The Agricultural Biodiversity Weblog recently posted a transcript from the BBC radio program Farming Today. In it, Brande Wulff of the Sainsbury Lab describes what the host characterizes as “a technological revolution that will change the way the world’s crops are grown.”

“Dr Brande Wulff (Sainsbury Laboratory, Norwich): Well this is a huge leap forward. Traditionally it would have been a, a marathon of five years or so to do this type of work or possibly even a long distance endurance event of ten years or so. Now we’ve reduced that to a short sprint of one or two years. So it’s, time is in, is the essence in this type of work and so it’s really a huge leap forward.”

So what did they do?

1. They mutated an elite line of rice with a chemical mutagen (EMS)
2. They created advanced mutant generations (e.g. M2) so that recessive mutations would be visible
3. They identified several plants that showed new traits (in this case, pale green leaves and semi-dwarf stature – the latter of which is an agriculturally important trait)
4. They crossed each of these individuals to the wildtype parent line and generated segregating F2 populations
5. They pooled all F2 plants that showed each new trait and re-sequenced their genomes
6. They compared this mutated genome sequence to the wildtype parent reference sequence and identified the genes that were associated with the new traits

What part of this is a technological revolution?

1. Identifying single genes of major effect? No, this is already easily done.
2. Improving our ability to sort out quantitative traits (many genes of minor effect)? No.
3. Creating novel genetic variation through mutagenesis? Nope.
4. Identifying genes associated with a trait just from genomic data? No.
5. Improved phenotyping? Not at all.

From what I can tell, they’re simply TILLING by sequencing, which is already performed as a service by biotech companies and academic labs. They have some clever tricks, but I don’t think any of them improve the state of the art very much.

The problem really comes down two points.

First, it’s very rare for important agricultural traits to be controlled by single genes – both because most traits are far more complicated than this and also because these easy to identify genes have largely been sorted out already. I’d be surprised if there’re many of these low-hanging fruit left to be harvested. Second, the biggest bottleneck in all forms of crop improvement is phenotyping. It’s relatively easy to identify one semi-dwarf plant out of several thousand full stature plants. It’s incredibly difficult to quantify complex, environmentally-sensitive traits like yield and stress resistance. I’m not going to go into all the reasons why this is true, but it’s the reason why traditional mutation breeding has been mostly limited to obvious traits.

And here’s the thing I really don’t get. They picked out their new phenotype (as far as I can tell) in the same inefficient way everyone has since the beginning of breeding – the only thing they apparently improved was their ability to identify a single gene of major effect that causes an already identified phenotype. Which is the easy part.

I’m disappointed that the state of breeding was so oversold to the media. I frequently hear such incremental scientific progress sold as technological breakthroughs. It makes for more exciting news stories, but it also raises public expectations to unrealistic levels that ultimately make science advocacy more difficult. One lesson I think we can all take from this is to make sure we’re communicating with professionals in other sectors of our field. There’s no reason for plant molecular biologists laboring to improve plants to misunderstand the challenges and limitations of actual applied programs.*

* And in this case, I’d announce to all that developing a new crop variety, no matter the method, rarely takes much fewer than ten years – and no one is likely to consider buying your variety if you don’t have data from a few years of multi-environment trials in the target environments.

Abe A, Kosugi S, Yoshida K, Natsume S, Takagi H, Kanzaki H, Matsumura H, Yoshida K, Mitsuoka C, Tamiru M, Innan H, Cano L, Kamoun S, & Terauchi R (2012). Genome sequencing reveals agronomically important loci in rice using MutMap. Nature biotechnology PMID: 22267009

New book by Robert Trivers, Deceit and Self-Deception

Few variables are as important in our lives as our perceived moral status. Even more than attractiveness and competence, degree of morality is a variable of considerable importance in determining our value to others—thus it is easily subject to deceit and self-deception. Moral hypocrisy is a deep part of our nature: the tendency to judge others more harshly for the same moral infraction than we judge ourselves—or to do so for members of other groups compared to members of our own group. For example, I am very forgiving where my own actions are concerned. I will forgive myself in a heartbeat—and toss in some compassionate humor in the bargain—for a crime that I would roast anybody else for….

In this foundational book, Robert Trivers seeks to answer one of the most provocative and consequential questions to face humanity: why do we lie to ourselves?

Deception is everywhere in nature. And nowhere more so than in our own species. We humans are especially good at telling others less — or more —than the truth. Why, however, would organisms both seek out information and then act to destroy it? In short, why practise self-deception? To biologists this has long been a mystery. Our sense organs have evolved to give us a marvellously detailed and accurate view of the outside world. So why should natural selection then lead us to systematically distort what we know?

After decades of research, Robert Trivers has at last provided the missing theory to answer these questions. What emerges is a picture of deceit and self-deception as, at root, different sides of the same coin. We deceive ourselves the better to deceive others, and thereby reap the advantages. From space and aviation disasters to warfare, politics and religion, and the anxieties of our everyday social lives, Deceit and Self-Deception explains what really underlies a whole host of human problems. But can we correct our own biases? Are we doomed to indulge in fantasies, inflate our egos, and show off? Is it even a good idea to battle self-deception?

With his characteristically wry and self-effacing wit, Trivers reveals how he finds self-deception everywhere in his own life, and shows us that while we may not always avoid it, we can now at least hope to understand it.

Syndicated from GMO Pundit aka David Tribe.

Frank likes bees too.

When I was an undergraduate, I spent about a year or so working as a beekeeper. It was a fun job, and I learned all sorts of fun facts about bees. By this time I had been interested in parasitoids for nearly a decade and a half, having raised parasitic wasps out of caterpillars since I was five. Naturally, I attempted to see if there were any parasitoids which attacked Apis mellifera but I always ended up empty handed and disappointed. This always confused me because there were parasitoids which attacked ants, termites and caterpillars living in ant nests. I never understood why parasitoids had never been documented attacking honeybees.

This changed earlier this week, when a description of a parasitoid fly which attacks bees was published in PLOS ONE: A New Threat to Honey Bees, the Parasitic Phorid Fly Apocephalus borealis by Core et al. Unfortunately, the authors tried way too hard to connect the fly to Colony Collapse Disorder, but I’ll discuss that later. First…

What are Phorid flies? What are parasitoids? Why do we care?

Figure 1 from Core et. al 2012. I labeled the identifying characteristic of the family Phoridae with a black arrow and the ovipositor which is convergent with a wasp stinger with a red arrow.

Parasitoids are insects which are parasitic as larvae, free living as adults and which kill their hosts after development is complete. Most parasitoids are either flies or wasps, with wasps being the best studied. They’re important to agriculture because they’re good at regulating the populations of their hosts by killing them in large numbers. My studies revolve around how these insects evade the immune system, which gives us a springboard to learn more about how insect immunity works on a biochemical level.

Parasitoids in the family Phoridae are particularly interesting. Most species, such as the very common Megaselia scalaris, are actually scavengers but some species have made the leap to parasitism. The paper lists a particularly great example of parasitoid phorids, the decapitating flies which are used as fire ant biocontrol. These flies can be identified by a bunch of scrunched up veins on their wings, labeled by a black arrow in the first picture.

Figure 1 B from Core et. al 2012. The fly is visible laying it's eggs into the abdomen of the bee to the left of the picture.

Parasitoids go through standard holometabolous development of egg, larvae, pupa and adult. The adults lay eggs either on or inside their hosts. The larvae develop within the hosts, pupate, and then hatch into adults. Each of these stages requires particular adaptations, and parasitoid wasps and flies use completely different strategies. Larvae, for example, must evade the immune system. Wasps tend to suppress the immune system through venom or polydnaviruses. Flies, on the other hand, tend to hide in tissues which aren’t easily accessible to the immune system. They also have a tendency to hijack the immune system in some rather impressive ways like using melanization machinery to build snorkels to keep the parasitoid larvae supplied with air.

Sometimes, however, parasitoid flies and wasps solve similar problems with similar solutions. This parasitoid oviposits inside the host like the wasp, but uses a hard spike on it’s fleshy ovipositor to help it insert it’s eggs into the bee. I labeled this with a red arrow in picture A.

In the picture above, you can see the fly laying it’s eggs into the abdomen of the bee. From here, the eggs hatch and hatch into larvae which feed on the bee’s tissues. After this the larvae emerge in a particularly gruesome and characteristic fashion, between the head and thorax. The larvae emerge from under the ‘chin’ of the bee after the bee leaves the colony at night.

Fly larvae emerging from honeybee host, highlighted with red arrows.

This is a particlularly interesting example of a host shift. Apocephalus borealis is a specialist on bees and wasps, so a shift to Apis mellifera makes sense because it has a similar immune system. Honeybees hail from Africa, whereas this parasitoid is uniquely American so this is a definite example of a native parasitoid infecting and adapting to a new host.

What about Colony Collapse Disorder?

Despite the good job the authors did documenting the development of this parasitoid inside the honeybee, they lose my enthusiasm when they get to the colony collapse stuff. I really think they did some good work on natural history in this paper, that is they did some good work on looking at how the flies develop in the bees in labs. However, there are some things which weren’t very well fleshed out in this paper which mostly pertain to CCD.

I really think they tried too hard to connect this fly to CCD and this part of their work wasn’t very well performed. In their defense, I think the main purpose of this paper was the natural history work on this parasitoid. The CCD work appears to be done as almost an afterthought, but given the high profile of the paper I thought this warranted it’s own dissection.

To investigate internal hive behavior and possible infections within a hive, we kept an observation hive in a laboratory near our primary study hive. Samples taken from the observation hive in June 2010 confirmed infection with A. borealis. Rates of infection varied between June 2010 and December 2010 (Mean = 25% Range = 12%–38%) peaking over the sample period in November at 38%. In September, the number of bees in the hive declined and we observed phorid pupae and empty pupal casings among dead bees at the bottom of the hive, indicating emergence of adult phorids within the hive and the potential for A. borealis to multiply within a hive and infect a queen.

Let’s overlook the fact this was observed in a single hive kept differently than how most bees are housed. There’s a bigger issue here.

At my university, I am the curator of the insect zoo. We used to have some pretty big problems with Megaselia scalaris in our roach colonies. M. scalaris is a very common phorid fly that develops on dead and dying insects. Weakened hives aren’t able to fight off scavengers, so it’s possible in my view that Megaselia could have been in the hive after the populations declined because the large number of fresh dead bees would be the perfect environment where this scavenger could develop. The authors didn’t explicitly explain how they differentiated Apocephalus puparia from Megaselia puparia, and I think this is a fatal flaw in their work. These are two very similar looking Phorids with ecological habits that couldn’t really be more different. Megaselia does not develop as a parasitoid, and would thus pose no threat to the bees.  I think this is a rather important oversight and I wouldn’t trust their conclusions without further explanation of how they differentiated between the two. Put bluntly, I don’t think this piece of data should have been in this paper without that information.

Secondly, they did a bunch of tests looking for bee pathogens in the Phorids. They looked for genetic material, correctly noting this didn’t necessarily indicate that the pathogens were growing inside the flies. Quite frankly, I think it would be very strange if a parasitoid which fed on tissues of a bee didn’t consume any of it’s pathogens even if those pathogens didn’t infect the fly. Many science writers have been confused by this result, and many articles give the impression that the authors thought the flies vectored the pathogens. I find that doubtful but I won’t completely rule it out. Either way, I need to point out that it doesn’t come anywhere near proving it because there is no data indicating the pathogens were growing inside the flies. They also pointed out a correlation between Phorid emergence and the point of the year when colonies collapse, but demonstrating causation needs more data. The authors explicitly stated all of this, but some writers didn’t realize this.

Third, the majority of the data dealing with how the bees act when infected with the flies appears to have been conducted on a very specific building of the campus of San Francisco State University. That’s well and good, but urban beekeepers are a very specific subset of beekeepers and this data might not be relevant to most beekeepers, and thus irrelevant to the hives most important to agriculture. I think they need to do a lot more work on behavior before we can make any solid conclusions on how parasitized bees act in the wild before emergence of the parasitoids.

I don’t blame them for trying to connect this parasitoid to CCD, because that’s the hot topic right now in bee biology. However, I don’t think this fly really has much to do with the collapse of honeybee colonies. Despite this, this is still a really important find because this fly could shed more light on CCD, but not in the direct way the researchers imply in this paper. This is an insect which invades the bee and evades it’s defenses. Figuring out how the fly evades the bee’s defenses could shed light on how the bee’s immune system works. Figuring out how the bee’s immune system works might help us figure out how whatever pathogen actually does cause CCD is also able to evade the defense mechanisms of the bees. Once we fully understand the bee’s defense mechanisms, we can then think about potential interventions based on this data.

And now… some gratuitous parasitoid videos. These are particularly impressive examples of physical grace and biochemical warfare from some of the most incredible critters in the world.

A special thanks to Bug Girl for pointing out the Biodiversity In Focus article.

Core, A., Runckel, C., Ivers, J., Quock, C., Siapno, T., DeNault, S., Brown, B., DeRisi, J., Smith, C., & Hafernik, J. (2012). A New Threat to Honey Bees, the Parasitic Phorid Fly Apocephalus borealis. PLoS ONE, 7 (1) DOI: 10.1371/journal.pone.0029639

By Emily Willingham

Rice.

A study from a Chinese group led by Chen-Yu Zhang of Nanking University and published in Cell Research, has uncovered the fascinating result that when people eat rice, they can absorb microRNAs (miRNAs)–tiny sequences of RNA–from the rice into the blood. These rice-originating miRNAs turn up in blood and tissues of people who eat rice and…here’s the kicker…one type of rice miRNA interacts with human proteins that are responsible for removing LDL (“bad” cholesterol) from the blood (!). It’s the first report of plant miRNAs ending up in people by way of diet and the finding that at least one of them alters an important process in the body.

The implications could extend in many a direction, but not as far as writer Ari Levaux would like to take them in this remarkably confusing article published on the Atlantic Website. Before taking on the errors and the overstretch that are that piece, let’s look at something far more interesting: miRNAs themselves.

These little bits of RNA, consisting of 22 building blocks linked in a single strand (a human DNA molecule has billions) get around with surprising facility, and their purpose is to regulate genes. They don’t regulate by latching directly onto a DNA sequence but instead lurk in the cell and interfere with processes that come after the gene’s role is complete. If you consider the gene sequence as the directions for building a protein, one job of RNA is to serve as a copy of those directions. It takes on the risky business of toting that copy out of the safety of the nuclear vault in our cells and into the big, bad scary cytoplasm outside. In the cytoplasm, the fluid-ish environment of the cell, RNA has many, many roles, but all of them center on executing the directions encoded in the gene for building proteins, the molecules that help make up our tissues and perform the tasks required to keep us alive.

In some cases, though, RNA occurs in the form of miRNAs, and their job may well be to bollix up the protein-building works. These little molecules–which researchers have identified in the hundreds in humans–can, for example, latch onto an RNA that is a copy of the protein code and cause it to break down or keep the cell from using it. These tiny RNA sequences help fine-tune the process of protein building well beyond the starting point of directions copied from a gene sequence. Thanks to miRNAs and many other steps that can promote or interfere with protein building, the cell–and the organism–has several chances to modulate how much of a specific protein it makes, allowing agile, real-time responses to changing conditions.

Researchers have discovered myriad ways that miRNA influences human development and disease, and these discoveries open the way to using that information to cure disease. But all of the miRNAs investigated thus far in people have come from people themselves, either present for normal functions or overabundant and linked to disease. The flashy take-home from this latest rice study is, We can pick up these tiny regulators from what we eat…and they can interfere with the functions of proteins we make.

This take-home could have huge implications for how diet influences our health and development if other non-human miRNAs turn up that fit the same profile: absorbable after we eat them and modifying how our bodies function. The effects could be good, bad, ugly, or neutral. This paper is simply an open door. Now, for years and years, investigators will walk through it to find a number of research paths to explore, from seeking more non-human miRNAs and identifying their effects to evaluating how modifying diet might influence disease or human development via miRNAs.

In spite of how much lies ahead and how relatively little lies in the present about this discovery–one rice miRNA, one human effect–the piece that appeared today in the Atlantic argues that the implications are immediate and dire and related to genetically modified organisms. I initially read the piece trying to identify how someone could make that leap but instead found myself distracted by how poorly the article presents the science itself.

First, the headline: The Very Real Danger of Genetically Modified Foods. I read the Cell Research paper. I can’t find mention of GMOs in it. I don’t find mention in the paper the the rice miRNA in question derives from a genetically modified rice strain. So, I don’t see that this headline appropriately represents the science here.

Then there’s the dek: “New research shows that when we eat we’re consuming more than just vitamins and proteins. Our bodies are absorbing information, or DNA.” That’s not what this research shows. It shows that the body takes up a specific rice miRNA when people consume it. Not DNA or “information.”

The lede leaves out a crucial modifier: the word “rice”: “Chinese researchers have found small pieces of ribonucleic acid (RNA) in the blood and organs of humans who eat rice.” Actually, miRNAs are present in the blood and organs of…all humans, whether they eat rice or not. I think the writer here means “small pieces of rice ribonucleic acid.”

There is then a series of claims about what the research implies, including, mysteriously, that it will help us learn how some “herbal medicines function.” The original paper makes no mention of herbal medicines, although some research indicates that “natural agents” can alter expression of human miRNA. Also among the potential implications described in the piece is, “And it reveals a pathway by which genetically modified (GM) foods might influence human health.” That’s an enormous leap to make from “one rice miRNA in blood and tissues influences activity of one human protein.” A number of steps would be required for a GM food to exert a similar effect, none of which have been investigated yet. These steps include identifying that the modified sequence in the target food either also encodes a miRNA sequence or interacts with its expression or, later in the gene-to-protein process, somehow evades normal miRNA regulation thanks to this change.

Then suddenly, there’s Monsanto and a strange effort to explain the central dogma of molecular biology (DNA–>RNA–>protein) using a pizza/pizza restaurant analogy that involves the “DNA” knowing what kind of pizza “it wants,” although in truth, the cell is the entity in charge of which parts of the DNA it uses. The central dogma, a linear representation of how a cell copies DNA into RNA and then uses the RNA copy instructions to build proteins, is too simple for what we know today about how cells regulate protein expression. But the core dogma remains intact, including that DNA serves as the template for making RNA.

The article makes a number of other scientific errors, including in a bold pull quote claiming, “The Chinese RNA study threatens to blast a major hole in Monsanto’s claim. It means that DNA can code for microRNA (italics mine), which can, in fact, be hazardous.” No. That’s not what the Chinese study “means.” It’s not news that DNA encodes RNA of all kinds. It encodes the messenger form that carries the copy of the code. It encodes the ribosomal form that is a component of ribosomes, the cell factory workers that take the code copy and use it as an instruction book for building proteins. It encodes the RNAs that bring those factory workers the molecular blocks the cell uses for building proteins. And it encodes miRNAs. This latest paper does not carry the meaning that DNA encodes miRNAs–that’s a longstanding part of the Central Dogma, ironically, and not news. Nor does it threaten in any discernible way to “blast a hole” in much of anything. As I noted, the study opens a door.

In closing, Levaux writes,

The news that we’re ingesting information as well as physical material should force the biotech industry to confront the possibility that new DNA can have dangerous implications far beyond the products it codes for. Can we count on the biotech industry to accept the notion that more testing is necessary? Not if such action is perceived as a threat to the bottom line.

That's a lot of rice. U gonna eat that?

“Ingesting information”? The miRNAs are not “information” (they are noncoding molecules), and like all other things of this world that we’ve identified, they’re not somehow distinctive from “physical material.” There is naught in this study that implies that “new DNA” can have “dangerous implications” far beyond the products it “codes for.” The miRNAs in this paper are not “new.” They are from rice, the most-prevalent grain crop in Asia, and presumably something humans have been taking in for hundreds of years. It’s unclear from this study even what the implications of the findings are for consumers of regular rice, much less what they’d be for modified organisms. Furthermore, we are not the only entities that modify organisms. Nature does so, often by way of viruses. I wonder why the fact that miRNAs are also present in viruses and could “potentially regulate host genes” didn’t set off the anti-GMO alarms, too.

The article goes on for several grafs about Monsanto and substantial equivalence–indeed, the writer devotes a mere 180 words or so of 908 to the study itself–and observes that the lead author on the Cell Research paper (wisely) declined to comment on any implications about these findings for GM foods. If only the Atlantic and Ari Levaux had done the same, the real implications of this remarkable work could simply stand on their own.
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For an article that focuses more on the research findings from the study, including design and other dietary miRNAs identified, see this piece by Anne-Marie C. Hodge at Scientific American.

ETA: As for the study itself, the effects the authors found weren’t earthshattering, and it seems that there was an issue with images provided that required a rapid erratum after the paper was published.

Follow-up: The author of the piece, Ari Levaux, has responded here, and I have replied just below that.

Follow-up follow-up: Ari Levaux has tweeted that he is going to rewrite the piece, taking the scientific critiques into account. I’m looking forward to seeing the update.

Emily Willingham has a bachelor’s degree in English and a PhD in biological sciences, both from The University of Texas at Austin, with a completed postdoctoral fellowship at the University of California, San Francisco. She blogs at The Biology Files about how science and writing about science take shape around the audience known as You. She is the author of The Complete Idiot’s Guide to College Biology and currently working on a book about lice. Yep, “lice.” She bets you’re about to scratch your head right now.

Environmental Outlook: Labels for Genetically Modified Foods

In 1992 the FDA ruled against requiring labels for genetically engineered foods. Join us for a panel discussion on the rationale for that decision and why some are urging the FDA to reconsider its stance.

Thomas Redick: Global Environmental Ethics Counsel

Gardiner Harris: Science reporter for The New York Times and author of the mystery novel “Hazard.”

Gary Hirshberg: President, Stonyfield Farm, Inc.

The development of the roster of guests was rather interesting, and bears mentioning. It has gone through numerous rounds of change. Initially, Val Giddings, President of Prometheus Agricultural Biotech, was going to be on the show, and then they also decided to add Doug Gurian-Sherman from the Union of Concerned Scientists. Then they switched to inviting our own Pam Ronald from UC Davis, and for a brief time period her name was also on the website. I heard from Pam last night that they decided that they did not want to have a science section on the show, and canceled that part of it.

In this whole process, it seems, the producers were trying to “balance” the show, but each iteration of the process showed that a false balance was being achieved. The journalist Chris Mooney has described the trap that some journalists fall into when covering science-related issues is to give equal time to scientists that represent the consensus of the scientific community and those that represent outlier or minority positions. This show was about to go even farther by giving this minority viewpoint more time on the show than for responses from the practicing scientist guests, and as a result, there was difficulty negotiating the interview.

But the end result may be more appropriate. The newly-added guest, Thomas Redick from GEEC sounds interesting, and it appears that he argues against labeling, as evidenced by a book he co-authored, Thwarting Consumer Choice: The Case against Mandatory Labeling for Genetically Modified Foods. I am not familiar with him or his arguments in specific, so that will be new to me.

So have a listen, I will be, and represent science by calling in as early as you can to ask questions! Feel free to discuss the show below live or afterward.

(This just in: at the last minute, they have added and advertisement for a pro-labeling e-book by Hirshberg and other critics of GE, making it pretty clear the intent of the show.)

I like to think of myself as a skeptical blogger. I like to engage in critical thinking about scientific issues because this is an important aspect of my job as a graduate assistant. When I move into the workforce, I’ll still need some basic skills to parse evidence because this is my job as a scientist. Mythbusting is a great opportunity to do this, and I enjoy discussing things which may help people who read my posts whenever I can. Being an entomologist gives me some rather interesting opportunities to do this, which is leading me to discuss head lice of all things.

Pediculus humanus capitis by Gilles San Martin via Flickr.

In my last post, Do OTC Head Louse Treatments Work? Part 1: Mechanisms, I explained how the most commonly used FDA-approved treatments worked. In addition to those science-based products, there are many products that have no evidence of efficacy behind their claims, and that rely on fear to make a sale. What I’ve seen deeply concerns me not only as a scientist trying to make the world a better place, but as a parent trying to raise my daughter the best that I can. In this post, I’ve taken a few commonly sold products and listed some ways in which I think they play fast and loose with their claims.

A very brief review of how the nervous system works and how pesticides work in general can be found in the video below:

How do we know if treatments work?

Before getting down to the business of mythbusting, I think it’s appropriate to discuss how we know various products work. Treatments are assessed through clinical trails where infested volunteers subject themselves to putative treatments which are known as in vivo trials. In some cases, the lice are removed from the volunteers and exposed to the treatments in petri dishes which are known as in vitro treatments. In vitro treatments must be performed with the louse’s biology in mind because removing the louse from the host means that the louse is no longer in its natural environment. If the louse is not in it’s natural environment, the results gained from such a test may not be applicable to a real infestation. In vitro tests can disprove that a product works under ideal conditions, but proof of efficacy ultimately requires that the product be tested in real world conditions.

Clinical trials must have large numbers of people (and large numbers of lice) and untreated control groups. After all, insects are surprisingly fragile critters and even water or non-insecticidal shampoos may result in a small amount of mortality which is insignificant to treatment. Water or noninsecticidal shampoos can also temporarily clog the insect’s spiracles, resulting in immobile lice which could be interpreted as dead by a careless counter. Removal can physically injure the lice, which could cloud trial results if results are drawn from collected lice.

Another important aspect of clinical trials is blinding and randomization which make sure the person who is counting the lice isn’t aware of the treatment the person received. The human mind is a surprisingly bad tool for science because we tend to see patterns where none exist, and we may unintentionally superimpose patterns that don’t exist. Since everything in nature has some amount of variability (Anastasia is about six inches shorter than I am, Bug Girl is about a foot shorter than I am, and my boss is about a foot taller than I am for a quick example) we use statistics to tell us what the probability is that our results are due to random chance, eventually ending up with something known as a P-value. Followup observations are also required to show that the patient remained louse free, that is that there weren’t any hidden adults or unhatched eggs because the unhatched eggs can restart infestations.

Last week, I discussed some common OTC head louse treatments. While effective, there are some problems with resistance for some OTC treatments which results in failure of some treatments. This is a product of evolution where some lice are able to survive treatment because they have some random mutations which just so happen to be beneficial in a pesticide filled environment. The mechanisms of this resistance are actually similar to agricultural pests which have been treated with the same product.

One thing astute readers may have noticed is that I didn’t shy away from the use of the word ‘pesticide’ when discussing these treatments. One of my very first posts on Biofortified revolved around the definition of the word ‘pest’ which is completely anthropocentric. A pest is any critter which annoys us in the slightest, and a pesticide is a compound which kills a pest. Insecticides are used to kill insect pests and head louse treatments are referred to as ‘pediculicides’ because they kill lice. All pediculicides are insecticides (because they kill lice, which are insects), and many of the less toxic insecticides used in agriculture have been repurposed as pediculicides. Often times with head louse treatments, you hear companies claim with great pride that their products are pesticide free, are great at killing lice and that no resistance has evolved to their treatment.

Well… how do these claims stack up?

Uncomfortable Truths

Current packaging of products discussed in this article. Product images taken from the websites of their respective companies, used in accordance with the Fair Use Clause in US Copyright Law.

The use of agricultural insecticides to treat head lice is somewhat of an uncomfortable truth, and many companies have taken advantage of this to market head louse treatments. Despite what any label you read may say, any product which claims to kill lice is an insecticide by definition. It doesn’t matter if these are plant extracts, because pyrethrum falls straight into this category and it is classified as an insecticide. In fact, I would even go so far as to argue that a product is engaging in false advertising if it claims to kill headlice while being pesticide free. This, of course, doesn’t mean that all products must directly interfere with the inner workings of lice to be potential treatments.

Some compounds like mineral oil are used as insecticides in agriculture to kill aphids by suffocating them. The product marketed as ‘Lice MD‘ in the picture above claims to kill lice through a similar mechanism. The fact that these chemicals do not interfere with the neurological systems of insects does not mean that the product isn’t an insecticide. If the product claims to kill lice, as Lice MD does, it is claiming to be an insecticide.

A couple of examples of products that play fast and loose with advertising, in my opinion. Remember: natural products can be just as bad as synthetic products. Also, any product that claims to kill something is certainly not pesticide free. Both images taken from the websites of their respective companies, and used in accordance with the Fair Use Clause in US copyright law.

Uneasiness about insecticides has also given rise to many products which are derived from natural sources; these are popular because of a general assumption that natural products are safer than synthetic insecticides. The advantage of this from a company’s point of view is that these products don’t have to go through safety or efficacy testing, depending on how they’re marketed. The Dietary Supplement Health and Education Act of 1994 allows many products to go straight to market without testing under the guise of ‘supplements’ which allows them to make sometimes outlandish health-related claims. Homeopathic products are similarly exempt from safety and efficacy testing, which gives companies a great loophole to sell products which make medicinal claims.

This is a successful tactic because it plays on the unease parents have about treating their children with insecticides to kill lice. Unfortunately for these uneasy parents, the assumption that natural products are less harmful than synthetic products doesn’t always hold true. The LD50s for many synthetic pyrethroids are higher than their natural counterparts. Ricin and amantin are both incredibly powerful poisons derived from plants and fungi respectively. Eucalyptus oil, if used improperly as a head louse treatment, can have dire consequences including seizures and death. Many natural components can have chronic effects, too. Cyclopamine, derived from Vetratum californicum, causes some rather disturbing birth defects by inhibiting developmental pathways. Rotenone, a pesticide once used widely in organic agriculture, has been linked to Parkinson’s disease in workers exposed to sublethal doses of the toxin over the course of a very long time. Aflatoxins are powerful carcinogens produced by fungi which threaten food supplies all over the world. Even something as seemingly innocuous as a cockroach sex pheromone can be carcinogenic.

To be safe, it doesn’t matter if a chemical is derived from natural sources. Instead, safety depends on how the chemical interacts with the molecular machinery that keeps us alive. The safest way to make a new product is to construct it with chemicals where we know what everything does, as opposed to treating with soups of unknown composition. Unfortunately, this isn’t always possible because purifying and testing a compound for effects is extremely expensive and can take years of effort.

One of the components in the Quit Nits formula is a plant called Delphinium, a plant genus which is famed for its toxic alkaloids that poison cattle and make this plant genus a pest of cattle pastures. I’ll discuss this claim further in another paragraph, but the plant is in the formula at a concentration that is most likely too low to harm either lice or people. Other claims on this product are technically honest, but misleading. Some components of this product have been used in agriculture as insecticides. Lice consume a blood diet, and would probably have to eat these pesticides to see any effect. Components of the shampoo are toxic, but the concentrations these components are used in are harmless to people and are probably harmless to lice as well. As far as I can tell, most of these components haven’t been tested against lice in literature available to researchers. The statements made in the Quit Nits product comparison chart are misleading on multiple levels.

Misleading Statistics

Study methodology and results from the Lice Sheild website. This usage of the information from the company's website is in accordance with the Fair Use Clause of US copyright law.

Many products give misleading statistics that aim to trick parents into believing the product works. For example, let’s take a look at a product called Lice Sheild. They give a description of an experiment on their website that seems like a good test on the surface but is missing any information that actually allows you to draw any conclusions. For instance, they give P-values in their experimental setup, but do not give any information needed to verify their results. The P-values given imply statistical significance, but without any information on repetitions, sample sizes, means, or deviations the information is basically useless. There’s no way to check their math to see if the statistics were correctly performed. There are also no details on how many lice they used for the experiment. If they used two repetitions of five lice (the minimum required for 80% repellency with four lice moving between hair strands and away from the treatment), this would be a negligible result. If they used ten repetitions of 500 lice, the results would be a bit stronger. There simply isn’t enough information here to determine if the statistics were correctly performed.

Also lacking is a description of the experimental arena which is important because there are many ways in which you can test repellency that would potentially interfere with louse movement. If they placed the louse in a container in a patch of hair, one wouldn’t expect lice to move away from the hair at an appreciable rate. Many products are tested by placing the lice on a piece of filter paper and looking at the percentage of lice which move away from the product. While a test like this may appear to show some repellent activity, it’s not actually a very good measure of how good your product repels lice in real world conditions. Using in vitro tests means you’re trapping the lice in a place with the repellent and giving them essentially unlimited time to make their choice. This is a big problem because they’re using a timeframe that’s irrelevant to head louse transmission. Lice are mainly transmitted through hair to hair contact, and it’s rare for two people to be in hair to hair contact for this amount of time.

In short, showing 80% repellency is very different than saying that you have a 80% reduction in your chances of getting head lice. The company which makes Lice Shield uses questionable statistics to claim their product repels 80% of lice under conditions that don’t reflect the conditions where lice are transmitted, then turns around and claims in their FAQ this means that there is an 80% reduction in head louse transmission without any evidence for this claim. These two claims are quite different, because repellency doesn’t necessarily translate to a reduction of infestation.

Homeopathic Medicines are Marketed Differently than FDA Approved Drugs

Homeopathy is a system of beliefs which claim that serially diluting a ‘medicinal’ substance makes it stronger. These dilutions are pretty specific, for example the letter X denotes a 1:10 dilution. If a product is diluted 6X, it’s diluted to 10^-6 which is about one millionth of the original concentration. The idea that diluting a potential louse treatment makes it stronger is ridiculous because if the chemicals in any treatment interfere with insect biochemisty, they must be within a certain range to have an effect. Too much, the person gets poisoned (but the lice still die). Too little, and the lice survive and resistance can build up after the more susceptible individuals are culled from the population.

Homeopathy defies essentially every principle in science from biology to physics. Homeopaths claim that water has memory but, to paraphrase Tim Minchin, this ‘memory’ of water seems infinite when paired with some substances but water seems to have a case for amnesia when it comes to more harmful substances. Homeopathy has no a plausible mode of action.

The next paragraph of my post may get me into hot water with some of my skeptic friends. Many skeptical bloggers have taken on homeopathy. Let me restate: homeopathy has no plausible mode of action. I want to put this in writing to avoid the inevitable criticism from other skeptical bloggers. I also want to avoid the quote-mining from naturopaths who may want to say that I support homeopathy. I am not claiming the efficacy of homeopathy because there is no evidence that it works, and there is no plausible mechanism by which this practice could possibly work.

I am considering some homeopathic products as potentially effective. Why? Homeopathic formulas are exempt from safety and efficacy testing by the FDA which gives many products a free pass when it comes to clinical trials. Many products aren’t actually homeopathic because they contain ingredients in concentrations that could potentially have an effect. These products are often classified as homeopathic so they can make medicinal claims. A cold remedy product marketed under the name Zicam is a good example of this. Zicam was a solution of zinc which was marketed to treat the common cold after it was shown that zinc ions could interfere with viral replication in in vitro tests. The product was eventually recalled by the FDA because it was found to destroy the sense of smell. Another example of a product sold as a homeopathic remedy with potentially active components is sold under the name of Quit Nits.

Unlikely Modes of Introduction

Quit Nits bills itself as a homeopathic remedy and contains a bunch of plant extracts from several different species. As a result of intense selection by insect herbivory, all plants have some sort of anti-herbivore defense. Many plants have toxic components as a result of being under selective pressure to develop such components over the course of millions of years. Plants represent a wonderful treasure trove of different types of novel pesticide chemistries. After all, this is how we got pyrethrum. Despite the fact plant extracts are potentially plausible pesticides in and of themselves, we shouldn’t assume that any plant can kill any insect.

The first thing that raises a red flag for me in the Quit Nits formula is the mode of introduction of this pesticide. Some pesticides (see this RNAi post, for example) must be eaten to be toxic, and these are referred to as stomach poisons. Others can be absorbed, and are referred to as contact poisons. While this product does have toxic components, the fact these plants have natural toxins doesn’t automatically mean that they’ll be absorbed by the lice. Because the lice feed by inserting their mouthparts into the host, it seems very unlikely to me that they’d actually be able to pick up any pesticide by eating it unless the pesticide was in the blood of the host in appreciable amounts. Thus, any active ingredient would have to be absorbed through the exoskeleton.

A second thing that I am concerned about is the formulation. Spraying plant extracts on crops and lathering the same stuff into hair and then washing it off are very different modes of introduction. Pesticidal activity may not be preserved by the shampoo, even if the substance is downright toxic to bugs when dissolved in water. This stuff needs to be tested on lice in the formulation offered for sale before it can be said to have insecticidal activity. The mode of introduction and dosage play vital roles in the insecticidal activity. It’s possible the active ingredients wouldn’t retain their insecticidal activity in shampoo or that they wouldn’t be in contact with the lice long enough to be toxic. No pesticide kills every insect with equal efficacy in every situation. This is why the ultimate test of any pesticide is to test it on the pest in the situation you’re going to use it in, in the formulation in which it will be used.

Third, the mode of action of the two active ingredients means that they are unlikely to affect lice. Extract of the plant Delphinium and extract of a plant called Sabadilla (Schoenocaulon sp.) are listed as active ingredients at one part per million. There appears to be little work evaluating Delphinium for insecticidal activity, but Sabadilla and Delphinium both contain veratridine which acts as a stomach poison in insects. Because lice feed by inserting their mouthparts into the skin of the host and sucking blood from capillaries under the skin, I have a tough time believing they’d actually pick the insecticide up in appreciable amounts unless the toxins were absorbed directly into the bloodstream. Since the active ingredient is toxic to humans, there would probably be some major issues with the product if it made it’s way into the bloodstream. The mode of action here renders me skeptical that the lice would pick up a toxic dose of the pesticide in the first place.

Pesticides Used in Doses Unlikely to be Effective

The biggest problem with Quit Nits is the concentrations of the active ingredients. It’s the dose that makes the poison and if you look at the label of the product in question, there are two ingredients that are listed as parts per million and one component that’s in there at a 1:100 dilution.

Purified components of Sabadilla have been used as pesticides for high value orchards like oranges and mangoes. The lowest concentration for semi-purified Sabadilla alkaloids is about .1 g/l, or about one part in 10,000 if we’re going by weight. The extract of the plant seeds, of which the alkaloids are only a small part, is about a hundred times lower than this in the quit nits shampoo. The seeds of Schoenocaulon contain 2-4% insecticidal alkaloids by weight, which means the alkaloids from Sabadilla are present at one part in 25,000,000 in the shampoo.

Delphinium contains veratridine in appreciable amounts as well and has a large amount of other toxic alkaloids in addition to veratridine. It’s difficult to know what concentrations the insecticidal alkaloids are present in Delphinium because there are simply many potentially insecticidal alkaloids in these plants. However, we can make some educated guesses because researchers have purified alkaloids from Delphinium. The individual components are present in milligram amounts with all the alkaloids being present at about 6 grams per kilogram of plant tissue. If we assume the insecticidal alkaloids are present at a concentration of five grams per kilogram of plant material to make our math easy, this means that the insecticidal components comprise about one part in two hundred per unit weight. The concentration of plant in the shampoo is about two parts per million, which means the alkaloids are present at one two hundredth (1/200) this concentration. Given generous assumptions of grams per kilogram amounts, the active ingredients would be present part per hundred million concentrations if we assumed all of the alkaloids in the plants had insecticidal activity.

These plants combined are in about one part in 500,000 in the shampoo. This means that the concentrations of the insecticidal alkaloids is about one part in 4-6*10^-8 parts depending on the alkaloid concentrations of the plants used. Because the lowest concentration of this pesticide used in agriculture is one part in ten thousand, this comes out to a ballpark figure of somewhere around 1,000 times lower than the lowest dose used in agriculture. The dose the lice will be exposed to in the shampoo won’t be great, as there will only be a couple grams of the shampoo used on the entire scalp. To give you an idea of what the pesticidal concentrations are in other louse products, pyrethrum is generally in antilouse shampoos at one part per hundred (one percent). Malathion is generally present at one part in two hundred parts, or one-half percent. This means that the crude alkaloids from the plant extracts would be present at one one millionth the concentration of the active ingredients that have known insecticidal activity. The improbable mode of action combined with the low amounts of active ingredients in the plant means that I would assume these ingredients are essentially inert without proof that they kill lice at these concentrations.

These ingredients aren’t the main stuff in the Quit Nits treatment, though. The plant extracts listed above are in parts per million, but Quassia amara extract is present at a 1:100 dilution…about 10,000 times higher than Sabadilla and Delphinium. Furthermore, it’s in the ballpark of the Pyrethrum extract. So what about Quassia?

Ingredients with No Proof of Efficacy

Quassia amara is an interesting plant because it contains one of the most bitter substances in the world. These substances are called quassinoids, and have been examined for insecticidal and antifeedant activities against a wide range of pests. In many cases extracts and purified components from Quassia have been shown to have insecticidal and antifeedant activity, but it wasn’t always clear to me whether the antifeedant activity was so strong that it led to mortality. In other words, it was difficult to tell if the substance made the food taste so bad to the bug that they’d rather starve than eat. Either way, we’re interested in it’s activity against lice in particular.

There have only been two papers which have examined Quassia extracts against lice. One appears in a Dutch journal in 1978 and another in a Spanish journal in 1991. Since these papers are in rather obscure low impact journals, I was not able to access them directly through my library and instead had to rely on their descriptions in review articles. The review articles weren’t exactly favorable towards Quassia as a louse treatment. The Dutch paper claimed high efficacy, but the experiment was apparently ran as an un-controlled, un-randomized, un-blinded experiment and counts as nothing as far as proof goes. The Spanish paper claimed high efficacy, but the review states that the Spanish paper concluded that Quassia would only have repellent effects but didn’t mention whether the extract had a clinically relevant success rate. There have been no well performed tests of Quassia as a head louse treatment, and the few tests that have been performed have yielded conflicting results. There’s simply no proof that the “active” ingredients in Quit Nits work.

Quit Nits also sells a repellent spray that has undergone independent testing. One paper compared it’s repellent activity using a filter paper repellency test, incubating the lice with filter paper treated with repellent on one side and water on the other. The objective was to measure what percentage of the lice moved away from the treatment. At the earliest time point measured (two hours), Quit Nits performed about as well as water. At later time points, there was some non-significant repellent activity. Another paper looked at the repellency of Quit Nits under real world (or close to real world) conditions and looked at whether lice would transfer to hair under approximated hair-hair contact conditions, if the lice would move on the hair treated with Quit Nits repellent spray, or if the lice would feed on the forearm of one of the authors who performed the study. For the hair tests, KY jelly was used to simulate greasy hair and Quit Nits fared no better than this. For the skin tests, bare skin not receiving any treatment was used and the lice exposed to Quit Nits treated skin fed just as well as those on bare skin. Quit Nits repellent spray simply doesn’t repel lice, as far as the current experiments show.

Some Products Have no Plausible Mode of Action

The first example of a product with no mode of action is a product called X-pel. In fairness, I’ve only seen this at a few small grocery stores in Iowa, but the fact something like this is sold at all really worries me. The product is a shampoo which consists of ground up honeybees, phenol, and an uncommon species of Rhododendron at femptogram concentrations (15X), or one part in one quadrillion. On their website, they give a couple of vague descriptions of various tests. The tests contain very little methodology and give no statistical information about their results. They claim a few ‘major universities’ were involved in the testing of the product, but neglect to give any sort of contact information or any publications generated as I described in the Quit Nits treatment. They have a video on their website, below, where they show an in-vitro test that consists of them drowning a louse in the shampoo. Because lice can be inactive for a long time following immersion in water, there is no evidence given that the lice in this video were actually killed. They also show an uncontrolled, un-randomized, un-blinded test of a single subject without any apparent followup as proof that their product works. Phenol here is the most likely ingredient for insecticidal activity, as the concentration of the Rhododendron is far too low to do anything at all. Quite frankly, I’m not sure how honeybees are supposed to kill head lice unless we assume the venom glands were somehow involved, but I find this unlikely. The ingredients used in this product are only used in vanishingly small concentrations, and there’s really no way to justify using ground up honeybees to treat head lice.

Another product marketed under the name Licefreee! is little more than a concentrated sodium chloride solution. While it’s plausible the product could suffocate the lice, the data for suffocants in head lice treatment isn’t exactly convincing. Because lice are coated in a waxy layer that prevents dehydration, I find the claim that a 10% salt solution will kill lice suspect. As far as I can tell, there’s no evidence of this product works either because I’ve only seen this mentioned in passing under ‘folk treatment’ sections of review articles. I’ve seen no primary literature articles dealing with concentrated salt solutions as lice-killers.

Conclusion

Many of these companies use a variety of tactics to sell their products that have nothing to do with efficacy. Many use highly questionable advertising methods, like capitalizing on patient fears of synthetic medicines and pretending to identify with their customers to sell them products of uncertain effectiveness. Some of these products even go as far as to claim to be pesticide free while still claiming to kill lice. Many of these products claim to have been invented by parents, but as a parent myself I cannot imagine marketing a questionable head louse treatment and this is a big part of why I’ve written this post.

The science-based products currently on the market that I mentioned in Part 1 have been thoroughly studied and activity proven with the obvious exception for strains of lice that are resistant to some treatments. Even though there is a risk to any product you’re bound to use, the risks of these products have been investigated and have been taken into consideration when formulating treatment regimens. I can certainly understand anxiety about exposing kids to pesticides, but when looking at alternative treatments one needs to ask whether they’re safe and effective. Extraordinary claims require extraordinary evidence. If a product you spend money on makes any sort of claim, you should consider the claim extraordinary and ask for evidence behind the claim.

Burgess, I. (2009). Current treatments for pediculosis capitis Current Opinion in Infectious Diseases, 22 (2), 131-136 DOI: 10.1097/QCO.0b013e328322a019

Leone, P. (2007). Scabies and Pediculosis Pubis: An Update of Treatment Regimens and General Review Clinical Infectious Diseases, 44 (Supplement 3) DOI: 10.1086/511428

Canyon, D., & Speare, R. (2007). Do head lice spread in swimming pools? International Journal of Dermatology, 46 (11), 1211-1213 DOI: 10.1111/j.1365-4632.2007.03011.x

Heukelbach, J., Canyon, D., Olivera, F., Muller, R., & Speare, R. (2008). Efficacy of over-the-counter botanical pediculicides against the head louse based on a stringent standard for mortality assessment. Medical and Veterinary Entomology, 22 (3), 264-272 DOI: 10.1111/j.1365-2915.2008.00738.x

Lebwohl, M., Clark, L., & Levitt, J. (2007). Therapy for Head Lice Based on Life Cycle, Resistance, and Safety Considerations PEDIATRICS, 119 (5), 965-974 DOI: 10.1542/peds.2006-3087

Leone, P. (2007). Scabies and Pediculosis Pubis: An Update of Treatment Regimens and General Review Clinical Infectious Diseases, 44 (Supplement 3) DOI: 10.1086/511428

Greive KA, & Barnes TM (2011). In vitro comparison of four treatments which discourage infestation by head lice. Parasitology research PMID: 22030833

Canyon, D., & Speare, R. (2007). A comparison of botanical and synthetic substances commonly used to prevent head lice (Pediculus humanus var. capitis) infestation International Journal of Dermatology, 46 (4), 422-426 DOI: 10.1111/j.1365-4632.2007.03132.x

Rossini, C., Castillo, L., & González, A. (2007). Plant extracts and their components as potential control agents against human head lice Phytochemistry Reviews, 7 (1), 51-63 DOI: 10.1007/s11101-006-9026-0

When lice strike

"We all have lice" by Antonia Hayes via Flickr.

Head lice are something almost everyone has to deal with, and head lice treatments are something someone buys every once and awhile. These are big business in and of themselves. Because they’re big business, many firms have started popping up offering louse treatments with varying degrees of effectiveness.

A while back, I went through my own head louse ordeal with my daughter. Treatment was complicated by a family member who didn’t realize they were infested. We originally thought the lice were resistant to treatment, so I had to get a second treatment. Since then, I’ve become curious about what is for sale in stores for Over The Counter (OTC) head louse treatments and generally take a look at whatever treatments I can when I get the chance. Over the years, I’ve become surprised at how many dubious treatments are offered for sale (although perhaps I shouldn’t be) and how many of these use questionable advertising techniques mostly built upon fear rather than science. Many treatments offered for sale over the counter are either unproven, or have been proven not to work.

First, let’s discuss some headlouse biology. Then, let’s discuss how the treatments currently FDA approved work. In Do OTC Head Louse Treatments Work? Part 2: Questionable treatments, I’ll discuss the dubious treatments.

Disclaimer: I have worked in entry level positions at companies which sell these products. This, has not influenced my position. I should also mention that I’m not a medical professional and will not be discussing side-effects or risk-benefit analysis. I am an entomology graduate student who studies insect physiology and although I’ll mention the side effects of these products in passing I will not discuss them in detail. This post will discuss the science behind head louse therapies, how they work, and why some aren’t thought to work. I’ll also discuss the evidence that would be required to show that they work. This post deals with insect physiology and should not be mistaken for medical advice. Always consult a doctor if you think you may have health issues because blogs are notoriously bad places for medical advice*.

Lice biology

Male head louse, via Wikipedia.

Head lice are small hemimetabolous insects - basically booklice that have evolved to be parasitic. They start life as an egg or nit attached to hair, then go through a series of nymphal stages before maturing to an adult.  The adults and nymphs both feed, injecting saliva that causes small localized immune reactions which is why you itch. They’re very well adapted to hair and grasp it with clawlike legs. They can only grasp onto some kinds of hair which is why you don’t get pubic lice and head lice occurring on the same body parts. They spend all their lives on hair, even staying on the hair while they feed. Actually, off hair (or similar

fibrous material) human lice are nearly useless and have trouble getting around. They must feed every few hours, otherwise they quickly starve to death or die of dehydration off the host. Lice are transmitted mainly through direct hair to hair contact, with objects like combs and hats playing a potential minor role in transmission.

The nervous system of head lice is surprisingly similar to ours, with differences that are minor as far as we’re concerned. The nervous system is composed of several thousand cooperating neurons and is involved with every aspect of a louse’s life, movement, feeding and reproduction and many products target this system. When a nerve fires, sodium and potassium channels open which causes potassium to flow out of the cell and sodium to flow back in. Often, this process is touched off by the binding of another messenger such as acetylcholine which causes these channels to open. The charge changes from a negative charge to a positive charge, known as depolarization. The positive charge is very localized and moves down the nerve cell as a result of the sodium/potassium channels opening and closing in a very tightly regulated sequence that is essential to function. Other channels can prevent the nerves from firing such as GABA which binds to a receptor and causes the opening of chloride channels which prevent the nerve cell from firing by causing it to attain a very negative electrical charge. The pesticides used in headlouse treatments target all these systems, all of which can lead to a dysregulation of the nervous system and a collapse of nervous system function.

How do louse treatments work?

The safest products are sold over the counter and are used as commonly available first line treatments. Pyrethroids are generally considered to be the least toxic product, and are the most widely available. Lindane is a bit more toxic than either pyrethrum or malathion but most adverse reactions are still due to misuse. All three of these pesticides target different systems in the louse. Resistance has been documented in lindane and pyrethroid insecticides, but not malathion in the US. Pyrethroid based insecticides are used as a first line of attack with lindane and malathion being listed as a second and third route of attack respectively due to resistance of lindane and lack of resistance to malathion.

Pyrethroids are compounds similar to pyrethrum which is derived from the chrysanthemum plant.

Chemical structure of pyrethrum, the most commonly used pyrethroid derived from chrysanthemum plants.

Pyrethrum is a botanical product, while pyrethrins are artificial versions of this compound which have varying degrees of effectiveness on insects. In general, the artificial versions are more toxic to insects and less toxic to mammals based on LD50 values. Pyrethrum is the compound used in head lice treatments. Pyrethrum acts by propping open the sodium channels, allowing a sodium influx into the nerve cells. The nerve cells then become depolarized in unison, which results in the discoordination of the nervous system. The nervous system eventually shuts down, followed by the louse’s vital systems.

Resistance to this pesticide exists in two forms, knockdown resistance and cytochrome p450 degredation. Cytochrome p450s are enzymes which detoxify various compounds and catalyze a wide variety of breakdown reactions. These enzymes are present in humans as well, and also serve to detoxify the small amount of pyrethroids which are absorbed during treatment. In many resistant strains, the cytochrome p450s are upregulated, or overproduced. The overproduction of specific cytochrome p450 enzymes results in the increased breakdown of the pesticide. To combat this, a common additive called piperonyl butoxide is added as a cytp450 inhibitor. Knockdown resistance occurswith a change in the sodium channel that decreases the sensitivity to the pyrethrum, which is more difficult to combat. This is a wonderful example of evolution in action because it’s something which has evolved in direct response to usage of pyrethroids in headlouse treatment.

Chemical structure of lindane, courtesy of wikipedia commons. The molecule consists of a 6 membered ring decorated with chlorine atoms.

Lindane acts by binding to the GABA receptor and permanently inhibiting it. This results in the influx of chloride ions. With the GABA receptor stuck to the ‘on’ position, the nerves are unable to transmit any signals. This  mechanism is semi-complex mechanism but briefly the chloride ions reduce the charge in the cells, so much so that when the potassium flows out the nerve cell is still negatively charged and never fires. The nerves are unable to fire, and are in effect turned off. With the nervous system turned off, the louse becomes permanently paralyzed and dies as a result of not being able to feed. Resistance has been documented to lindane, but I’m not sure what the mechanism is. This product is one of the more toxic substances on the market for head louse treatment, and generally isn’t prescribed for children.

A third mechanism revolves around acetylcholinesterase, an enzyme not directly involved in the transmission of nerve signals. Acetylcholine Is used as a neurotransmitter, being sent between nerve cells to cause them to fire. When an action potential reaches the end of a nerve cell, the nerve cell releases acetylcholine which results in the nerve cell firing. Acetylcholine is degraded by an enzyme called acetylcholinesterase. Without acetylcholinesterase, the nerve remains permanently depolarized and the ion gradients collapse.

Chemical structure of malathion. The active portion of the molecule is the phosphate-like group on the far left which modifies the place in the enzyme responsible for catalyzing the reaction which shuts off nerve cells temporarily.

Even though acetylcholinesterase isn’t directly involved in the transmission of the signal, the enzyme is still important in ensuring the proper working of the nervous system. Organophosphates such as malathion knock the enzyme out, killing the insects. Malathion is an interesting molecule in and of itself. Toxicity requires degredation to another product, which happens better in insects than in mammals. Malathion is sold in a solution that contains isopropyl alcohol and tea tree oil which both synergize the effects of malathion by mechanisms which aren’t well understood. They work either by denaturing protiens in the lice as in isopropyl alcohol or by acting as a supplementary antiacetylcholinesterase as in tea tree oil.

Another method which has been used to cure head lice is what I refer to as the ‘nuclear option’ (or, to use a rare euphemism… landscaping for crab lice), and that’s simply removing the child’s hair. Without hair, the lice cannot hold onto their host and simply fall off. While side effects of the above treatments are relatively rare when the pesticide is used properly, this is by far the safest and most effective method of louse control. Unfortunately, this may not be acceptable for many people. When my daughter had head lice, she did not want to have her head shaved and this is the case for many little girls.

Are there treatment risks?

Although I’m keeping this post focused mainly on the mechanisms of these pesticides, remember that it’s the dose which makes the poison and any substance can be toxic when given in a high enough dose. Exposing yourself to a small amount of pesticide is OK so long as you allow it to break down and leave your system. Repeated exposure over a very long period isn’t a good thing because these products do inhibit neuronal function, leaving the door open for possible neurodevelopmental effects. Because of this, these products are not reccomended for long term use and treatment regimens are designed to last as short as possible. Head lice generally take about ten days to two weeks to mature into adults which is why retreatment is recommended within a week. Many products (except lindane) do not kill eggs, so any leftover eggs will hatch and eventually grow to reproductive adults if a followup treatment isn’t performed. The active ingredients have proven useful in a variety of contexts, including agriculture, but in this case the trick is to treat the patient with a dose high enough to kill most of the lice but low enough to not cause symptoms in the human.

Classifying these chemicals as pesticides sounds scary to many, and many companies have figured out how to take advantage of the unease many parents feel about treating their kids to sell products which have no evidence of efficacy. Next week, I’m going to expose many of these products and further explain the science behind clinical trials for these products.

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* One of my favorite fellow entomobloggers, Bug Girl, even has a page titled ‘I will not diagnose you’ and this applies to me as well. Do not contact me asking for any diagnosis because any E-mails of this character will be sent directly to my junk E-mail folder as it is outside of my duties as an entomologist to perform this sort of work and would be completely irresponsible.

Facepalm by Alex E. Proimos via Flickr.

On Twitter yesterday, @seekblunttruth shared a link with @franknfoode that I thought deserved greater scrutiny. The link is to an ISIS post* titled Bt Crops Failures & Hazards.

Others may spend some time criticizing ISIS itself, and that criticism may be worthy, but here I’d like to focus on the post. I’ll let you check out the post content  yourself, but I want to focus on the works cited list.

There are 29 citations. We find 11 sources that are by ISIS authors. It’s ok to refer to your previous work, we do it on Biofortified all the time, but having almost 40% of the citations be self-citations feels like an attempt to pad the citations list. Many of the rest of the sources are either by biased organizations or have been previously debunked either in the literature or in the blogosphere.

The following 6 sources are not peer-reviewed. Really, only one of these (the Bloomberg article) is a useful source (assuming that you feel that non-peer reviewed media is useful).

1. EPA memorandum saying they plan to review insect resistance – This is not really useful, maybe ISIS meant to cite something else?
2. Article in Bloomberg – Reasonably balanced and useful article about development of insect resistance to Bt.
3. ISAAA brief on global status of biotech crops – Source used for number of hectares planted in biotech crops. Reasonably useful information source for this particular piece of info, but take with a grain of salt because this is a self-described pro-biotech organization.
4. Report by Navdanya International – I’ll let you decide the seriousness of the report from the cover (hint – there’s no biotech traits in wheat).
5. “Compendium of Cotton Mealybugs” by India’s Central Institute for Cotton Research – I don’t know enough about this organization to judge (and I don’t have time to read the whole report at the moment).
6. Pesticide Action Network report – By a self-described anti-pesticide and also anti-biotech organization.

The following 12 sources are peer-reviewed (41%). Of these, 5 have been thoroughly thrashed elsewhere, and citing them without critique is dishonest, in my humble opinion. One (#4) reminds us that biotech isn’t a silver bullet. The rest don’t really say “Bt good” or “Bt bad”, they’re details to be examined.

1. Inter-laboratory comparison of Cry1Ab toxin quantification in MON 810 maize by enzyme-immunoassay 2011 in Food and Agricultural Immunity. Cited to show variability in Bt concentrations.
2. Temporal and intra-plant variability of Cry1Ac expression in Bt-cotton and its influence on the survival of the cotton bollworm 2005 in Current Science. Same as above, although examines expression differences by genotype. Genotypic differences in gene expression are not unique to biotech traits, and are expected by breeders, so this isn’t unexpected.
3. Seasonal expression profiles of insecticidal protein and control efficacy against Helicoverpa armigera for Bt cotton in the Yangtze River valley of China 2005 in Journal of Economic Entomology. Again, differences in expression, this time in different plant parts. Again, not an unexpected result.
4. Mirid bug outbreaks in multiple crops correlated with wide-scale adoption of Bt cotton in China 2010 in Science. This paper showed that when you stop spraying pesticides, pests come back. Unfortunate, but not an unexpected result. This paper is a great example of how biotech pest resistance needs to be paired with integrated pest management. There are no silver bullets.
5. Genetically modified crops safety assessments: present limits and possible improvements 2011 in Environmental Sciences Europe. This paper, by Séralini and Vendômois (and others) is based on a flawed paper that has been discussed elsewhere, including by the European Food Safety Authority.
6. Cry1Ac pro-toxin from Bacillus thuringiensis sp. kurstaki HD73 binds to surface proteins in the mouse small intestine 2010 in Biochemical Biophysical Research Communications. I have not seen previous analysis of this paper. Perhaps a Biofortified reader would like to discuss it further. One question I have is whether other proteins from plants and bacteria have similar reactions with proteins on the intestine. Another question is whether the proteins binding has any actual physiological effect.
7. Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada 2011 in Reproductive Toxicolology. This paper has been discussed elsewhere, including by Marcel Kuntz and Food Standards Australia New Zealand, then subsequently on Biofortified.
8. Reduced fitness of Daphnia magna fed a Bt-transgenic maize variety 2008 in Archives of Environmental Contamination and Toxicology. I have not seen previous analysis of this paper. Any Biofortified readers familiar with it?
9. Transgenic pollen harms monarch larvae 1999 in Nature. This famous paper by Losey (and others) has been extensively discussed elsewhere, including by Iowa State entomologist Hellmich.
10. Decline of monarch butterflies overwintering in Mexico: is the migratory phenomenon at risk? 2011 in Insect Conservation and Diversity. The hypothesis of this paper is pretty silly. It proposes that an increase in glyphosate resistant crops resulted in more milkweed being sprayed with glyphosate so less food for monarchs. Never mind increased deforestation and conversion of natural lands to cropland (resulting in less milkweed) in the same time frame. Never mind the fact that if glyphosate wasn’t being used, some other herbicide (that also kills milkweed) would be used. This is not an argument against glyphosate resistance, or against Bt, or against biotech traits. It may be an argument for careful land use, set-asides of land for natural habitat, and integrated pest management – all of which can just as easily be done with biotechnology as without.
11. Transgenic DNA introgressed into traditional maize landraces in Oaxaca, Mexico 2001 in Nature. As Mercer and Wainright point out, Quist’s results haven’t been replicated. I have written a post about gene flow that may be relevant to understanding the Quist paper.
12. Toxins in transgenic crop byproducts may affect headwater stream ecosystems 2007 in Proceedings of the National Academy of Sciences. This paper by Rosi-Marshall (and others) has been critiqued elsewhere (see the responses at the bottom of the article). I wrote about this paper back in 2008 (and in 2007).

The author of the ISIS post failed to do a proper literature search, so didn’t find any of the sources that showed anything but their preconceived notions of Bt. This is definitely worthy of a facepalm, if not a headdesk. If anyone has relevant points to add to this analysis, post a comment and I’ll update the post.

* They call it a report but if that is a report than most if not all of the posts on Biofortified are also reports.

The Genome Generation, Elizabeth Finkel Melbourne University Press 2012 ISBN 978-0-522-85647-7

From the back cover:
The year 2001 marked more than just the beginning of Stanley Kubrick’s space odyssey, it marked the beginning of the genome era. That was the year scientists first read the 3 billion letters of DNA that make up the human genome. This was followed by a veritable Noah’s Ark of genomes—sponges and worms, dogs and cows, rice and wheat, chimps and elephants-180 creatures aboard so far.

So what have we learned from all this? How has it changed the way we practise
medicine, grow crops and breed livestock? What have we learned about evolution?

These are the questions science writer and molecular biologist Elizabeth Finkel asked herself four years ago. To find the answers she travelled the science frontier from Botswana to Boston, from Warracknabeal to Mexico and tracked down scientists working in the field. Their stories, told here, paint the picture of what it means to be part of the genome generation.
Elizabeth Finkel holds a PhD in biochemistry and spent ten years as a professional research scientist before becoming an award-winning journalist. She is a contributing editor to Cosmos magazine and also writes for the US magazine Science. Her numerous awards include a Queensland Premier’s Literary Award for her book, Stem Cells: Controversy at the Frontiers of Science. In 2011 she was named the National Press Club’s Higher Education Journalist of the Year.

Elizabeth Finkel tells the evolving story of DNA

in an intriguing and accessible way.

The Genome Generation is absolutely riveting. These tales from the frontier

are a ‘must read’ for everyone who wishes to understand our past—the logic of

evolution—or take a peep into our exciting future at the creation of ‘super plants’

through ‘digital agriculture’.

Is the genomic revolution an overhyped flop or are we on the edge of a life-changing revolution? This book stares down the myths and lays out the answers in engaging, compelling stories. This is an accomplished work of scientific literacy.

The Pundit’s considered comments about the Genome Generation will appear at this site as soon as he gets a chance to read the story. But the book is certainly handsomely produced, and Elizabeth Finkel is a wonderful science writer with a fabulous track record.

The ghost of Norman Borlaug, haunting foodies since 2009. Artwork in CIMMYT Seed Bank

I responded that contrary to such lofty conclusions, a combination of missing details, shortened quotes, and silver-bullet single-solution thinking was at play. The ensuing discussion was heard around the food blogosphere with Michael Pollan tweeting for people not to miss reading our exchange, and Mark Bittman advertising it as well. I would like to continue and expand the discussion here, and bring up some things that have been glossed over and forgotten in this discussion.

How much Nitrogen?

The main thrust of our disagreement was over the issue of the source of nitrogen for growing crops that are going to feed the world. Tom quoted Norman Borlaug as saying that organic would not be able to feed the world, and tried to address it with the ISU brochure. But as I pointed out, Tom cut off the quote, avoiding a key phrase that indicates he is talking about nitrogen production. Here is the full quote:

That’s ridiculous. This shouldn’t even be a debate. Even if you could use all the organic material that you have–the animal manures, the human waste, the plant residues–and get them back on the soil, you couldn’t feed more than 4 billion people. In addition, if all agriculture were organic, you would have to increase cropland area dramatically, spreading out into marginal areas and cutting down millions of acres of forests. At the present time, approximately 80 million tons of nitrogen nutrients are utilized each year. If you tried to produce this nitrogen organically, you would require an additional 5 or 6 billion head of cattle to supply the manure. How much wild land would you have to sacrifice just to produce the forage for these cows? There’s a lot of nonsense going on here.

This key phrase underscores the perennial problem of switching from fertilizers to an organic-only approach. The first question is where you are going to get the nitrogen that plants need to grow? It takes a lot of energy to pull nitrogen out of the air and break its triple-bonds to turn it into a form that plants can use. This is a major energy cost for conventional farming, but it also secures its higher yield. The only way that organic agriculture can get nitrogen is by harvesting it from other living things in one way or another. Nitrogen can be “fixed” from the atmosphere by legumes, which can be grown as a “cover crop” that is planted after the fall harvest, or in the spring to cover the land in an off-year and gather nitrogen that will be plowed into the soil. You can also plant a “catch” cover crop with a grain such as barley or oats, intended to capture excess nitrogen during the winter, which can be plowed into the soil in he spring. Or, you can gather nitrogen in the form of animal manure – which comes from previously-grown crops, and thus, previous sources of nitrogen. You could also go for fish slurry – and harvest your nitrogen from the ocean, or weirder still, argue over naturally-occurring deposits of Chilean nitrate (PDF) and their status in organic agriculture. In any case, the nitrogen has to come from somewhere. Ironically it would seem, nitrogen from human waste is not allowed. The ISU research that Tom was enthusiastic about was a little fuzzy on where the nitrogen was coming from:

The organic plots receive local compost made from a mixture of corn stover and manure.

Nitrogen Cycle, from landscapeforlife.org

Where did this manure come from? How many acres of land were required to produce this manure, and where did the nitrogen come from to produce it? These are questions that are not detailed, and it shows one layer to the complexity of long-term sustainability. Tom responded to defend organic agriculture with a paper that estimated that with cover crops alone (PDF), the world could produce enough nitrogen to replace all synthetic fertilizers. The Badgley et al. paper had many assumptions, but also some good information. Their basic approach was to estimate how much available nitrogen can be produced on all the non-forage croplands in the world. Essentially, how much can we gain by planting legume cover crops? But this is where the incompleteness of the paper began to unravel.

The paper assumed that none of the croplands currently in production were being planted with cover crops already. So the acreage of non-cover-cropped lands was overestimated. Next, it also assumed that legume cover crops would actually grow on all of these acres. Statistics about current practices are very hard to find, and the one that I could find (PDF), for New York vegetable growers (not grain), said that 50% of their acres had cover crops, and 20% of those were legumes fixing nitrogen. As I have learned, besides the timing of planting and the weather, certain cover crops can make pest problems worse, and if you follow a legume crop with a legume cover crop, you can have issues with rotting. Before you can estimate whether cover crops can provide enough nitrogen to replace fertilizers, you first have to estimate what can be practically achieved in actual cropping systems. Even the Rodale research did not plant legume cover crops every year.

I then had a thought. If you are going to plant a legume cover crop (as with any cover crop), you are going to need seeds. Those seeds have to come from somewhere, and will take up a certain amount of acreage to produce. Out of curiosity, I thought I would calculate how many acres of farmland would be required to grow the seeds necessary to cover the world’s croplands in hairy vetch, a common and highly regarded legume cover crop. The results were stark.

The Badgley paper estimated the total available croplands as 1362 M hectares (Table 4), and if all were planted with legume cover crops, it would produce 140 Million Megagrams of Nitrogen (or 140 Teragrams). The paper reports that the world uses 82 M Mg of Nitrogen (82 Tg), which means that according to these numbers, to exactly replace the amount of nitrogen being used by farms today, you would need 1362 * 82 / 140 = 798 M hectares of legume cover crops – so about 800 million hectares. How much seed would you need to plant that?

Hairy Vetch. Photo by neckonomania

The recommended seeding rates for hairy vetch are 30 pounds per acre. The only source I was able to find about seed production of hairy vetch reported that you can only get 200-540 pounds per acre of seed (PDF). This means that for every acre of cover crop, you would need 1/6 to 1/18 of an acre to produce the seed you would need. (You also need to produce the seed for the seed crop – making it slightly higher). Without knowing the true average for seed production, I just averaged the high and low-end of the range to arrive at 1/12 of an acre of seed fields to produce enough hairy vetch for one acre of cover crop. To plant 800 million hectares of hairy vetch cover crops, we need about 67 million hectares (or 164 M acres) of hairy vetch seed production to supply it. For seeds to plant the seed fields, add another 6 million hectares to give you 73 million hectares of land.

For perspective, I looked up the total cropland of my awesomely-productive home state of California, which according to the USDA, has 4 million hectares under cultivation. This means that we would need almost 20 California’s of cropland to grow enough hairy vetch seed to plant these 800 million acres, and if you converted all Californian farmland into seed production (goodbye meat, dairy, etc) you still only have 10 M hectares, and you would need the farmland of 7 Californias.

Where are we going to find this extra land? Or should we decrease the total cropland area in the world by five and a half percent? (73 / 1362 = 5.4%) This is the opposite of feeding the world, and it presents a real challenge for cover crops. But not the last challenge, either.

Another detail worth noting is that the yields of these organic plots can have higher total nitrogen applied when compared to conventional plots. In this paper (PDF) on nitrogen rates and leaching, also from Rodale, almost twice as much nitrogen was applied every year in the organic plots relative to conventional, in order to maintain their yields (Table 4). This translates, as admitted in the paper, into greater rates of nitrogen leaching into the surrounding environment. Nitrogen in the soil is a very mobile nutrient – it washes out easily. Nitrogen runoff from farmlands contributes to water pollution, leading to things such as the Dead Zone in the Gulf of Mexico. It turns out that according to more Rodale research (PDF), not only do organic farms leach just as much nitrogen as conventional farms, but farms with legume cover crops leach even more. 20% of the applied nitrogen leaches out of organic manure and conventional systems, while 32% of the nitrogen applied to legume cover-crop systems leaches out. There is a lot of research on nitrogen leaching and cover crops, including some that don’t sound so bad for leaching, but there is a shortage of good long-term leaching studies. There is also evidence that the cover crop can harm the yield of the following crop. Not only does the amount of nitrogen applied to maintain yields call into question the sustainability of these sources of nitrogen, but also the environmental sustainability of the downstream effects of legume cover crops as a silver-bullet solution to the world’s nitrogen needs.

So even post-mortem, Norm still beats Tom in an argument. Cover crops in an organic system have a long way to go to get to “feeding the world.” This is not to say there isn’t potential in cover crops – because there is. But one thing we must not slip into is silver-bullet thinking – nor excluding a tool from a toolbox because someone calls it a silver bullet.

The Role of Genetics

Modern genetics includes a whole range of tools that we have in our toolbox, all of which are going to be essential in the decades to come. Not only do you have your basic breeding, gene banks for diversity, and genome sequences to help you find important genes, but modern technologies such as marker-assisted selection and genetic engineering are playing an increasing role in crop improvement. One of the ways you can help a plant gather more nutrients from the soil so they don’t run off is to strengthen its root system and its ability to uptake nutrients. In the last few decades, fertilizer use has stayed about the same, while crops have been yielding more, which means that they have been bred to be more nitrogen-efficient. With nitrogen efficiency as a goal, you can increase the yield of a crop without requiring more nitrogen to be applied, or perhaps maintain the same yield while applying less nitrogen. For you breeders out there, this can mean testing out your new hybrid contenders in nitrogen-limiting environments to see just how much yield you can squeeze out of a drop of N.

In the genetic engineering arena, there is a nitrogen use efficiency trait developed by Arcadia Biosciences, which I understand they have licensed to several seed companies and for a variety of crops, and even a nonprofit technology transfer organization for Africa. Transgenic rootworm resistance has been linked to nitrogen use efficiency (because it protects the roots so they can take in nutrients), however a field trial going on at UW-Madison has not been able to observe a consistent benefit from it – sometimes it requires less nitrogen, but not always (PDF summary). Still, one can write an entire book chapter on the potential for genetic engineering to contribute to nitrogen use efficiency.

There is another way that genetics can play a role in the nitrogen needs of the planet, one that might not come to mind right away: breeding a better cover crop. Currently, cover crops are evaluated on a species-basis. Red clover or hairy vetch? Why not take a survey of red clover and hairy vetch germplasm, looking for those that fix nitrogen at high rates, have good winter survival, and decay at a reasonable rate to provide fertilizer for crops the following year, and then combine those traits? (And while you’re at it, you could try to do something about hairy vetch’s horrendous seed yield. Non-shattering trait, anyone?) This kind of research potential is not just limited to legume cover crops – as grains are often used to capture nitrogen from the growing season to mix back into the field the following year as mulch. Why not breed or engineer a cover crop grain plant that is really good at scavenging nitrogen in the soil?

The future of sustainable agriculture is going to look a lot more like organic than most of what we have today, however, there are ideological barriers within that approach that are limiting its ability to not only expand but to use new technologies that can actually help it reach its goals. Imagine a nitrogen-efficient high-yielding corn crop that follows a legume cover crop that fixes nitrogen at an accelerated rate, followed by a winter wheat that grabs the excess before it can leak into the Mississippi. If we were to actually have this system, as organic and sustainable as it sounds, ironically it would not likely be eligible for certification.

Many Pieces to the Puzzle

This summer I visited CIMMYT in Mexico, and one of the most dynamic presentations was given by Kenneth Sayre out in the field, amongst research and demonstration plots of Conservation Agriculture (CA). This approach combines rotations and cover crops with reduced tillage to reduce erosion, increase soil carbon and nitrogen, and reduce water stress and weeds. Besides discussing the benefits of these approaches, it was also pointed out that CA does not suffer from limitations against judicious use of fertilizer, or even genetically engineered crops. Are there perhaps some limitations to this approach, and ways to improve it that have not yet been thought of? Yes, as with everything else. While usually the CA plots do better than the non-CA plots, this year at the station the reverse was true.

We need better crops, improved soils, more efficient water and land use, more rotations, better nutrient recycling, precision farming, and improved social and political structures to make it all work. Too often, questions in agriculture are popularly addressed with narrow, single solutions, with lip service to diverse approaches. “Organic is the solution” vs “genetic engineering is the solution.” Honestly, I hear more of the former than I do the latter, but they are both misguided. It is interesting that while Tom and I were debating the merits of nitrogen issues in organic agriculture, he framed it as him versus a “GMO enthusiast,” and Mark Bittman framed it as “organic vs conventional.” These misleading frames of reference are part of the problem because they keep discussion adversarial and exclude the practical middle-ground. To paraphrase Jon Stewart: Stop. You’re hurting us.

There are many pieces to the puzzle and when it gets set up as one worldview versus another we all lose – because all current worldviews are wrong. Whether you are talking about the nitrogen needs of the world or water, energy efficiency, pests and disease, there is a lot more that we don’t know than there are things we know. Starting with the answer and trying to support it is going to inevitably lead to failure, and so the best approach, as it  always seems to be, is to have an end goal in mind and let the pragmatic application of scientific research figure out how to get us there, using multiple interlocking and interacting approaches. Do you want to feed the world sustainably, securely, and healthily for generations to come? Let’s figure out how to get there.