, but I’d prefer to avoid shitting out worms and parasite eggs on a regular basis. But Velasquez-Manoff references those good old days wistfully as the “world of yore” and claims that scientists “working on autism” just aren’t “generally” aware of this evidence linking our modern-world lack of worm parasites, subsequent inflammatory condition, and autism. Poor, stupid clueless autism researchers. He then goes on to cite two people who are not autism researchers.

One of these scientists not working in the field of autism, William Parker of Duke University, compares sewer rats and clean rats in his work (fun!). The sewer rats have a lot of parasites and the lab rats don’t. The sewer rats have “tightly controlled” inflammation; the clean rats don’t.  This researcher and “many others” (unnamed others) think that we should still be sewer rats. [NB: Just as we are not mice, we also are not rats]. Then Velasquez-Manoff quotes Parker noting that it was all cool when we just had some allergies and autoimmune disease because we were too clean, but then adding, “but autism? That’s it! You’ve got to stop this insanity.” If I’m inferring correctly, we have to stop the insanity that is autism--not my phrasing--by picking up some worms and acute infections. Autoimmune diseases? OK! But autism? Insane.

And then the kicker. Velasquez-Manoff actually says that we can stop the insanity: “Fix the maternal dysregulation,” he writes, “and you’ve most likely prevented autism” (italics and jaw-dropped boldface mine). This unequivocal statement is a core untruth of this article. And possibly without meaning to, Velsaquez-Manoff now echoes an even more dangerous refrain from the history of autism research: refrigerator mothers. Except here, the mothers are “dysregulated,” with dangerous wombs and frantic immune systems that have not achieved the appropriate Zen-like state during her pregnancy. I'm expecting Freud to pop in at any moment and start lecturing us about hysteria.

This article no doubt will have many mothers of autistic children scanning their memories of whether they had infections during pregnancy. It no doubt will have pregnant women feeling at least a little paranoid every time they develop an upper respiratory illness or sneeze. No doubt, women with autoimmune disorders, which have a severe female bias whether you're western or not (and generally aren't linked with behaviors associated with autism, even when the nervous system is involved), will worryworryworry, given this specter of the autism "insanity" and their own genetics. And again, I don’t see how desiring to prevent autism with a return to days when everyone had “acute infections” jibes with the implication that maternal infections during pregnancy are linked by subsequently induced inflammation to autism.  

How do we fix this non-Zen-like maternal dysregulation? Worms. Parker proposes “pre-emptive restoration” of what he calls “domesticated” parasites into all people, everywhere, as though parasitic worms were like docile farm animals grazing away in our intestines. [NB: the definition of parasite is an organism that lives in or on a host and harms the host.] In case you think that’s what is insane, there was a clinical trial planned at the Mt. Sinai School of Medicine to try the eggs of these worms to treat adults with autism. The recruiting status of this trial has not been updated in awhile. Velasquez-Manoff writes that a trial is "under way" at Montefiore Medical Center and the Albert Einstein College of Medicine, but I find no hits at clinical trials.gov reflecting that. At the Albert Einstein website, I find such a trial described with a note that says, “This study is still pending.” Perhaps potential candidates have seen pictures of the worm in question and found themselves declining. Regardless, “pending” is not the same thing as “under way.”

The worm in question is a whipworm that typically parasitizes pigs, and there doesn’t seem to be a disease or disorder it or its wormy brethren are not claimed to help. Some of it may be valid and looks quite interesting, but the successful trials have been in autoimmune disorders. No data exist to support using them to treat or prevent autism, much less to claim that they would be preventative. Lest we handle this too lightly, I’ll add that infections with parasitic worms afflict an estimated 740 million people and can cause anemia and malnutrition. Having a bunch of worms growing in your intestines generally isn’t preferable to not having them there.

As he closes with two paragraphs in which he uses, without preamble, the word “superorganism” twice, Velasquez-Manoff then violates science yet again by calling this plan to colonize all people with worms an “ecosystem restoration project.” Never mind the plain fact that you simply can’t go home again when it comes to ecosystems and that colonizing our guts with pig parasites isn’t exactly replaying our evolutionary history. Either way, we are not the organisms we were 10,000 years ago or even 1000 years ago, not even counting the worms, and we won’t be again. Talking about “days of yore” and “time immemorial” doesn’t backtrack the collective changes our species has accumulated since the good old days of rampant parasitic infestations and high infant mortality. And my hope is that articles like this one won’t backtrack us to viewing all of autism as rooted in immune dysfunction and find ourselves once again staring into the abyss of vaccine panic.

What we have here is an argument that relies on shaky and shifting hypotheses of autism and autoimmune epidemics and hygiene, built using sparse data and scientific hints, a poor understanding of basic evolution and ecology, and a paradox of calling for a return to a more infectious past to “cure” autism while blaming immune-dysregulated, occasionally infected mothers of the present for …  autism. In his closing, Velasquez-Manoff argues that evolution provided us with a roadmap of the original microbial and parasitic ecosystems we once were, one that, presumably, if we follow it, will guide us out of the “insanity” and “affliction” that is autism. If it’s possible, that’s where he’s most wrong. Evolution isn’t something that happens with a plan. To describe it in those terms is to have a profound failure of understanding of what evolution is. Where we’re going, evolutionarily speaking, there are no roads.  And it would be better for most of us if there weren’t any parasitic worms, either. 

-----------------------------------
**By "rather limited," I mean by comparison to other autism-related studies, such as gene variant studies, although some of those involve immune-related genes, and that most of the studies available are correlational, thus sketching only a relationship without a cause-effect established. For a comparative, search PubMed for combinations of autism, genetics, genes, immune, immunity, inflammation, etc., with particular attention to mechanistic and functional studies available.
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Update: The writer of the original op-ed has posted an annotated source list on his personal Website. I have analyzed the list and the annotations in the context of the "cause" argument here.

Friday, August 24, 2012

Stem cell clinical trial for autism: proceed with caution


Recent headlines have trumpeted an FDA-approved clinical trial of cord blood–derived stem cells for autism, involving 30 children and two i.v. infusions of cells from each child’s own banked cord blood. The stated rationale is a link between inflammation and autism, but I, for one, find that rationale spurious.

The inflammation–autism concept found its footing in part thanks to a study that appearedin 2005 [open access] and described findings linking inflammation in the post-mortem brain and autism. The researchers, based at Johns Hopkins, had examined donated brains from 11 people with autism, six of whom were children, and in particular found evidence of what they called an “inflammatory process” in the cerebellums of brains from autistic people. The autistic group in this study was highly heterogeneous in terms of ages, causes of death, and the presence of epilepsy.  

The Hopkins work and a handful of other papers led some researchers to focus on inflammation, particularly neuroinflammation, as causative in autism. In spite of some faint signposts pointing to an association, however, the Johns Hopkins group that published the 2005 paper warns on its Website that “there is no indication for using anti-inflammatory medications in patients with autism.” Medications like prednisone, they say, would not affect the brain cells they identified as inflamed because the steroids influence a different part of the immune system.

Although research has yet to link autism and neuroinflammation definitively or even sort of definitively, as with many investigative niches in science, a handful of groups dominates the landscape. Among these groups is a Stanford CalTech team led by Paul Patterson, who has written a book about purported links between the immune system and autism. Their most recent findings [paywalled] in a mouse model of autism suggested an association between what they call maternal immune activation (as might be triggered by a viral infection) and autism. In this work, the authors also irradiated affected mice and performed bone marrow transplants that, the team reported, reduced some of the “autism-like” repetitive and “anxiety-like” behaviors.  On his blog, Patterson emphasizes that this work was done in mice, not people, and does not provide an indication for invasive and traumatic bone marrow transplants for autism. Indeed, he notes, “We have yet to establish whether it was the infusion of stem cells or the … transplant procedure itself--complete with irradiation--that corrected the behaviors.”

The point of a bone marrow transplant is in part to replace and replenish cells that participate in immunity. Stem cells form the replacement material, and of course, medical science now has identified many sources of stem cells. One of these sources is umbilical cord blood, which also contains several other cell types. Parents who want to spend the money for peace of mind can arrange to have their infant’s blood taken at birth and stored privately in a cord blood bank. The self-described “largest and most experienced” bank in the United States is the Cord Blood Registry, which also conducts clinical trials with stem cells from the blood samples. I note that the American Academy of Pediatrics discourages private cord blood banking unless an identified need for stem cell therapy already exists.

Stem cells are, obviously, both controversial and potentially big business. Like gene therapy before it, the field of stem cell therapy was expected to be the Next Big Thing, and for some diseases, it might be keeping that promise. The source of the stem cells can be a big factor in ethics, safety, and efficacy, but the safest and most ethically neutral source for an individual receiving a transplant is presumed to be cells that come from that person. Because cord blood stem cells are taken before mutations make cells cancerous, these cells can be effective in transplants to treat, for example, leukemia.

Possibly the most high-profile potential application of stem cells is as treatment for cancers like leukemia and degenerative neurological disorders. Autism is not a degenerative neurological disorder, but because it is neurological and because of some hints at an involvement of the immune system, groups like Patterson’s have homed in on stem cells as a way to replace ostensibly pathological immune system cells with a fresh, presumably healthy batch. Cord blood seems like the perfect source and relatively safe, and the most desirable approach to administration would be a simple intravenous infusion. A Korean group has tried exactly that for a different disorder, cerebral palsy (CP), infusing a specific type of cord blood stem cells called mononuclear cells into a group of 20 children with CP. Five of the patients, or 25%, showed some improvement. Because this type of trial and treatment is in its infancy, no one know what the long-term implications of such treatments are, but the safety profiles thus far are good.

These results and others applying cord blood stem cells for CP have led to interest in trying out a similar treatment for autism, although not enough time has passed for determinations of long-term outcomes, good or bad. Already, some parents seek stem cell transplantation abroad as a treatment for their children’s autism, even as safeguards for the blood products and their contents are lacking and many for-profit clinics overpromise, at best. In fact and not surprisingly, fraud is common. There is likely no more vulnerable population than parents who are desperately seeking to help their children.

In part in an effort to focus on stem cell interventions for autism in a better-regulated environment, the FDA has just approved a clinical trial that will involve intravenous injection of stem cells derived from cord blood into autistic children, with each child receiving cells from his or her own cord blood. News reports have referred to this planned trial as “groundbreaking,” and one outlet went so far as to announce in a headline that it would “cure autism.” Not everyone, however, received the news with unfettered joy.

The trial is the result of a collaboration between the Cord Blood Registry and Sutter Health pediatric neurologist Michael Chez, who also focuses on an immune link with autism and has written a book about the medical management of autism. Given the news saturation the announcement received, I wouldn’t be surprised if phones at the Cord Blood Registry weren’t buzzing all day long as worried parents anticipating a birth dial in, inspired to bank blood as a treatment against their future child’s possible autism. The Cord Blood Registry appears to want to hammer that point home, offering up this graphic on their clinical research site for the study, emphasizing the CDC’s recent report of a 1 in 88 prevalence of autism in the United States and the five-times greater rates among boys. It’s a clear message to expectant parents who know they’re having boys.

But the graphic and accompanying text don’t say much about the research supporting the endeavor. What we have is a few studies suggesting an autism–immunity link, although not all findings support one [paywall], some partial effectiveness of cord blood cell infusion for cerebral palsy, and no data regarding what effect, if any, a cord blood infusion would have in autism. The rationale for the work appears to be the CP trials and Patterson’s work with a mouse model of inflammation.

In a review that Chez co-authored in 2010 [PDF] about the potential for immune therapy in autism, he cites the 2005 paper from the Johns Hopkins group that assessed inflammation in post-mortem autistic brains. In that review, he also notes that each autistic person has a “uniquely different clinical appearance in each individual” and that there are “subsets of autistic patients” with neuroinflammation. One group from Italy has sought to identify these subsets and characterized four groups: one with immune abnormalities, two with little or no immune abnormalities, and a final group with a mix of traits from the other three groups. Of their population of 245 patients, about 18% fell into the “immune abnormality” group.

The cord blood autism trial will include 30 children, all of whom have cord blood banked with the Cord Blood Registry. Fifteen will receive a stem cell infusion and 15 will receive a placebo injection. After 24 weeks, the two groups and their treatments--stem cell or placebo--will be switched. The endpoints of interest are improvements on behavior scales. Pull together the terms “stem cells” and “autism,” and this trial--based on the news reports at least--looks like a hot science winner.

In the midst of all of this celebration and starry-eyed excitement about stem cells, however, the consumer would do well to proceed with caution. The trial suffers from two paradoxical issues. First, there doesn’t seem to be a specific autism-related rationale for treating children with stem cell injections. Cerebral palsy and autism can have some overlap and be co-morbid, but they are not the same thing. Yet, if the trial must go on, the proposed population seems too small. As Chez himself has noted, autism is highly heterogeneous. As the Italian group found, a minority percentage seems to represent a subset that might have immune problems. The inclusion criteria for the trial don’t mention any immune-related endpoints. With a small group and a high heterogeneity, even if cord blood–derived stem cell infusions have an effect, the results might be so individual and sporadic that rather than giving answers and hope, the trial may just end with a soft thud of equivocal results.

There is a real essence of “stem cells are hot and autism is hot so lets throw some stem cells at autism” here. Science and clinical trials involving a pediatric population in particular shouldn’t rely on the “throw it at the wall and see if it sticks” mode of testing. Regardless of how safe the protocol is, administering even intravenous infusions to an autistic child can be traumatic for everyone involved. A trial like this seems hasty and the ballyhoo surrounding it overstated and overpromising. Finally, if they do find an effectiveness of cord-blood–derived stem cells for treating autism--how does that translate into clinical practice? Currently, autism is diagnosed many months or years after birth. Any family hoping to benefit, at least from direct infusion, would have to have had the foresight to privately collect and store their children’s cord blood for any results of this trial to be applicable. And as I’ve noted, that requires no mean outlay for a possibility—autism— that still remains at around 1%.

See also this post from the California Institute for Regenerative Medicine

Tuesday, August 21, 2012

Why fact-checking matters

Several stories have surfaced lately about writers who have taken, let's say, liberties with facts, quotes, or other people's words. A couple of these incidents arose from work that appeared in books, but the most recent debacle centered on a national magazine, Newsweek. As the brouhaha boiled up, Newsweek noted that it does not use fact-checkers to vet the content of what it publishes:
"The magazine does not have a fact-checking department ... "we, like other news organisations today, rely on our writers to submit factually accurate material."
I'm not one to use exclamation marks often, but ... !!!

Facts, you see, are a low-rent commodity. What's more important these days, where the money needs to go, evidently, is to the Boldfaced Name Writers whose very byline can sell a story or a book. While they rake in sufficient funds to live off of what they write, careless of accuracy or sourcing or originality, other writers who perchance have a more precise and methodical approach to ensuring the quality and originality of their prose sit unpaid and poor. Lots of us are, indeed, rather poor. Regardless of our methods, however, we all need fact-checking, badly.

I'd like to think that facts and accuracy are still worth something to the people who read what nonfiction writers write. The saying is that you shouldn't believe everything you read. Have we now reached the point at which we shouldn't and can't believe anything we read? Savvy consumers with time on their hands and good Google fu can do their own fact-checking. Yet even they may have to get into some meta-meta-fact-checking given that even "trustworthy" publications have demonstrated how very little they care about promoting that trust by ensuring confirmed and accurate information.

How much is the erosion of trust worth? What does Newsweek, for example, have to gain from publishing inflammatory and inaccurate articles, ending up on the defensive in the face of some impressive and highly public correctives? Was it really worth it, Newsweek, not to pay someone to check the facts first? 

I do three jobs for money: writing, editing, and fact-checking. The least well-paid of these is fact-checking. My fact-checking work requires meticulous analysis of research papers, the intent of phrases, interpretation of statistics, and the standard confirmation that digits haven't been reversed in values. I do this work for continuing medical education courses targeting specialty physicians. If my client hadn't hired me to do this work, the level of inaccuracy and downright misinformation that these physicians would receive would not only be indefensible, it could even be dangerous. I've identified mistyped dosage levels and frequencies for medications and misinterpreted conclusions from papers that could have affected clinical decision-making. The fact-checks that I return to my client are cluttered with comments from word one through the conclusion. 

The thing is, each of these courses has a writer, a writer who is an MD with expertise in the specialty at hand. But even experts can screw up, mistype, misinterpret, and miscalculate, sometimes in critical ways. I love the fact-checking work because I feel like I am serving as a detective for the truth, on a small but important scale. As any writer with sufficient humility can tell you, a second and third set of eyes on anything we write is critical. As any writer with sufficient experience can tell you, even when we have deep expertise in our subjects, we can make glaring and embarrassing mistakes, and having someone else check our facts against original sources and interviews is a huge comfort ... and a safety net for everyone involved.

As a behind-the-curtains detective for the truth, I have a hard time understanding why high-profile publications that already suffer from audience erosion would take the chance of screwing up major stories by not having them fact-checked. Fact-checkers don't get a king's salary. Is the loss of your audience's trust in your publication really worth that level of nickel-and-diming?

Wednesday, August 8, 2012

Forced pregnancy testing to attend school: What could be wrong with that?

Let me count the ways this Louisiana high school's policy of pregnancy testing girls and excluding those who test positive or refuse testing* from school fails, well, in just about every way. I have eight.

  1. It punishes only one partner in the "crime" of conception. Will there also be paternity testing and exclusion of the boys or men responsible from school?
  2. It deals with a runaway horse after it's left the barn. Could these monies be better spent on, say, appropriate sex education or--gasp--birth control distribution?
  3. It violates the law. Excluding a girl or woman from a free and appropriate, least restrictive education for a health condition? Nope. Not OK.
  4. It sets a very dangerous precedent. What will schools be able to test for next, without cause? In this case, the only "cause" necessary is having ovaries. Do we really want to go to the edge of that slope?
  5. It is an irrational response to what a pregnant teenager needs. She needs an education, she needs to know that society won't shun or shame her while protecting the anonymous person who fathered the child, and she needs to know that being pregnant and planning to carry a child to term does not have to mean that her life, her reputation, and her self respect are all dead.
  6. It violates health privacy laws. The only person who should have any awareness of whether or not a teenage girl is pregnant is the girl herself and her health care provider. 
  7. It is unnecessary in any educational sense. School officials do not need to have this information in-hand to execute their duties as educators appropriately; pregnancy has nothing to do with whether or not a student has a capacity to learn in a free, unrestricted, appropriate environment.
  8. It is designed to shame. Period. I am baffled about the cognitive dissonance required to holler about respecting life and embryos and fetuses while simultaneously acting as though having sex and being pregnant were the most shameful things a woman can do--not a man, of course--and require public shaming and shunning.
I'd like to think or hope or wish that the days of the Scarlet Letter are over--it's been centuries, after all--but given the continuing war on women--and high-school girls--clearly, we have a long way to go, baby. 

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*Added after posting. Also, the school's policy is described here as quoted below, with a link to the policy document:
According to its student pregnancy policy, Delhi Charter School "reserves the right to require any female student to take a pregnancy test." If the test is positive, "the student will not be permitted to attend classes on the campus of Delhi Charter School."

Tuesday, August 7, 2012

Where do we draw the line on who gets--or deserves--an organ transplant?

You'd think that being young and otherwise reasonably healthy might be a good criterion for getting you on a list for an organ transplant if you need one. Or that having a donor, say for a kidney, at hand and at the ready in your own family might make it OK for you to receive a transplant. What you don't want to think--really, consider this--is that you'd be denied a transplant because of your mental condition or level of intellectual ability. If ever there was a slippery slope in medicine, this one is a black diamond coated in ice.

In January, a three-year-old girl made the news--and her story went viral--when the medical powers that be denied her the opportunity to receive a kidney transplant from her own mother. The girl, Amelia Rivera, became the subject of various petitions and amidst a general outcry, the hospital that denied her transplant, Children's Hospital of Philadelphia, officially approved Amelia to receive the transplant, again from her own mother. Amelia has Wolf-Hirschhorn Syndrome, a rare genetic disorder, and will die unless she undergoes a kidney transplant. Her mother detailed her early experiences with the medical staff during this decision process here. The medical professionals tried to draw a line between being intellectually able enough to warrant a kidney and a life and being so intellectually disabled that life is not worth saving or prolonging.

Amelia's case was so clearly one of misguided decision-making--have I mentioned that she had a donor at hand, her own mother?--that any other outcome than a "yes" to her transplant would have been indefensible. But today, we've got another case. This one involves a 23-year-old man who needs a heart transplant. Obviously, he has no donor at hand, as people cannot donate hearts and live. And, it would seem, medical decision-making can involve more than deprivation of a beating heart and a life. It also can involve a different kind of heartlessness, a cold calculation that might have made Darth Vader flinch before his own postmortem rehabilitation.

Again, the trigger here is a rare disorder, in this case a reduced capacity for ejection of the blood from the left ventricle of the heart, the muscular chamber responsible for shooting that blood out of the heart and into your circulatory system. It puts the "pump" in the "pumps blood" part of the heart's primary duty. You can imagine some of the possible outcomes if this pump fails. Right now, Paul Corby's 23-year-old pump is operating at about 20%, not unlike the heart of his father, who died at age 27 before his rare heart condition was discovered. That means that Paul Corby is at least at greater risk of stroke and certainly under threat of heart failure and an early death. Indeed, according to Joslyn Gray, who broke this story at Babble, Corby's already had a handful of mini strokes. Did I mention he's 23?

He also is autistic.

According to the doctor who determined that Paul Corby shouldn't be placed on the transplant recipient list for a life-saving heart transplant,
I have recommended against transplant given his psychiatric issues, autism, the complexity of the process, multiple procedures, and the unknown and unpredictable effect of steroids on behavior.
In other words, his autism precludes his being a suitable transplant recipient. His mental condition precludes it. His history of angry outbursts--presumably the reason for concern about "unpredictable effects of steroids"--precludes it. And for some reason, the fact that a heart transplant is complex and requires multiple procedures, something that presumably applies to anyone receiving one, is also relevant in his case.

For some context, let me introduce you to someone who received a heart transplant just last March. He is 71, a smoker for 20 years who has survived five heart attacks and was in end-stage heart failure at the time of his transplant. Evidently, his mental state was not a contraindication for his having a transplant, so after 20 months on the list, he received one. His name is Dick Cheney.

Is it appropriate to prohibit someone from placement on a transplant recipient list because of a developmental disorder like autism or because of issues of mental health? In essence, this exclusion of Paul Corby, a never drinker and never smoker and author of a self-published book, from the transplant recipient list, is a message that if you are an Other, if your mind does not meet some critical cutoff for mental health, if your behavioral history does not come up to snuff, if you have a developmental disorder, if you are autistic, you are not worthy of having your life saved, or even of a chance to get on the list of those hoping for it.

Who else would find themselves excluded under these criteria? Anger concerns? Will people with narcissistic personality disorder who rage find themselves excluded? Unpredictability? Look out if you've got a history of bipolar disorder. Developmental disorder is a contraindication? If you or your child has a diagnosis of ADHD or autism, then guess what? You're Not Worthy.

The Babble piece quotes a professor of bioethics, Jeffrey Kahn, as saying,
You want to make the best use of a very precious organ. You want to make a successful use, not waste it. And ‘waste it’ doesn’t mean that the person doesn’t deserve it, it’s that we don’t think it will be successful. If there is a real medical concern, that is legitimate.
What seems absent here is a medical rationale for excluding Paul Corby from the transplant recipient list. Obviously, if there were a genuine medical contraindication, then a transplant would be precluded. But based on what the hospital wrote, nothing in the list of reasons specifies a medical contraindication. It's all behavioral. It's all about mental health. What is the legitimate, evidence-based reason for mentioning autism or even mental health at all?

The Babble piece quotes Kahn as adding,
I think that the key distinction,” Dr. Kahn said, “is that we as a society are not willing to say, ‘that person’s life is worth more than another’s,’ based on their contribution, the quality of their life, their intellectual capacity. If that’s what’s happening in this case, that seems to be an outlier. It’s not the way that we have decided to allocate this scarce resource.
Making god-like determinations about what constitutes a worthy life, based on intellectual capacity or mental state? Not something that we, with our limited human vision, should be doing. Imagine whom we would have lost in the arts, sciences, literature, and most important, our simple day to day lives and loves if those were our criteria for determining who is worthy.

I hope that the medical professionals involved here, including those at Penn Medicine responsible for this denial of Paul Corby from the transplant list, reconsider what they've done. With this decision and their stated rationale for it, they send the message that the Powers That Be can decide, with impunity, that you are Not Enough, not for medical reasons but for who you are, how you behave.

And make no mistake, not a single one of us is Enough in some way or another. Not one of us meets every standard of normality or OKness in our being and behavior. Would it be all right with you if you--or even worse, your child, God, so so very much worse--were denied a chance at living because someone determined that their differences, their variance from some norm, made you--or them--unworthy? Have we not, in this world, seen enough of this kind of deadly decision-making based on assumptions and presumptions about what constitutes a worthy human life?
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Corby's mother, Karen, has started a petition at Change.org to lobby on behalf of her son. A similar petition may have had an effect in the Amelia Rivera case.

Sunday, August 5, 2012

Is a PhD required for good science writing?

Short answer: No. But you can make these funny hats
and gowns part of your permanent wardrobe.
Photo via Wikimedia Commons.
What's required to make stories about science accessible and accurate for the nonscientist? Daniel Bor discussed this in a comment on a piece he wrote about the Jonah Lehrer deception. In the comment, Bor said,
I think scientific journalism could immediately be improved by assuming that you need at least a PhD for the job.
Not surprisingly, while acknowledging the soundness of Bor's original post, many science writers took issue with this assertion. Bor did take a step back and say that he was happy to admit he'd gone too far making the PhD point. As much as I'd like to see expanded job opportunities for science PhDs, I agree that this method ain't the way to do it.

In fact, as someone who has a PhD in science but has been a writer longer than I've been a scientist, I'd argue that it might be better not to have specific training in science if you're reaching for an audience of nonscientists, depending on what your goal as a writer is. If your goal is to tell a great science story that keeps the nonscientist reading and thinking, "wow" or "I get it," then scientific training might be an anti-requisite. If your target is critique and analysis of science, then scientific training could be quite useful as long as you don't let your deep background blind you to what your readers might not understand as well as you.

Arguments like these always seem specific to the sciences. Economics looks like a jargony wasteland to me as someone little familiar with its terminology and landscape, but I can't recall seeing requirements that journalists covering the economy must have economics degrees, much less PhDs in the field. What is required to become a respected journalist extends beyond esoteric knowledge. A respected journalist builds trust with an audience and earns that respect with a track record of overall accuracy, decent writing, and a dedication to openness. Good journalists in any subject area build their hours of understanding the way they build what we used to call the Rolodex of contacts: with hard work and asking the right questions.

And it's asking the right questions that really matters. My experience has been that the closer I am to a subject scientifically speaking--i.e., when it's relevant to my field of research--the worse I am at asking the right questions about it, filling in gaps for a nonexpert, and writing about it comprehensibly and comprehensively. In fact, my worst work for the nonexpert audience has always involved my areas of scientific research. A deep understanding of a topic acquired by way of contributing to the research field has done me no favors when it comes to writing about that subject for a nonscientific audience. We are talking major suckage here.

My best work has emerged when I have a relatively limited grasp of the science--probably at the level of anyone who has completed a college physics class. I know enough to start the questions, I know enough to read a research paper and get the gist, but I don't know so much that I leave out critical questions in interviews, questions with answers that might help both a reader's understanding and my own. Possibly even as critical for writing a good piece (Slate's editorial stance notwithstanding), I end up getting great expository quotes from experts. That's not easy to do, and if your approach is one of already knowing everything and avoiding asking the "obvious" questions, you're not going to get those good quotes from good interview subjects. And that means you'll miss one of the greatest joys of journalistic writing.

Rather than being dangerous, a little knowledge can be a great tool as long as a writer uses it appropriately and has no compunction about revealing ignorance in a subject area. That's another place where having extensive training in the sciences could be an obstacle. What scientist--or formerly practicing scientist--wants to get into a conversation with a colleague or peer and show general scientific ignorance? I don't know about other people who have combined writing for a nonexpert audience and scientific training, but for me, I have to watch myself carefully in interviews. I'll sometimes find myself interpreting back to interviewees or explaining before they finish explaining, in part, I think, from reflexive need to let them know, peer to peer, that I get it. I have to stop myself, let them finish, ask the "ignorant" questions. Ego's gotta stay out of it or Ego will interfere.

Where ego and training and depth of understanding can be an asset rather than a liability is if your wheelhouse is criticism, commentary, or general opinionating. Deep expertise--whether acquired through graduate training in science or putting in 10,000 hours of journalistic effort in a topical niche--confers the necessary grounding and cachet a writer needs to build audience trust in and respect for those opinions and critiques. Without getting too starry eyed or blindly invested about it, I'd trust a critique of microbiological resistance studies from Maryn McKenna just as much as I would trust such a critique from any peer reviewer. If Deborah Blum's got something to say about the chemistry of a news story, as background or the story's focus, she gets my attention just as much as any trained chemist would--probably more so, thanks to her lyrical writing, a double treat for a science writer/reader. If Carl Zimmer pens articles about human lakes, viruses, or science-related tattoos, I'll tend to trust in what he writes because he's focused relentlessly, accurately, and gracefully on these topics for a long time. None of these writers has a graduate degree in science or even majored in science. They have instead dedicated their hours to the combined pursuit of science and writing, with wonderful results. 

But in the case of critique, I'd be just as willing to rely on insights from a scientist trained in the specific field involved. Like the writers I've named above, deep scientific training qualifies scientists to critique within their subject areas. If they give up the lab bench for writing, that expertise will inevitably broaden around a core interest, and the combination of science training and hours of writing experience can take them to the level of a Blum, McKenna, Zimmer, or David Dobbs when it comes to critique and analysis in combination with reporting. But if those scientist-to-writer types are anything like me, they should stay far, far away from their dissertation topic as a writing focus unless critique is the goal.

No one's concocted a magic formula for the best combination of science training and writing when it comes to science writing for the nonexpert audience. What I do know from my own experience as a writer, which happens to bookend earning a doctorate in biology, is that having a PhD can be a hindrance as much as a help and certainly cannot be considered the sine qua non qualification for writing about science. The bottom line is that regardless of how you succeed as a science writer in building trust with your audience, your success will depend in large part on three factors: your dedication to accuracy and its pursuit, your willingness to check Ego at the door, and your focus on crafting work that reaches and resonates. No PhD required.


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ETA: Back in February, journalist and now-PIO Matt Shipman also addressed what makes a good science writer. As he notes on Twitter, we agree