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.
——————————————————————–
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.

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

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.

Question number one asked people to self-report their understanding of GE food. While self-reporting has its own problems (Like people who say they completely understand GE foods yet don’t really know anything about them), it does provide some information about how aware different groups are about GE. The survey reports that 65% of people are aware that some foods in the store are genetically engineered, and high-income and highly-educated people are up in the 80s. As for the understanding of the concepts, check out these results:

As you might expect, education level influences people’s self-reported understanding of GE food, and the column with the asterisk shows a significant result, which should be a no-brainer: People with a high school education or less report that they have a low understanding of genetic engineering. This understanding appears to be a result of higher education, and as we have discussed on this blog before, secondary education has room for improvement. You can look at the data for age and income in the paper, but I thought the education level was the most interesting.

Next, they asked the survey participants their opinion about the safety of GE food, and this reveals a result that is partly surprising, and partly expected.

Most people are undecided about the safety of genetically engineered foods. This should come as no surprise to anyone in this debate, although quite frequently people on the anti-GE side (and sometimes the pro-GE side) think that most people believe that these foods are unsafe. This is entirely not the case, as the peer-reviewed literature shows that most people are undecided in general about GE, and that includes safety. But there are a few surprises in these results.

When I describe the shape of public opinion on GE, I often say that the people who have decided in favor or against GE as being roughly equal, but both minority groups next to the majority of undecided people. This Reuters survey reveals that in fact more people in the US believe that GE foods are safe than those who do not. And as you move from younger to older, less to more income, and lower to higher education that you see the greatest differences. Amongst people over 65, who make $100k per year or more, or have advanced degrees, there are twice as many people who believe GE foods are safe than those who believe that they are unsafe.

This has several important implications, including the fact that companies that advertise their products as being “non-GMO” tend to have people of higher income and education as their niche market – and therefore marketing their products on the basis of GE foods being unsafe may not resonate with these customers. These results also mean that there is a positive correlation between education and belief about the safety of GE foods.

The survey asked a question about labeling of GE foods, and found an unsurprising result:

Consistently, surveys have shown that about 90% of people, when asked, believe that GE foods should be labeled in the store. Anti-GE organizations tend to state that this is because most people want to avoid GE foods. Most of these surveys don’t delve into why people want them labeled, but some published papers do. Consumers want more information about genetically engineered food, which makes perfect sense considering how many people are still undecided about its safety, benefits, impact, etc. For those who dislike the idea of GE foods, naturally they would want to avoid them. Amongst those in favor of GE, there is probably more diversity of opinion about labels, ranging from no need whatsoever, to wanting to know if something is GE because you would want to buy it. I would rather know that some foods were GE than not, myself. But the important factor in deciding how much people want a mandatory food label is the strength of the desire, not an answer to a simple binary yes/no question. This can be (and has been) asked in several ways, such as how much people would be willing to pay for GE labels, or for people to rate different kinds of labels in order of importance. Examining attitudes on labeling outside of these contexts does not give guidance for public policy.

Now here comes the real news – would people eat GE foods?

This is the result that most people who talk about the acceptance of genetic engineering should pay attention to. Despite lack of knowledge about GE crops, uncertainty regarding its safety, and a desire for labels – most people surveyed would eat genetically engineered plant-based foods, to the tune of 60%. This 60% represents people who would eat GE foods if they knew they were genetically engineered, so even if you were to institute mandatory labeling for GE crops, this is 60% of those people who would happen to read that on the label – people who do not would not change their decision. Furthermore, we can also see that acceptance of genetic engineering in animals is lower – at about 40% for both fish and meat. This is similar to where opinion on plants was years ago, and we have not yet had genetically engineered animals on our dinner plates. So this result could either reflect an inherent difference in attitude between genetic engineering of plants and animals, or, a difference in attitude that reflects the time since the introduction of GE plants.

There are, as with all studies, certain caveats. This survey was conducted on 3,025 people, with an error rate of 1.8% That’s pretty good, however it does not reveal the limitations of the type of data collected. This is data based on self-reported assessments of current and/or future hypothetical behavior – something that is known to give an inaccurate picture of actual behavior. Survey respondents can sometimes give what answer they believe they should give, rather than how they would actually behave. And people can sometimes be really bad at self-assessment. For instance, when asked about generosity toward charitable organizations, respondents rate themselves as being much more generous than they actually are. The best kind of research you can do on human behavior is to actually study human behavior, or set up hypothetical situations that more closely reflect reality. This is the stuff of peer-reviewed research, and not the kind of thing you can do with phone surveys.

The Non-GMO Project reports on their website that a 2008 CBS/New York Times poll, “53% of consumers said they would not buy food that has been genetically modified.” Yet, we find that this survey find that fully 60% self-report that they would eat GE plants, and 40% for animals. How can we put these two results together? First, the statement on the Non GMO Project website that these 53% “would not” buy GE foods is false – the study did not give results that are clearly delineated like that. Although I have been unable to find any data from the original 2008 poll, this book chapter(PDF, pg 7-40) describes some of the results in more detail. The 53% figure represents the people who personally rate buying a GE food “not very likely” and “not likely at all.” These are expressions of likelihood, not determinations of the binary behavior of whether or not they would in practice. The 53% figure also lumps together people who feel moderately disinclined and strongly disinclined to buy them – and if their results follow other existing research, then the people who feel strongly disinclined are in a minority. It was also a question about buying attitude, not eating behavior, and the sample size was one third that of the new Reuters survey. Finally, 50% is right in the middle of 60% for plants, and 40% for animals, so it could reflect the average attitude of people toward GE.

However, There is another difference: time. The CBS/NY Times poll was conducted in 2008, and the Reuters survey was conducted in 2010. There has been much discussion about GE in the past few years, perhaps attitudes have changed somewhat – a possibility that we cannot rule out. The survey also found that 70% of people were aware of GE foods in the marketplace, whereas the CBS poll found only 44% were aware of them in 2008. Clearly, more people are aware of them, and perhaps have become educated about them. I’d like to know where they learned about them! (By coincidence, Biofortified was founded in 2008.)

I would like to make one last point about labeling of GE foods. Several groups are pushing for mandatory labeling, often suggesting that there will be widespread rejection of these GE foods once labeled. This survey shows that when asked, and when aware that food have been genetically engineered, still 60% self-report that they will eat GE foods that are on the market. We already know that people don’t read the labels, as found by Charles Noussair in 2002. And this quote from Noussair bolsters my comment about the difference between opinion surveys and actual behaviors:

“Opinion surveys capture the respondent in the role of a voter, not in the role of a consumer,” he says. “The two behaviors can be quite different, as many studies have shown.”

Japan is arguably one of the most GE-cautious nations in the world, yet, 94% of its soy is imported, 71% of which is from the U.S., and 93% of that is genetically engineered. Therefore, despite the presence of mandatory labels, at least 62% of the soy in Japan is genetically engineered, and people buy and eat it there. Labels will not eliminate GE foods from stores, because people will buy and eat them nevertheless. Adding an extra cost to everyone’s food based on public opinion and not actual behavior or demonstrated need should give you pause. If it is your own desire you are expressing by pushing for these labels, remember that this survey shows that public opinion on the safety and acceptance of genetically engineered foods is not in your favor. If anything, it shows the need for more information, and what happens when more people get it.

*As noted in a comment below, the survey is from 2010, but it appears to have resurfaced recently, so I thought it was just released, but that the data was from 2010. The first sentence has been edited to reflect this fact.

What kinds of environmental risks? Things like basic genetics research, comparing breeding to biotechnology, and downstream effects of environmental release. There is even a section for it you want to submit a research proposal to study co-existence between GE and non-GE crops. You could even study pyramided, or “stacked” GE crops and compare them to single-transgene varieties. So many possibilities.

This call for grant applications is important for several reasons. Research coming out of this program would build upon, and compliment existing research, much of which is listed on this page on our blog. When published, it would also go on this list. (Out of curiosity I called up NIFA to inquire if a project like our GENERA project could be funded under a grant such as this. Sadly, no – the focus is on experiments and not catalogs of them, unless we were to take other people’s raw data and reanalyze under a new algorithm.) Sanely investigating and evaluating the kinds of environmental risks involved in genetic engineering is of utmost importance, and the research must put it in the context of plant breeding and agriculture in general. It is also my fond hope that for whatever projects are funded by this grant program, that the investigators keep in mind how their research would be conveyed to the public.

This is the first time I’ve promoted a grant for scientists to apply for on the blog, and it may not be the last. I thought that we could get some discussion going about what kinds of research we think would be worthy of pursuing? I have two main ideas.

The first is that we have had and heard a lot of discussion about using genetic engineering techniques to move and modify genes between plants of the same species, known as Cisgenics, and more recently, Intragenics. While it seems to be the case that consumers find this to be more appealing than cross-species genetic engineering, I find from discussions with scientists that there is considerable debate about the ups and downs of this distinction. Some see it as little different and merely a way to make an end run around regulations, others see it as a potentially less-disruptive way to alter the genomes of plants. This blog post by Kevin Folta was picked up for one of my department’s journal club discussions, and there were some interesting comments about it, including, how long must a gene be in a species for it to be worthy of being picked up and moved and have you still call it Cisgenics? Can you take Bt out of corn and stick it into another corn?

Correct me if I am wrong, but it seems to me that we have limited data to really answer the question about whether or not moving genes within or between species are inherently different in their risks, versus the same. Some argue that taking a gene from another species is riskier because if opens up new possibilities for interactions between genes because the proteins didn’t co-evolve. On the other hand, some take the co-evolution argument to the other side to point out that interactions also co-evolve and that two genes that have worked together in the same species may be more likely to interact, and there is still the null hypothesis that there is no significant difference at all.

There is some evidence and theory behind each position, but what we would need, then, is an experiment designed specifically to address the question of whether there is a difference, and what kind of difference. I suggest that one way you could go about this is with an experiment that goes something like this. There are genes in many species which serve similar functions due to common ancestry, which are called homologous genes. But, they may have evolved slightly differently in each species, so you could test whether the closeness of the species source matters by simply generating many GE plants with each of these homologous genes, and then comparing the result. You could look at gene expression to see if there are any significant differences between them, for example.

Scientists in the audience might point out that the place in the genome where you engineer the new genes will matter, so you would probably have to generate several transformations in different sites and compare the distributions of effects. You could also look at phenotypes to see if anything odd comes out consistently with one and not the other, or investigate what proteins might interact with the different transgenes. Do this for several sets of homologous genes from progressively more distant organisms and you’ve got yourself a way to test this hypothesis! Add another plant species to insert them into and it will broaden applicability.

Alfalfa by TwoWings via Wikimedia Commons.

I would also like to see some research on coexistence come out of this. What would be some good management practices that will minimize gene flow and spillover effects between neighboring farms? How much time must there be between flowering, or what kinds of borders are necessary, and what would crops that won’t cross with other varieties due to cross-incompatibility genes mean for these practices? Moreover, there is some opportunity for an interdisciplinary research in this area.

As I have shown before, we don’t know a lot about exactly what are the thresholds for consumers when it comes to cross-pollination between GE crops. The Consumers Union did a biased poll with loaded terms, and yet, couldn’t get consumers to care very much about it. Organic groups and exporters are worried about consumer rejection (or rather, processor rejection) if there is cross-pollination, and it seems to me that coming up with thresholds for cross-pollination in a coexistence regime necessitates knowing what consumers think, in a robust and scientific manner. If consumers like the 1% rule, are fine with a 5% rule, or wouldn’t touch a 0.0001% transgenic-pollinated organic crop, those would lead to different situations entirely. Imagine a project where both the methods to achieve coexistence are studied alongside consumer attitudes toward the results of those methods, and you’ve got a nice interdisciplinary project.

What would you like to see get worked on? Any thoughts about what I described above? There’s $4 million of research to be funded – wouldn’t it be grand if an idea started here and made it into a selected proposal?

In the realm of food politics we hear claims that genetic engineering is ‘the solution‘ to world food problems, or that we just need more food per acre. We also hear that it is all about distribution or diet, and that we do not need more food to feed these people. The fact is that both of these dichotomous views are wrong. The task of adequately and consciously feeding, clothing, employing, and protecting 7 Billion people will take all of these things, and a lot more. About a month ago I watched this video created by the University of Minnesota’s Institute for the Environment – and I think it is the best video I have ever seen that sums it up. Watch it.

The Inconvenient Truth is not only that we have this huge task ahead of us, but that many of the people we need to come together to do this would rather bicker about petty political differences. Now how do we get all those people at the table without chucking food at each other?

Glusosino-What?

There has been considerable interest in investigating the composition of foods to determine what parts of them can contribute to our health. (And what detracts from it too.)  Broccoli and other cruciferous vegetables have garnered considerable attention for their effects on the development of cancer. Research has revealed an important class of compounds called Glucosinolates, particularly one known as Glucoraphanin. When this sulfur-containing compound is metabolized by a plant enzyme called Myrosinase, it becomes one of two different compounds: Sulforaphane and Sulforaphane Nitrile. These two Isothiocyanates have been found to have preventative effects against cancer, and Sulforaphane is by far the more potent of the two. And this year, an important paper found that even the precursor, Glucoraphanin, also has important effects.

I apologize for the dizzying array of chemical names. So let me see if I can make them easier to understand. Glucosinolates include many similar kinds of compounds, and Glucoraphanin at the top of the picture here is one example. It gets the Gluco- from having a glucose sugar molecule bonded to it, which is that ring on the right hand side. Isothiocyanates are another class of compounds, and the main example is Sulforaphane. You can distinguish them by that N=C=S group on the Sulforaphane above. There are many Glucosinolates and Isothiocyanates important for this topic, so rather than bring up so many names I’ll only talk about the groups (end in -ates) and the two specific ones I mentioned (Glucoraphanin and Sulforaphane both have -raph- in them).

How do they work? Well, there is a huge amount of research on this topic, and while I could send you on a journey through a google or PubMed search, there are a few clear things that we know. Broadly speaking, cancer is uncontrolled cell growth that usually happens with DNA is damaged, but there are other causes as well (such as cervical cancer being caused by papillomaviruses). Chemicals that damage DNA are known as mutagens, as they can alter the string of letters in the DNA to read differently, and since the mutations they cause can also cause cancer, they are also called carcinogens. We encounter carcinogens in our everyday lives, from artificial chemicals we’ve produced for one reason or another, to the oxidative stress caused by normal cellular respiration, to the UV light naturally emitted by the Sun. Carcinogens are also found in our food.

Yes, our food produces carcinogens. More specifically, there are chemicals naturally present in our food, that when eaten, can become carcinogens. Since plants cannot run away from their predators, they have evolved to defend themselves using chemical and biological weapons, while animals have evolved enzymes and other ways to protect against those defenses. We produce a host of enzymes in our livers that detoxify chemicals that we eat in our food every day, and they are classified as Phase I and Phase II ‘xenobiotic’ metabolizing enzymes (there are also Phase III but we won’t get into that). Phase I enzymes take a foreign chemical and add or expose a functional group that Phase II enzymes can then add a molecule to, which allows the modified chemical to be excreted from the body. However, sometimes the chemicals produced by Phase I enzymes turn out to be carcinogens, which can cause damage before the Phase II enzyme is able to safely destroy it. Some chemicals that are known to have carcinogenic activity are among the Coumarins, Flavonoids, Glucosinolates, Isothiocyanates, and Phenols found in many plants – including broccoli.

Some of these compounds can also affect the activity of Phase I and Phase II xenobiotic enzymes, and often both. A chemical that induces the first class might cause more carcinogens to be produced, while one that induces the second class would more quickly eliminate them from the body before they can cause damage. Sulforaphane was discovered in 1992 to selectively induce the second, and not the first. And the more Sulforaphane you consume, the more it induces this activity. What this means is that consuming Sulforaphane will increase your body’s ability to protect itself against many forms of cancer. Indeed, and although some early research on Glucoraphanin suggested it might be harmful because it induces Phase-I enzymes, the new 2011 paper indicates that it upregulates cytochrome p450 along with Phase-II enzymes and therefore also contributes to the anti-cancer properties of broccoli itself.

You may have noticed that since Sulforaphane is an Isothiocyanate, and Glucoraphanin is a Glucosinolate, that they are members of two of the classes of compounds I mentioned above that have known carcinogens among them. Breeding for enhanced levels of one could affect the levels of others, so there is a great deal more complexity to this issue than I have described here. In addition, some Phase-I enzymes eliminate carcinogens, and some Phase-II enzymes create carcinogens as well. There are other compounds present in cruciferous and other vegetables that contribute in other ways as well. But on the whole it is true that these compounds have a beneficial effect, despite these complexities. And since Sulforaphane is produced from Glucoraphanin in cruciferous vegetables such as broccoli – then eating broccoli that is higher in Glucoraphanin will protect against cancer even more.

To top it off, a paper published this year found that Sulforaphane also inhibits the activity of two enzymes in cancer cells, leading to cell death. So its benefits may not be limited to preventing, but perhaps fighting certain kinds of cancers.

Breeding Better Broccoli

Now the question becomes, how can we get broccoli on our dinner plates that has more of these beneficial compounds? There is considerable variation in the amounts of Glucoraphanin and other Glucosinolates in broccoli, and this review paper by E.H. Jeffrey et al discusses what is known about this variation. They show that Glucoraphanin and other Glucosinolates can vary from as little as one tenth to as much as three times the amount found in your average broccoli. Not all broccoli is bred the same.

Differences in the levels of these compounds can be caused by genetics, environment, interactions between the two, and post-harvest storage and processing. It turns out that in one study for Glucoraphanin and other similar aliphatic Glucosinolates, 60% of this variation is genetic, while only 5% is environmental. 10% is due to an interaction between genetics and the environment, which is like saying that one variety makes more in one environment, while another variety makes more in another environment. Genetics comes out as a clear winner if you want to improve the anti-cancer properties of broccoli, and where there is genetic variation for a trait like this, a plant breeder can select for plants that have that trait and improve it over generations.

Plant breeders at the John Innes Center in Norwich, England, and Monsanto’s vegetable seeds division used the genetic variation for Glucoraphanin levels in wild broccoli to breed for higher levels in a modern, commercial broccoli. This is accomplished by crossing cultivated and wild plants, and in successive generations selecting for plants that have higher levels of Glucoraphanin as well as the traits you want in a modern broccoli. They report that by testing in 23 locations against other leading commercial broccoli varieties, that their new Beneforté broccoli variety contains an average of about 2.7 times as much Glucoraphanin as your average broccoli. Since the effects increase with dosage, this means that you would be expected to gain more cancer-protective benefits by eating it. How much benefit, however, is not clear.

The environment it is grown in and what happens to the broccoli after it is harvested still matters, however. As Glucosinolates contain sulfur, fertilizing the soil with sulfur can quite understandably boost their levels. And while organic growing methods can affect some minor Glucosinolates both positively and negatively, Glucoraphanin is unchanged by this practice. How the broccoli is stored and processed also affects what levels remain in the vegetable, and finally, how you prepare it also matters. The enzyme Myrosinase that converts Glucoraphanin into Sulforaphane does this when the broccoli is chopped and chewed, but only if the broccoli is uncooked. Cooking destroys the enzyme’s activity, and also reduces the levels of Glucosinolates. Either eat them raw, or blanch them briefly! And since Myrosinase activity can be affected by the climate and season, there can still be an important environmental factor to this trait.

And one final note about breeding. While Glucoraphanin is the most abundant Glucosinolate in broccoli, it is part of a complex pathway and a complex trait, so breeding for the levels of one compound may affect levels of the others. The best breeding program will look at a broader array of Glucosinolates and other effects that breeding, environment, storage and packaging will have on the final product. Indeed, since some genotypes will do better in particular environments than others, and some may hold onto their chemicals during storage better than others, these downstream effects can inform the breeding process significantly.

Other genetic tools are helping to develop traits such as these, as this paper demonstrates that you can predict levels of Glucosinolates you will get when you made hybrid broccoli.

The Beneforté website indicates that this particular variety of broccoli is grown in a particular location in California, rather than in many places around the country. While you may not like the idea of produce shipped thousands of miles, this does mean that they have essentially fixed the Genotype by Environment interaction. In non-breeder terms, this means that they picked the best environment for the best variety of broccoli to get the highest levels of Glucoraphanin, amongst other traits. This suggests that they also took the environmental contributions into account when developing the Beneforté. The entire process took them about ten years.

While the exact amount of benefit to be had by eating the Beneforté broccoli is unclear, it does appear that it is likely to help in the area of cancer prevention. Keep in mind I am no dietitian, nutrition researcher, nor doctor, however the prevailing scientific literature indicates that it should. It would be nice to see some data published on this and other broccoli varieties, more information about other Glucosinolates in this variety, and perhaps a feeding model as well, but if I saw the Beneforté and I had the cash to get it, I probably would. The story of its breeding is almost reason enough besides the Sulforaphane!

Andy Bellatti

Back to Bellatti

Now that you know all you ever wanted to know about Broccoli and what we know about how its chemical composition prevents cancer, it is time to return to Andy Bellatti’s ill-informed piece purporting to “Bust” the Beneforté Broccoli.

The first point that Bellatti takes issue with is with regard to growing conditions.

“Similar growing conditions” — there’s an interesting tidbit. For all we know, then, Beneforté’s glucopharanin content could pale in comparison to that of organic broccoli.(sic)

Actually, if Bellatti did his research, he would know that organic growing methods do not significantly affect the levels of Glucoraphanin (which he misspells as glucopharanin), as I indicated above. The growing methods described on the Beneforté website appear to be describing climatic factors rather than the organic-conventional dimension. And it is quite odd that he takes issue with a straightforward and scientific manner of studying and reporting differences under similar growing conditions, which is necessary for comparison. But rather than try to find out the facts and report an analysis of them, he goes off the organic health halo to make what is an empty quip.

Next, he criticizes the focus on Glucoraphanin.

Of course, this obsession with glucoraphanin is a silly and myopic distraction. Broccoli, by virtue of being a vegetable, is healthful and does not need to be improved upon. None of the myriad of chronic health issues affecting millions of Americans are due to “faulty broccoli” with low levels of glucoraphanin.

Again, proper research would have prevented him from making a categorical double-error such as this. Being a vegetable does not automatically make something healthy. What is a vegetable but an edible non-reproductive part of a plant? Being healthy is not part of its definition. But more importantly, his ignorance of plant genetics betrays the second error. There is genetic variation for healthful aspects of vegetables, which means that you can have vegetables that are more or less healthy than each other, all on account of genetics. As I put it above, no two broccoli’s are the same. He is enjoying vegetables that are the result of a long plant breeding process of genetic improvement, and his suggestion that ‘This is as good as it gets’ is way off. In the case of broccoli – given that it is the same species as cauliflower, cabbage, and Brussels sprouts which vary widely in their content of Glucoraphanin, that means that the very broccoli trait in question is likely the result of human improvement already. Plant breeding is a continual process of constant improvement that should not stop.

He has also contradicted himself here – by suggesting that organic may be an improvement over conventional (which it is not in this aspect), he is suggesting that vegetables as most people eat them can and should be improved upon. If the mere virtue of being a vegetable was enough, then conventional non-organic broccoli should be enough for him.

Chia, hemp, flax. "Magic bullets" of Omega-3.

Now I will address the more important point, and that is that focusing on Glucoraphanin “is a silly and myopic distraction.” Granted there are more complexities to the cancer-preventative effects of broccoli compounds as I described above, but Glucoraphanin is still the most important part of it. But, some people have food philosophies that focus more on changing what specific foods people eat rather than changing the composition of those foods. To understand his comment in context of his food philosophy, I took some time to read his blog.

He is a vegan, who in his own words “approaches nutrition from a whole-foods, plant-centric framework.” Still, I do not see how improving the genetics of broccoli does not fit into this philosophy. You are still eating a whole plant food. Perhaps, still, the specific composition of those foods does not matter to him?

However, his blog posts reveal a different story. He is in fact quite concerned with the specific composition of foods, ranging from listing the nutrients in each of his posted recipes, to complaining how he had to learn about how food service establishments work instead of the compositional differences of chia, hemp, and flax seeds. As a matter of fact these seeds show up an inordinate number of times in his recipes – and I daresay that “none of the myriad of chronic health issues affecting millions of Americans are due to not eating enough chia, hemp, and flax seeds.” Of course it would be silly to expect these seeds to be magic bullet cure-alls, but that is the standard that he held the broccoli to, so fair’s fair.

So it becomes very clear that Andy Bellatti is highly concerned with specific nutritional compositions of and differences between foods. In fact, the hypocrisy reaches levels that will bust everyone’s irony meters. While Bellatti tries to give enhanced levels of Glucoraphanin in the Beneforté broccoli a bad ‘raph, he is quite delighted to advertise such chemicals as important reasons to eat cruciferous vegetables in the first place!

In this blog post extolling the virtues of broccoli rabe, Bellatti says the following,

For example, it offers high amounts of isothiocyanates, compounds that fiercely battle carcinogens in the body.  High isothiocyanate consumption has been shown to significantly reduce risk of developing breast, esophageal, lung, and prostate cancers.

Compare that to what he said about the Beneforté:

Of course, this obsession with glucoraphanin is a silly and myopic distraction.

Andy Bellati: Eat it for the Glucoraphanin! Err...

Apparently Bellatti is quite familiar with silly and myopic distractions himself. He gives completely opposite opinions of these compounds depending upon the end goal of his argument. It is apparent from his blog that his food philosophy includes focusing in on these nutrients, and so by rejecting the nutrient-focus of this broccoli, he is also rejecting what seems to be his own nutritional philosophy.

Politics, Politics, Politics

He then proceeds to reveal what I think is the real reason for his distaste with the Beneforté, that it is made by Monsanto.

The biggest irony of this product lies in Monsanto’s claim that Beneforté “help[s] maintain your body’s defenses against the damage of environmental pollutants and free radicals.”

Environmental pollutants? As in, the ones that have have increased exponentially as a result of genetic engineering?

He cites The Organic Center’s 13-year report on pesticide use, which we have already discussed here and noted that it compared pesticides of wildly different impacts on human health and the environment as being equivalent by weight. In other words, one pound of a nasty herbicide such as atrazine equals one pound of roundup, which is far less nasty. Genetically engineered herbicide tolerant crops have caused a shift in herbicide use from sprays such as atrazine to safer ones such as glyphosate – which are physically heavier have a lower environmental impact quotient (EIQ) per pound, so The Organic Center reports it as an increase in herbicide by weight even though it is a safer one. The study’s author, Charles Benbrook, is well aware of this problem. The report also demonstrates that GE has reduced insecticide use, but minimizes the actual impact of this by subtracting the pounds from the total. His approach makes math easy, but misleads about the overall picture.

Andy Bellatti also cites the Environmental Working Group page on herbicides, which only reinforces this point. What examples of nasty herbicides do they use to talk about health effects? Why, atrazine! One of the one’s that genetic engineering has replaced with roundup on many farms. While he was trying to catch Monsanto in an irony, he fell into one himself.

And, above all, let’s not allow Monsanto to get away with gimmicky healthwashing.

The real reason that Andy Bellatti set out to criticize this broccoli variety was not because it was a bad idea, but was because it was an idea held by a company that he dislikes. Actually, considering that Monsanto only just bought Seminis Vegetable Seeds in 2005 to form the company’s vegetable seeds division, it was probably an idea already set in motion before Monsanto had anything to do with it.

That’s a ‘Raph

Rather than base an opinion of the Beneforté broccoli variety on a consistent nutritional philosophy, a consideration of the scientific evidence, or even basic research that both his degrees in Journalism and Dietetics should have prepared him for, Bellatti decides to instead base it on his opinion of the company that is marketing it. How much of his dietary advice follows the same pattern, I am left wondering? Are clients hiring a dietitian or a food policy activist?

He completely missed an opportunity to discuss what we know and don’t know about Glucoraphanin and the precise details about how it interacts with our bodies, and then express an opinion about the relative merits of this improvement. But he rejected even the idea of learning anything about it before uttering a cynical burp of bad sulfurous broccoli breath.

There are more things to think about that I haven’t even gotten into. Would the promise of a greater benefit lead to more broccoli consumption, or perhaps less? Are there other interactions that this trait might have for better or for worse with people’s health? What standards ought there to be for health claims based on achievements in plant breeding? There is certainly room for discussion below, but I saw this as an opportunity for everyone to learn more about a health-oriented crop variety which is one of the first in many that are sure to come. The real facts about the biochemistry, genetics, breeding, and marketing are far more interesting to talk about.

Professor Nina Fedoroff of the Pennsylvania State University is the lead protest letter signatory.

The biotech crop regulation changes mooted by the EPA were announced March 2011 in the Federal Register here (pdf).

Scientist co-signatories on the Fedoroff Letter say that the EPA is going down a troublesome path that is not based on science, and which will frustrate and delay innovations needed to provide farmers with better cropping methods.  Because of the delays and unneeded extra cost burdens such a  policy shift would create, it would surely undermine global food security.

The text of Fedoroff Letter is provided below (see here for the full original letter).

Nina Fedoroff has (together with Robert Haselkorn,and Bruce M. Chassy) written a very readable  editorial about this issue in the FASEB biology journal:
“EPA’s Proposed Biotech Policy Turns a Deaf Ear to Science” (pdf). This great FASEB editorial fully explains the nature of the problem that is brewing with the current EPA policy direction.

Such expanded regulation would serve only to increase costs, hinder research, undermine the long-term viability of public university research programs, and limit product development from the private sector. The proposed actions would threaten our ability to produce high quality food at an affordable price and to feed a growing population.

They would also weaken the competitive advantage of U.S. public research programs in the global research arena, all with no increase in safety for consumers, farmers, or the environment — indeed, the contrary would be the case in many instances.

The academic community is committed to ensuring that the environmental and food safety benefits of biotechnology-derived plants continue to accrue, and it is essential that all agencies respect the scientific basis for regulation and division of regulatory responsibilities established by the Coordinated Framework. It is critical that regulations focus on scientifically demonstrated hazards, rather than being driven by issues of perception or political expediency. Therefore, we urge that the pending EPA regulatory actions be reconsidered and the rule-making proposal be limited to requirements for substances that have traditionally been regulated by the EPA, such as PIPs, and then only to those requirements that are fully justified on the basis of sound science.

Readers of Biofortified should start bending the ears of congressional representatives — and get the  EPA’s attention by every available communication channel — to make sure this potentially serious misadventure does not happen.

We, the undersigned members of the National Academy of Sciences, write today to voice our concern over the latest proposal from the U.S. Environmental Protection Agency (EPA) to further expand its regulatory coverage over transgenic crops in a way that cannot be justified on the basis of either scientific evidence or experience gained over the past several decades, both of which support the conclusion that molecular modification techniques are no more dangerous than any modification technique now in use. The increased regulatory burdens that would result from this expansion would impose steep barriers to scientific innovation and product development across all sectors of our economy and would not only fail to enhance safety, but would likely prolong reliance on less safe and obsolete practices.

Since then, extensive research, coupled with years of experience, led to the conclusion that there is no scientific basis to single out plants produced by transgene insertion for a special regulati•ry review, nor to distinguish these products from others on the basis of the process used to create them. There is now abundant evidence that the most appropriate regulatory approach would be to require review only of truly novel traits introduced into plants without regard to the methods used for their introduction. Yet the regulatory apparatus in the U.S. has increasingly moved in the opposite direction towards ever greater regulation and increased data requirements for transgenic plants, despite the abundant accumulation of data attesting to their safety.

The scientific community has a strong interest in keeping regulations science-based and Commensurate with the risk of the products at issue. This past March, EPA announced in the Federal Register a draft proposed rule to codify data requirements for plant incorporated protectants (PIPS). This draft was forwarded by EPA to the U.S. Department of Agriculture (USDA), Department of Health and Human Services and Congress for review in accordance with the Federal Insecticide, Fungicide, and Rodenticide Act.

Based on initial reviews of that draft proposal and recent EPA actions associated with biotechnology-derived crops, it is clear that the Agency is departing from a science-based regulatory process, walking down a path towards one based on the controversial European “precautionary principle” that goes beyond codifying data requirements for substances regulated as PIPs for the past 15 years.

We are particularly troubled by proposals to expand EPA’s current oversight into areas such as virus resistance and weediness that have been adequately addressed by USDA since 1986. Already, EPA has expanded its oversight into virus resistance, which previously had been the purview of USDA’s Animal and Plant Health Inspection Service (APHIS) and which EPA prudently proposed in 1994 to exempt from its regulations. With the draft proposed rules, EPA would further expand its regulations and data demands to other areas historically covered by USDA-APHIS without the slightest justification based on either data or experience.

It is most troubling that EPA is also proposing to increase its regulation to cover matters which are still not deemed to be threats even after years of study, such as potential gene transfer from plants to soil microorganisms. In other actions, EPA has expressed its right to regulate plants engineered for altered growth (e.g., by suppression of ethylene production), the same way it regulates synthetic plant growth regulators. The Agency does so based on a generous interpretation of the enabling legislation, despite the absence of any scientifically credible hazard.

Such an expansion in regulatory purview would reverse long established and highly successful policy under the Coordinated Framework. Such a shift would (1) create a duplicative regulatory system for very low risk products delivering substantial, demonstrated environmental benefits; (2) increase costs, reduce efficiency and prolong the review timelines thereby discouraging innovation; (3) dramatically increase the hurdles already facing academic institutions and companies attempting to improve so-called minor use or specialty crops through modern biotechnology; and (4) adversely impact trade in safe and wholesome commodities produced by U.S. growers because of the stigma attached to anything characterized as a “pesticide” — a regulatory label for DNA that is unique to the U.S. — and with no concomitant increase in product safety. In addition, any expansion in regulatory oversight not resulting from documented risk could have global ramifications, as policymakers in other countries routinely consider U.S. policymakers as leaders in the regulation of crops derived from biotechnology.

Indeed, it is astonishing that EPA would attempt such an expansion of its regulatory activity in this sphere. We now have more than 25 years of experience with biotechnology-derived crop plants. None of the hypothetical risks articulated at the dawn of this era has been realized and caused new environmental problems. On the contrary, billions upon billions of meals derived from these crops have been eaten by humans and livestock around the world with no ill effects. Moreover, environmental impacts of production agriculture and the carbon footprint of agriculture have been significantly reduced through the use of transgenic crops. At the same time, farmers have benefited economically, socially, and through improved health. These indisputable results make a compelling case that existing regulatory burdens should be reduced and refocused. There is absolutely no justification in either scientific data or experience for the regulatory expansion proposed by EPA.

Over the last two decades, advances in sequencing and genomic analysis have revealed that biotechnology is more precise and less disruptive to the genome than traditional plant breeding. In point of fact, recent genomic, proteomic and metabolomic comparisons of varieties bred through conventional and transgenic methods demonstrate that transgenic plants with incorporated novel traits more closely resemble the parental variety than do new varieties of the same plant produced by more traditional breeding or mutagenesis techniques. These findings confirm that transgene insertion is not inherently risky nor does it present new and greater hazards than conventional plant breeding.

In conclusion, recent EPA actions signal an intent to expand the Agency’s regulatory oversight into products regulated by USDA for over two decades and to products for which there has never been a justification for regulation. These actions are not only inconsistent with regulatory directives mandated by the current Administration, they also erode the integrity of the Coordinated Framework. Such expanded regulation would serve only to increase costs, hinder research, undermine the long-term viability of public university research programs, and limit product development from the private sector. The proposed actions would threaten our ability to produce high quality food at an affordable price and feed a growing population. They would also weaken the competitive advantage of U.S. public research programs in the global research arena, all with no increase in safety for consumers, farmers, or the environment — indeed, the contrary would be the case in many instances.

The academic community is committed to ensuring that the environmental and food safety benefits of biotechnology-derived plants continue to accrue, and it is essential that all agencies respect the scientific basis for regulation and division of regulatory responsibilities established by the Coordinated Framework. It is critical that regulations focus on scientifically demonstrated hazards, rather than being driven by issues of perception or political expediency. Therefore, Administrator Jackson, we urge you to reconsider the pending EPA regulatory actions and limit the rulemaking proposal to requirements for substances that have traditionally been regulated by EPA as PIPs, and then to only those requirements that are fully justified on the basis of safety and sound science.

I sign this letter on behalf of the more than 60 members of the U.S. National Academy of Sciences listed below. The list includes many of America’ most eminent biological scientists, including Nobel Laureates Dr. James Watson and Dr. Gunter Blobel.

Sincerely,
Dr. Nina V. Fedoroff
Member, National Academy of Sciences
2006 National Medal of Science Laureate
Science and Technology Adviser to the. Secretary of State and to the Administrator of USAID, 2007-10
Evan Pugh Professor, Pennsylvania State University
Huck institutes of the Life Sciences
211 Wartik
State College, PA 16801
nvflPpsu.edu

The 1st Rule of GMOs: You Should talk about GMOs. I think this is exactly right no matter what your perspective is on this topic. Please take a moment to register for Threadless, and vote on this entry. I recommend giving it a 5!

The issue of genetic engineering in agriculture needs more people sanely talking about it, not trying to start “food fights.” This entry looks like the only one that really seeks to promote discussion, whereas others promote violence (between food groups to start with), misunderstandings, and extreme views. Take a look at some of the competition:

A familiar concept – one example of how dislike for genetic engineering can get extreme. Not only wound up like dynamite, but also radioactive – I hope it bombs so it doesn’t lead to more explosive dialog.

One of the many half-plant half-animal depictions of GE crops – this time a scorpion-tomato. The entry claims that this exists, however our own reader C Radar points out that this is probably a myth.

Another one of the many literal food fight designs that showed up in the contest.

Now this one deserves its own separate analysis for its implications and motivations. Apparently a project intended for humanitarian purposes is not only an invasion, but also an invasion of slant-eyed yellow-skinned enemies to be fought off by round-eyed white-skinned heroes. As Jon Stewart would say about this kind of crossfire – Stop. You’re hurting us.

If you register to vote in this contest, you can thumb through all the entries and vote down the really objectionable ones. Too bad that 1 is the lowest score you can give! I am genuinely interested to see what exactly gets voted up in this contest, and I hope for the sake of the public discourse that the end result is not too bad.

Makes me think we need to design a T-shirt that provokes thought and dialog, without provoking a fight.

(This post originally appeared on Sustainablog on 8/1/11)

In the debate about GMO crops, the “threat of genetic contamination” is often raised as a reason  to reject the technology.  Is this threat real?  Does it justify acts of vandalism?  Could it lead to the “End of Organics“?  Is it actually an over-blown issue?  To answer these questions it is necessary to put this issue in the context of basic plant biology.

What We Are Talking About Is Really Just “Plant Sex”

“Genetic Contamination” is an emotional term which obscures the fact that the underlying biological process in question is quite normal, natural and highly necessary. All living species, need to be able to reproduce.  They also need to generate the genetic diversity that will allow the species to adapt and evolve as needed to survive.  Plants can’t move, so to “mate” with other plants of their species they have to find ways to spread the male sexual cells (pollen) to the female reproductive cells (the ovaries in the female parts of flowers).  Some plant do this with the help of pollinators – the bees, flies, butterflies, birds, etc.  These helpful agents incidentally move pollen around.  Other plants simply rely on wind to move their pollen to other flowers.  This is the case with most “grain crops” like wheat, barley, oats, corn etc.

“Cross pollination” is the accurate, unemotional, term for this process.  GMO crops participate in cross pollination in exactly the same way that non-GMO plants do and always have.

What Do You Get If You Cross A … With A …

Perhaps we have heard too many such jokes, because many people believe that the genes from GMO plants have the potential to “contaminate” all manner of natural species or “Organic” crops The fact is that if you “crossed a chicken with an octopus” you wouldn’t get “drumsticks for everybody.” You would get nothing.  The same is true for plant species.  They do not cross pollinate (or contaminate) other anything except extremely closely related plants.

There are some cases where a very closely related, “weedy” sub-species can cross with a crop (e.g. cultivated sunflowers with wild sunflowers), but those issues were anticipated long before GMO crops were introduced.  For that very reason, no GMO sunflowers have been introduced in the US.

GMO crops have no greater or lesser ability to move genes to other species.  Those sorts of fears are groundless.

Crops Where Cross Pollination is A Management Issue

Long before the advent of GMO crops, farmers of certain crops have had to manage “genetic contamination” issues involving normal cross pollination.  Wheat is wind pollinated and farmers commonly save part of their crop each year to serve as seed for the next (“saved seed”).  Wheat is also a crop with very specific quality characteristics for its various uses (raised breads, flat breads, crackers, pastries, noodles…).  New wheat varieties are bred for those specific uses.  There is a network of dedicated wheat seed growers who produce “certified seed” with enough isolation from other wheat so that the seed they produce is >95% the desired variety.  If a farmer plants that certified seed (usually at a small cost above current grain price), the crop he/she produces will be what is desired for the end use.  If the farmer saves some of that crop and plants it a second year, it will be less pure because of cross pollination from neighboring fields.  After a few years, it is necessary for the farmer to buy new certified seed because his/her own supply is “contaminated.”  There are many more examples like this for “saved seed” crops.

Hybrid seeds are grown by dedicated seed growers and purchased by the farmers every year.  This system insures both genetic purity for specific needs and the extra vigor and yield potential that hybridization enables.

Whether it is a “saved seed” crop or a hybrid crop, GMO versions create no new issues beyond what farmers have always been managing.  It only becomes an issue when someone wants to set a zero tolerance unlike the rational tolerances that have made all of these crops work for a very long time.

Crops Where Cross Pollination is Irrelevant

A few years ago there was a ballot initiative in Mendocino, California to ban GMO crops from that county.  It was driven by concerns about “genetic contamination” of the Organic farms (many supporters didn’t understand the paragraph above).   The fact that there were not even GMO crops that were likely to ever be planted in this particular county was seemingly irrelevant to the debate.  I was talking with a PhD level scientist that worked for one of the wineries there, and asked why that company was supporting the ban.  She said it was because of concerns about how the genetic contamination risk could hurt their sales.  I was stunned because, as a scientist, she certainly knew that grapes are never grown from seed but rather “vegetatively propagated.”  If you take a seed from a Cabernet grape and plant it, you will not grow a Cabernet.  It will be some new variety, just as when humans have children, they are each a unique new combination of their mother’s and father’s genes.  For thousands of years farmers have known how to take cuttings of desirable fruits and get them to root, or how to take buds of the desired fruit variety and graft it onto a rootstock.  The grapes in Mendocino county had been propagated that way for centuries.  A block of Cabernet planted next to a block of Chardonnay is not a “genetic contamination” issue, because the seed is never planted.  This same principle applies to almost all fruit and to other vegetatively reproduced crops like potatoes, cassava, sweet potatoes, sugarcane and many others.  GMO versions of these crops would not represent any “genetic contamination risk”  at all.  That is why it is so sad and absurd that activists in France destroyed a GMO grapevine trial because of needless “contamination” fears.

Genetic Contamination: An Intentionally Overplayed Issue?

On several occasions I have written directly to individual, anti-GMO scientists, at Greenpeace and elsewhere, asking specific questions about how they imagine that a particular crop could represent a “genetic contamination risk.”  I have never received an answer with any scientific justification or even a plausible “what if” scenario.  Presuming that these individuals understand basic plant biology, they apparently choose not to acknowledge it in their public campaigns.

What is really going on (“cross pollination”) is a vital, natural process.  Farmers and the plant breeders who serve them have long been able to harness the positive potential of this genetic exchange to breed for improved varieties.  They have also been able to fully manage the cases where cross pollination could cause a genetic purity problem for the crop.  GMO crops have not changed this in any fundamental way that cannot be dealt with by rational decision making and regulation.

You are welcome to comment here or to email me at savage.sd@gmail.com.  My website is Applied Mythology

Pollinator fly (bee mimic) image from Savvey’s Photography Photostream