Featured in Newsletter Archives - Genetic Literacy Project: Recent Episodes
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A new review paper by researchers at Bayer Crop Science, titled Beautiful and delicious mutants: The origins, fates, and benefits of molecular sequence variation in plant evolution and breeding, explains how genetic mutations in plants are not just accidents of nature – they are the foundation of agriculture itself.Published in the scientific journal Plant Physiology, the paper argues that plant mutations — whether spontaneous or engineered — are at the heart of food security and agricultural innovation.
From chance to choice
For most of human history, crop genetic improvement has relied on luck. A farmer might notice a barley plant with larger seeds or a tomato with fewer cracks and save those seeds for the next season. Without realising it, they were harnessing mutations — random DNA changes that happened to produce useful traits.
Each generation of plant has natural mutations in its DNA which help to drive the processes of evolution and natural selection. Some of these changes will make the plant more or less successful in its environment, but humans have been able to harness this to benefit the development of agriculture. Over thousands of years, this slow process of selection and human intervention helped transform bitter wild almonds into sweet ones, sprawling teosinte grasses into compact, high-yielding maize plants, and tough wild apples into crisp dessert varieties.
But chance alone could only take us so far – it is slow and unpredictable. In the mid-20th century, scientists began deliberately inducing mutations with radiation and chemicals, hoping to accelerate the discovery of beneficial traits. This “mutation breeding” produced thousands of new crop varieties, from malting barley and high-yielding rice to colourful chrysanthemums. These ‘mutant’ varieties remain staples in our diets and gardens today.
In the Bayer paper, the authors emphasise that these older methods of inducing mutations are not fundamentally different from natural ones — the DNA changes are physically indistinguishable. The only difference is whether they occurred by chance or by human design.
Genome editing: evolution with a scalpel
The most recent chapter in this evolving story is genome editing. Tools like CRISPR allow scientists to introduce mutations at specific locations in a plant’s genome, rather than waiting for chance or using radiation. Imagine being able to edit an almond so that only its kernels lose bitterness, while its roots still produce natural protective compounds against insects. Or designing rice that can thrive in salty soils without sacrificing yield.
The paper argues that genome editing is, in many ways, just a more precise continuation of what farmers and breeders have always done: generating genetic diversity and then selecting useful traits. But unlike earlier methods, genome editing is much more precise – which saves time and reduces wasted effort by improving the chances of success in modern plant breeding programmes.
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One of the most compelling aspects of the paper is the way it reframes the mutations delivered by plant breeders over the years as sources of beauty and diversity. Consider:
- Polyploidy — the doubling (or even tripling) of entire genomes — has given us plump seedless watermelons, modern octoploid strawberries which stem from natural 18th century hybridisation, and the fluffy ornamental cockscomb flower. Though technically “errors” in cell division, these mutations are agricultural treasures;
- Structural changes like inversions or translocations have shaped crop qualities ranging from the colour of wine grapes to disease resistance in wheat;
- Tiny DNA changes can have massive consequences: a single base-pair swap made almonds safe to eat, while another created carrots rich in vitamin A.
Even transposable elements — so-called “jumping genes” once dismissed as genomic parasites — have sparked major agricultural shifts, including the transformation of maize from a many-branched wild grass into the single-stalk architecture found in modern cornfields, whose global production today exceeds 1 billion tonnes.
These stories remind us that our food system is built on centuries of accumulated mutations, selected and refined by both natural forces and human intervention.
The perception problem
But if mutations are so central to agriculture, why do they carry such a negative reputation? The paper notes that in popular culture, “mutants” are usually monsters, and in medicine, mutations are often linked to cancer or genetic disorders. Rarely do we hear about mutations as the reason we enjoy juicy peaches or seedless bananas.
This perception gap matters. Genome editing, despite producing the same types of DNA changes found in nature, is often regulated and debated as though it were fundamentally different. A CRISPR-edited tomato with enhanced nutrition may face more regulatory hurdles than a variety created decades ago by exposing seeds to radiation — even though both contain mutations of the same kind. This is why in plants genome editing is usually referred to as precision breeding. It allows a breeder to do something they could try to do with traditional techniques, but more precisely, and with far fewer of the unplanned mutations which come with every generation of conventional breeding methods.
The paper suggests that our focus should shift from how a mutation arose to what it does. Does it make food safer, more nutritious, or more resilient to climate change? If so, does the process by which that change occurred really matter?
Mutations for a changing world
As the global population grows and the climate becomes more unpredictable, the stakes of crop improvement are rising. Plant breeders need access to tools that can help them develop crop varieties to withstand drought, resist pests, and thrive in a range of soil type and conditions, all while satisfying consumer preferences for taste, nutrition, and shelf life.
Random mutation, whether natural or induced, will always play a role. But targeted genome editing allows us to guide the process more deliberately. Instead of hoping for a beneficial mutation to arise, we can recreate known combinations of genes in new crop varieties or even design entirely new traits.
The challenges of feeding a growing global population and doing so more sustainably are vast and traditional plant breeding is a time-consuming process of incremental improvement. Genome editing reduces the time it takes to develop new, better, and more sustainable varieties of crops.
Importantly, the authors also stress that no single approach is sufficient. Genome editing complements — rather than replaces — existing practices of conventional breeding, germplasm conservation, and farmer knowledge. The goal is not to abandon this diversity of methods, but to expand the toolbox available to tackle agriculture’s greatest challenges.
Beyond the lab: ethics and equity
While the paper focuses mainly on the science of mutations, it hints at broader questions. Who decides which mutations are desirable? How do we ensure that genome editing benefits smallholder farmers as well as large-scale agriculture? And how do we balance innovation with the preservation of traditional crops and farming practices?
These are not just technical questions but cultural and ethical ones. Food is deeply tied to identity, tradition, and trust. If mutations are the raw material of agriculture, society must decide how to use them responsibly.
But it is vitally important that those decisions, and the public conversation surrounding then, are based on a solid understanding of how these newer forms of breeding relate to the spontaneous and human-induced mutations which have underpinned the development of agriculture and food production for thousands of years.
A celebration of mutants
The review paper is, at its heart, a call to rethink how we view mutations. Far from being aberrations, they are the sparks of novelty that have given us the diversity of crops we depend on. Every mouthful of bread, fruit, or vegetable is, in some sense, a celebration of mutants — beautiful, delicious, and essential.
If history is any guide, the crops of the future – and with it our ability to feed a growing population in the face of a changing climate – will continue to be shaped by both chance and choice, by a combination of natural variation and human ingenuity.
Dr Anthony Hopkins joined the British Society of Plant Breeders (BSPB) as head of policy in January 2024. He was previously chief crops adviser at the National Farmers’ Union. Find Anthony on LinkedIn
A version of this article was originally posted at Science for Sustainable Agriculture and has been reposted here with permission. Any reposting should credit the original author and provide links to both the GLP and the original article. Find Science for Sustainable Agriculture on X @SciSustAg
We’ve been working on this article for weeks. Poring over studies on the Tylenol-autism topic. Just before we got it scheduled to post… another soundbite.At today’s Cabinet meeting, Health Secretary RFK Jr. claimed that “children who are circumcised early have double the rate of autism,” adding “it’s highly likely because they’re given Tylenol.” President Trump backed him up, saying there’s “a tremendous amount of proof or evidence, I would say as a non-doctor.”
Here’s just the tip of what’s wrong with this claim: Kennedy mentioned “two studies,” but didn’t specify which. A quick search turns up two likely candidates. One is a 2015 Danish registry study that found a modest statistical bump in autism diagnoses among circumcised boys, especially under age five. The authors themselves highlighted big limitations—such as incomplete circumcision data and the inability to prove causation. (By the way, the study never mentioned Tylenol, acetaminophen, or any pain medications. The researchers were investigating whether the circumcision procedure itself – the pain and stress – might be linked to autism.) The other is a 2013 ecological paper that used circumcision rates as a stand-in for acetaminophen exposure. Even its authors described it as “hypothesis-generating,” not proof. And just to underline how shaky the circumcision link was, a 2015 published critique of the Danish study pointed out that its autism findings rested on very small numbers and questionable assumptions.
But RFK Jr.’s real logical leap is collapsing these into one neat story: some circumcised boys get Tylenol for pain, and some are later diagnosed with autism—therefore, Tylenol causes autism. That’s like saying umbrellas cause car accidents because both are more common on rainy days. The studies don’t actually connect those dots. The Danish analysis wasn’t about Tylenol at all, and the ecological paper was little more than circumcision-as-proxy guesswork.
Kennedy’s stance? “None of this is positive, but all of it is stuff we should be paying attention to.” This immediately brought to mind that scene in Dumb and Dumber—when Lloyd Christmas hears his chances with Mary are “one out of a million” and responds: “So you’re telling me there’s a chance!”
Now, on to what we actually came here to discuss: the broader claims about Tylenol and autism that have pregnant women wondering if they really need to “tough it out”…
At a press conference on September 22, the Trump administration urged pregnant women to “tough it out” and avoid Tylenol, citing a link to autism. The claim surprised many, including the researchers whose work is being cited. Scientists say that’s not what the research shows. The strongest evidence to date shows that if there is any link, it’s not a cause-and-effect relationship.
Here’s what you should know…
For starters, acetaminophen is the active ingredient in Tylenol and many other over-the-counter medications, making this warning broader than just one brand.
The Review That Doesn’t Say What They ClaimThe centerpiece of the government’s claim is a review of 46 studies published in August. Yes, 27 studies reported some association between acetaminophen and neurodevelopmental issues. In science and public health, “association” means that two things are related or connected in some way, but it does not mean that one causes the other. A third thing might be influencing the relationship and causing both of the first two things to happen at the same time. The review’s own lead author, Dr. Didier Prada, confirmed: “We cannot answer the question about causation—that is very important to clarify.”
He even used a perfect analogy: ice cream sales and violent crime both rise in summer, but nobody thinks Rocky Road causes assault. (Association, not causation.)
They also relied on the Navigation Guide, a framework built for environmental toxins, not medications. With medications, we can measure exactly what people took and when. But with environmental toxins—think lead paint from childhood homes or industrial chemicals from old factories—researchers have to guess based on decades-old records. The Navigation Guide was designed for those messy situations. Applied to medications—where we have prescriptions and clear records—it treats weak hints like strong evidence. Medical standards like GRADE correctly start with more skepticism about observational studies; the Navigation Guide doesn’t. Small, questionable associations get inflated into findings that seem more certain than they are.
The review gave high ratings to studies with fundamental flaws—including one where every single baby had detectable acetaminophen in their cord blood, making a true unexposed comparison impossible—while penalizing a massive Swedish sibling study for not having trimester-specific timing data. Reviews like this are extremely sensitive to how studies are weighted—small changes in weighting can flip the overall conclusion from positive to negative. When the methodology lacks transparency about these crucial decisions, readers can’t evaluate whether the conclusion reflects the data or the authors’ choices.
Finally, the review leaned heavily on ‘dose-response’ as a sign of causation. If a drug is harmful, higher doses should mean higher risk. But most dose-response patterns came from small or poorly adjusted studies. In the large Swedish sibling study—our best evidence—the gradient vanished once family factors were controlled (as indicated by the purple line below). Low, medium, or high use all showed essentially the same risk which hovered around no effect (as indicated by the black dashed line at HR=1), suggesting the apparent dose-response patterns indicated in red, blue, and green came from confounding by genetics, maternal health, or the underlying condition being treated rather than the medicine itself.
Image created by Unbiased Science. Adapted from Table 2 in Ahlqvist VH, Sjöqvist H, Dalman C, et al. Acetaminophen use during pregnancy and children’s risk of autism, ADHD, and intellectual disability. JAMA. 2024;331(14):1205-1214. doi:10.1001/jama.2024.3172Credibility matters, too. The senior author, Harvard Dean Andrea Baccarelli, disclosed he was a paid expert witness for plaintiffs suing acetaminophen manufacturers. When a federal judge reviewed his testimony last December, she ruled it “lacked scientific evidence“ and dismissed every case.
What The Swedish Study ShowsThe administration is overlooking the most rigorous evidence available: Sweden’s sibling study, which followed essentially every child born over two decades—2.5 million in total, including 186,000 exposed to acetaminophen during pregnancy.
Looking at the population as a whole, researchers initially saw a slight association: about a 5% increased autism risk with acetaminophen use. But when they compared siblings—one exposed, one not—the link vanished. Same parents, same household, shared genes… but different exposure. The risk dropped to zero.
If acetaminophen truly caused autism, exposed siblings would show higher rates. They didn’t. As neuroscientistSam Wang explains, that likely demonstrates the crude link was reflecting family factors—genetics, socioeconomic status, maternal illness—not the drug itself.
Critics likeNIH Director Dr. Jay Bhattacharya argue that sibling studies can “wash out” real effects by over-controlling. But that misunderstands their purpose. When siblings share genes and family environment but differ in exposure, comparing them isolates the drug’s effect. If acetaminophen truly caused autism, exposed siblings would have higher rates than unexposed siblings. When that difference vanishes, it reveals the association was driven by shared family factors, not the medication itself. Moreover, suppose sibling designs truly “washed out” real effects. In that case, we’d still see them in other well-controlled studies—but the best prospective cohorts with biomarker validation show the same null results once properly adjusted.
Out of all the studies included in the review, the Swedish study did the best job of including additional variables in its statistical analysis. These variables, especially parental diagnosis of autism, could affect acetaminophen usage and risk for autism in their children. Even after accounting for more than 25 additional variables, the study found a slight increase in risk of autism with acetaminophen use during pregnancy. However, this effect disappeared when comparing siblings to each other, which suggests that unmeasured household and genetic factors—not captured by any of the studies—are what actually drive the apparent association between acetaminophen and autism.
Follow the latest news and policy debates on sustainable agriculture, biomedicine, and other ‘disruptive’ innovations. Subscribe to our newsletter.SIGN UPThose 27 Studies: What They Actually ShowThe government continues to cite the “27 studies” that showed a positive association in the Baccarelli study. But many weren’t about autism at all, instead looking at general behavior problems. Others relied on mothers trying to remember medications years after their child was diagnosed—an obvious setup for recall bias (mothers of children with autism naturally scrutinize their pregnancy memories more intensely, potentially “remembering” more medication use). In contrast, the Swedish study recorded acetaminophen use prospectively during pregnancy and captured prescription data through pharmacy records.
Image created by Unbiased Science
This diagram illustrates recall bias in research. When studies ask about medication use years after pregnancy, the results can be skewed because memory works differently depending on context. Some parents may review their pregnancy choices in detail (e.g., those with children diagnosed with autism), while others may be less likely to do so. This natural difference in how much people have reflected on past events can create patterns in the data that don’t represent actual cause and effect. What researchers can measure through surveys (blue) may not match the real relationship they’re trying to study (black).
The authors couldn’t actually combine the studies into a traditional meta-analysis (a statistical method that pools data from multiple studies to get a clearer picture of whether there’s a real effect). The exposure and outcome measures were too different—some asked about ‘any use,’ others counted days, some split by trimester, and one measured drug metabolites in cord blood. So they fell back on vote-counting: tallying how many studies showed an association versus no association, without considering their size, strength, or reliability. That meant a Spanish cohort of 2,600 children based on parental recall was put on the same footing as Sweden’s national sibling study of 2.5 million births with genetic controls.
Patterns are telling: when mothers reported acetaminophen use prospectively, before knowing outcomes, the associations were weaker or absent. When asked years later, after a diagnosis, the associations were stronger. That’s not causation—that’s recall bias.
And even the positive findings were modest, typically 20-30 percent increased risk. At first glance, that sounds substantial. But these numbers come from observational studies, which are notoriously prone to bias. When researchers account for family genetics, maternal health, or the reasons Tylenol was taken in the first place, the apparent increase often disappears. In other words, what looks like a sizeable association on paper may actually be a mirage created by confounding and recall bias. The few stronger signals came from tiny, self-reported studies. In contrast, the largest, best-controlled evidence—the Swedish sibling study—found no effect once family factors were considered. Most crucially, none of the studies could separate the drug itself from the reason it was taken. As Yale researcherZeyan Liew points out, fever in pregnancy is a known risk factor for developmental delays.
The Real Dangers of “Toughing It Out”While the president tells women to tough it out, let’s be clear about what he’s asking them to endure. Untreated fever during early pregnancy nearly doubles the risk of neural tube defects and is linked to heart defects and oral clefts. These aren’t theoretical risks—they’re established medical facts.
Many pregnant women experience fever and pain during pregnancy. What alternatives exist? NSAIDs like ibuprofen are contraindicated in pregnancy, especially after 20 weeks. Aspirin carries bleeding risks. Opioids bring obvious concerns. As one analysis warns, creating panic about the only safe option will cause real, preventable harm.
The Timeline That Doesn’t Add UpImage created by Unbiased Science. Data sourced from https://www.cdc.gov/autism/data-research/data-table.htmlAcetaminophen (Tylenol) entered U.S. markets in 1955, more than ten years after autism was first described by Psychiatrist Leo Kanner in 1943. If acetaminophen were a major causal driver, we’d expect a surge in the 1960s–70s as use became widespread. Instead, recorded autism rose mainly in the 1990s as diagnostic criteria broadened and diagnostic substitution occurred, especially in California. (Doctors did more strongly discourage aspirin in pregnancy by the 1990s, likely nudging some women toward Tylenol, but acetaminophen was already widely used and autism rates didn’t spike then—the increase in autism diagnoses aligns with changing diagnostic criteria.)
At the press briefing, officials pointed to aCalifornia MIND Institute study claiming those diagnostic shifts couldn’t explain the rise. But the study made a basic error: it retroactively applied 2002 criteria to children from the 1980s and 90s without re-examining them. That’s like lowering the passing score on a driving test and insisting the test hasn’t gotten easier.
California’s own Department of Health laterreanalyzed the same population and found what the MIND study missed: between 1987 and 1994, autism diagnoses rose by 9.1 per 10,000 while diagnoses of intellectual disability fell by 9.3 per 10,000. The increase and decrease tracked almost exactly—classic diagnostic substitution, not a new epidemic.
The president’s claim that countries without Tylenol don’t have autism? Cuba has both acetaminophen (sold as paracetamol) and documented autism services. Lower recorded rates likely reflect underdiagnosis and reporting constraints.
The “Consensus” That Isn’tThe administration points to a 2021 statement signed by 91 scientists calling for “precautionary action.” But they recommended exactly what doctors have always said: use acetaminophen only when medically indicated, at the lowest effective dose, for the shortest time. The American College of Obstetricians and Gynecologists (ACOG) immediately responded at that time, warning against frightening women away from necessary treatment. Notably, that consensus was not based on any new research findings—it was a reinterpretation of existing observational studies that major medical organizations found unconvincing. ACOG reaffirmed in September 2025 that “acetaminophen remains the analgesic and antipyretic of choice during pregnancy” when used at the lowest effective dose for the shortest duration. Of course, the ‘lowest effective dose’ language isn’t unique to acetaminophen—it’s standard medical and legal boilerplate for virtually all medications during pregnancy. It’s good practice for everyone, pregnant or not, to take only what’s needed.
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We did take note that the Swedish study reports only 7.5% of mothers used acetaminophen versus 50-65% in the U.S. While this might partly reflect measurement issues (the study asked about ‘medications’ generally without specifically prompting about acetaminophen), the sibling analyses still found no increased risk among those identified as users. The stark difference between Swedish and American usage rates—whether real or artifactual—does raise questions about pain management during pregnancy. Are Americans quicker to reach for medication? That’s a conversation worth having about judicious use. But it’s separate from whether acetaminophen causes autism. The Swedish sibling analyses found no increased risk, suggesting the answer to that specific question is clear.
What We Can Actually Say With ConfidenceAfter examining all the evidence: If acetaminophen has any effect on autism risk—and that’s an enormous if—it would be so small we can’t detect it in millions of children. It would be one tiny factor among many in a condition that’s 80-90% heritable, with over 100 genes identified as contributors.
The government’s transformation of these uncertainties into absolute declarations isn’t just bad science—it’s dangerous. Pregnant women will suffer through treatable fevers and pain. Some will experience preventable complications. All based on a certainty that doesn’t exist in the data.
A Message to MothersIf you’re pregnant and scared, or if you’re a mother wondering if that Tylenol you took somehow “caused” your child’s autism: The premise of this entire debate—that autism is something to be prevented or blamed on someone—is fundamentally wrong.
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The best evidence shows no causal link. Can I promise with 100% certainty that acetaminophen never affects neurodevelopment? No scientist can promise that about anything.
Scientists use careful language like “no evidence of harm,” not because we haven’t studied it properly, but because we can’t ethically do the randomized experiments that would prove causation. We must rely on observational data, which is inherently less definitive. And we can’t study every possible combination of dose, timing, genetics, and environmental factors. While we can’t scientifically declare “Tylenol definitely doesn’t cause autism” (proving a negative is nearly impossible), the evidence strongly suggests that for the vast majority of people, acetaminophen use during pregnancy doesn’t meaningfully increase autism risk.
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The desperate search for environmental “causes” of autism distracts from what really matters—ensuring autistic individuals get the support, accommodation, and acceptance they need. Your child’s neurology is not your fault, not a tragedy, and not something that needs to be fixed.
The truth is less dramatic than the president’s announcement: there’s no credible evidence linking acetaminophen to autism. The real harm isn’t in taking necessary medication. It’s in the suffering that will result from transforming uncertainty into false certainty, correlation into causation, and weak associations into federal mandates—leaving pregnant women to endure treatable pain and fever based on a scientific conclusion that doesn’t exist.
Jess Steier is a public health scientist dedicated to bridging the gap between complex scientific evidence and public understanding. Jess is the Founder of Unbiased Science, CEO of Vital Statistics Consulting, and Executive Director of The Science Literacy Lab (a 501c3 non-profit organization), she has built her career on translating complex scientific concepts into accessible language while maintaining unwavering commitment to scientific integrity.
Elana Pearl BenJoseph is a physician with a focus on pediatrics, health communication, and public health. Find Elana on LinkedIn
Izzy Brandstetter Figueroa is an epidemiologist, educator, and statistics consultant for Unbiased Science. Find Izzy on LinkedIn
Paige Boklaschuk is an epidemiology student who loves to go down rabbit holes about reproductive health, nutrition, global health, and exercise science. Find Paige on LinkedIn
A version of this article was originally posted at Unbiased Science and has been reposted here with permission. Any reposting should credit the original author and provide links to both the GLP and the original article. Find Unbiased Science on X @unbiasedscipod
As a biomedical scientist, it has never failed to annoy me that the term ‘organic’ has been co-opted to spread misinformation. Before we get into the topic as it relates to foods (and other consumer products), I just want to emphasize that the term organic in chemistry has a VERY different meaning. And we will talk a lot more about that in the future!Dr. Andrea LoveBut since the EWG is out there yet again circulating their fear-mongering “Dirty Dozen” list, it bears explaining what organic actually means.
The organic foods industry is a $181.5 BILLION dollar industry as of 2022, with an expected annual growth rate of 11.2% year over year. This industry didn’t even exist until 2002, and was borne out of consumer demand and misinformation. For context, it was worth 26.7 billion dollars in 2010. That is a huge amount of growth for a market that has zero science behind it.
Most people have been misled to believe that organic is superior and that’s not your fault. Even the American Academy of Pediatrics has figureheads spouting that lie. Of course people wouldn’t spend more money for something that’s equivalent, so clever messaging is used to insinuate that organic foods are superior. And that is reflected in consumer perception. The number one reason that people opt to purchase organic foods is because they believe that organic foods are healthier, safer, more nutritious, or otherwise superior.
The reality? Organic foods are not superior, just more expensiveThe EWG and other organic activists are deliberately trying to spread misinformation in order to drive people to purchase organic produce, which is on average, around 50% more expensive than conventional counterparts.Organic food is only 5-7% more expensive to produce, so the difference in price is pure profit, and as a result, organic food is almost synonymous with luxury and privilege. Organic farming is at least 22-35% more profitable than conventional agriculture, especially when factoring in the labeling “markup” that is often default: upwards of 30% more on the price tag and hitting your wallet.
All organic means in the United States is that produce (or crops) in question are certified to have been grown on soil that had no prohibited substances applied for three years prior to harvest.
So what counts as prohibited substances? Certain synthetic chemicals. Organic farming also prohibits the use of genetically engineered seeds in cultivation. But organic farming uses PLENTY of pesticides – they just have a specific list that they deem appropriate. (I’ll discuss myths about livestock and animal products in a subsequent post)
Follow the latest news and policy debates on sustainable agriculture, biomedicine, and other ‘disruptive’ innovations. Subscribe to our newsletter.SIGN UPOne of the biggest misconceptions about organic products are that they are pesticide-free. This is falseOrganic farming uses plenty of pesticides and fungicides. A Soil Association survey demonstrated that 95% of organic food consumers said their top reason was to avoid pesticides. Sorry to burst the bubble here, folks.Organic pesticides are merely pesticides that remain chemically unaltered from the chemical state derived from nature. Before you fall into the appeal to nature fallacy trap, remember that the suffix ‘-cide’ means “to kill”. It doesn’t matter whether a pesticide is a natural chemical or a synthetic chemical: they all kill certain things at certain exposures. Remember: the dose makes the poison.
Synthetic pesticides are chemicals that are produced from chemical alteration. But the source of a chemical has zero bearing on its potential harm or safety. and In reality, some naturally procured pesticides are deadlier or carry a higher risk than synthetic options. Remember: plants produce lots of noxious chemicals to deter predators from eating them.
Pesticides and herbicides added to crops reduce exposure to and damage by unwanted insects, bacteria, fungi, and weeds.
If we did not utilize pesticides for agriculture, yields of farm crops would be impacted, cost of food goods would skyrocket, and we would not be able to feed the 8.1 billion people on the planet. Organic farming uses 84% more land for the same yield, but yields are 55% lower by area than conventional.
Just because something is labeled organic or natural does not mean it is safer to the homeowner or unable to cause harm to the environment. Botanically derived pesticides are not always safer; in fact, some can be more dangerous. — Chris Enroth
Organic pesticides are not safer than synthetic ones.
There are over 20 chemicals commonly used in the growing and processing of organic crops that are approved by the US Organic Standards. But the volume of chemicals used in organic farming aren’t recorded or monitored, even though pesticides deemed “organic” are generally less effective, so require larger volumes for similar effectiveness.
According to the National Center for Food and Agricultural Policy, the top two organic fungicides, copper and sulfur, were used at a rate of 4 and 34 pounds per acre in 1971. In contrast, the synthetic fungicides only required a rate of 1.6 lbs per acre, from 2.5X to 20X less than the amount of the organic alternatives. More than that, many of these organic pesticides are more toxic (when looking at LD50 values), especially when used at the higher levels required for adequate control.
LD50 values are a way we can measure toxicity – it refers to the dose of something at which 50% of the test group dies – the 50% lethal dose. Lower LD50 values means something has greater toxicity. Remember: you can’t simply say something is toxic – the dose makes the poison. Toxicity includes dosage, which is often normalized to the size of a given organism too.
Natural pesticides refer to products that are derived strictly from sources in nature with little to no chemical alteration. Synthetic pesticides are products that are produced from chemical alteration. All pesticides are toxic (-cide means to kill) – and the dose makes the poison. In fact, some naturally procured pesticides are deadlier or carry a higher risk than synthetic options. “Just because something is labeled organic or natural does not mean it is safer to the homeowner or unable to cause harm to the environment. Botanically derived pesticides are not always safer; in fact, some can be more dangerous.”
Lots of things in nature are toxic, so let’s cease and desist with the appeal to nature fallacy. Everything is chemicals and the source of a chemical does not dictate its safety. More than that, many have the potential to be more harmful to key pollinator species that we rely on, humans, and other animals.
Examples of organic pesticides include: Nicotine sulfate, Methyl bromide, Copper sulfate, Sodium hypochlorite, Gibberellic acid, Chlorine dioxide, Peracetic acid, Sodium carbonate peroxyhydrate, Lime sulfur, Azadirachtin, Spinosad, Calcium hypochlorite, Veratran D, Lignin sulfonate, Ferric phosphate, Copper oxychloride, Hypochlorous acid, Potassium hypochlorite, Rotenone, and Pyrethrins.
A post shared by @dr.andrealoveNicotine sulfate: Nicotine is natural, and thus approved for organic farming to control aphids, thrips, mites and other insects. It is amusing to have seen so many pro-organic campaigners arguing against the use of neonicotinoids by saying that these synthetic pesticides were using nicotine. Yes BUT so were organic farmers. But how toxic is this natural, organic-approved neurotoxin? Very (LD50: 50-60 mg/kg). In the US, nicotine sulphate carries a Danger warning. It is an organic neurotoxin that interferes with the transmitter substance between nerves and muscles. Tests have shown that nicotine sulphate has caused abnormalities in the offspring of laboratory animals and a New Jersey State study revealed that nicotine sulphate poisoning of organic gardeners can lead to increased blood pressure levels, irregular heart-rate, and, in certain cases, death.Rotenone: occurs naturally in the seeds and stems of several plants, such as the jicama vine plant, and has been used copiously for decades. Touted as being ‘natural’, is extremely toxic at relatively low doses. Was temporarily discontinued as pesticide from 2005 to 2010 in US, but was re-approved in 2010. It is also routinely used as a piscicide in fishery waters.
Pyrethrins are derived from from chrysanthemum flowers. They act as neurotoxins in all organisms, but are particularly neurotoxic to bees and other insects, many of which are key pollinator species. They can also be neurotoxic to mammals (including humans).
Copper sulfate: used as “organic” fungicide. Copper sulfate has significantly higher toxicity than synthetic alternatives. The LD50 (50% lethal dose) of copper sulfate is 300 mg/kg versus the synthetic alternative Mancozeb (4500-11,200 mg/kg) — which means that copper sulfate is at LEAST 15X more toxic, and needs to be used in LARGER quantities compared to synthetic alternatives. Not only is copper sulfate toxic to fish, humans, and other species, but it also persists in groundwater and the environment long-term.
Follow the latest news and policy debates on sustainable agriculture, biomedicine, and other ‘disruptive’ innovations. Subscribe to our newsletter.SIGN UPRegulation and safety monitoring is more stringent for synthetic pesticidesThe U.S. Environmental Protection Agency (U.S. EPA) regulates pesticides, and has a rigorous process that requires the product demonstrate no risk to human health if used correctly. All pesticides must go through a registration process requiring a review of data on the safety of the product which include many pesticides used in organic agriculture. These data are used to construct pesticide labels which anyone who uses them must legally follow.However, most natural pesticides haven’t been tested for their toxic potential, as the Reduced Risk Program of the US Environmental Protection Agency (EPA) applies to synthetic pesticides only. Many natural pesticides have been found to pose potential – or serious – health risks, including those used commonly in organic farming. This is also why the EWG conveniently “omits” all of the organic pesticide residues: because they are not monitored or regulated as stringently.
Safety data for conventional pesticides include:
Evaluating if the product can cause harm to humans and under what circumstances (i.e. is it toxic to humans after inhalation, ingestion, physical contact, etc).
Evaluating dose that can cause harm at both acute and chronic exposures.
Evaluating exposure (timing and frequency) that may cause harm (i.e. how often a produce item is eaten for example would determine exposure).
Evaluating overall risk, combined information about the dose, exposure and conditions under which harm may occur.
The EPA sets tolerance levels of residues for synthetic pesticides on food (I discussed this more in depth in my piece on chlormequat). For some organically-approved pesticides, no tolerance level is set.
Organic foods are not healthier or more nutritiousThere is very little scientific evidence to support any health benefits for organic products. In fact, the growing body of evidence supports the statement that a diet rich in organic products isn’t actually better for you.A 2009 meta-analysis found no nutrient differences between organic and conventional foods. More recent studies came to the same conclusion. While a 2012 study found slightly higher phosphorus levels in organic produce, and a 2014 study found higher antioxidant levels and lower cadmium levels in organic food, the differences weren’t significant, and the levels don’t translate to clinical or health relevance. The 2012 study concluded there was a “[lack of] strong evidence that organic foods are significantly more nutritious than conventional foods.”
In 2012, another meta-analysis analyzed 240 studies: 17 comparing populations consuming organic and conventional diets, and 223 studies that compared either nutrient levels or the bacterial, fungal or pesticide contamination of various products (fruits, vegetables, grains, meats, milk, poultry, and eggs) grown organically and conventionally.
They report little difference in health benefits between organic and conventional foods, as well as no consistent differences in vitamin content of organic products. In fact, only one nutrient (phosphorous) was significantly higher in organic versus conventionally grown produce. Protein and fat content were also similar, and no differences reported (some of which is due to methodological disparities) were clinically relevant.
Trace levels of pesticides found in urine are frequently used as “evidence”, but have no biological relevanceFinding micro-trace levels of any chemical in urine is meaningless in and of itself. More than 3,000 chemicals can be detected in human urine; almost none poses any harm. Trace chemicals in urine are the residue of the kidneys doing its filtering job. EWG routinely assesses ‘urine levels’ of chemicals, either because they do not understand basic chemistry, or they are deliberately exploiting the widespread misunderstanding people have about how chemicals are processed by our bodies in order to spread fear.A study claimed that people who switched to organic foods primarily had a decrease in urine output of pesticides: but they only looked at pesticides used in conventional farming, not organic pesticides. Of course it stands to reason you’re not going to detect things you’re not testing for! Another study making claims about glyphosate in urine, that the median glyphosate levels in organic food consumers and individuals with known exposure are essentially identical (390 vs 400 parts per trillion, respectively).
Organic farming is not better for ecology and wildlifeWhile organic farming is perceived as more environmentally friendly, the data don’t support the claim that organic farming reduces environmental impact.Organic pesticides are not better for biodiversity.
Some organic pesticides actually have worse ecological impact than conventional ones. Also, organic farming prohibits GE crops which can actually reduce the amount of pesticides needed for effective pest control. Because organic pesticides are not permitted to be altered to improve specificity or biodegradability, many organic pesticides are less effective, can bioaccumulate more, and have worse ecological impact by killing non-target species, including beneficial insects and soil microorganisms, many of which can be natural predators of the target pest in question.For example, organic pesticides used for aphids can kill multicolored Asian lady beetles and insidious flower bugs, both of which are natural predators of aphids. Many require much higher concentrations to be applied to have similar impacts as conventional pesticides. In addition, because organic farming prohibits GE crops, pesticides need to be applied where in conventional farming, a crop could be naturally resistant to a pest. A GM blight-resistant potato grown conventionally would not need fungicides like copper sulfate applied in order to control blight in organic farming.
Organic food has a larger impact on climate because of the greater area of land required to farm itOrganic farming requires more land use for equivalent yield
On average, organic farming uses 84% more land for similar yield. Organic agriculture yields lower crop productivity due to poorer nutrient availability and less effective weed and pest control. Organic produce generates higher nitrogen leaching, nitrous oxide emissions, ammonia emissions and has more acidification potential per unit of product. Nowadays, organic agriculture is now done mostly by big corporations instead of local producers, so combining lower yields with intensive machinery use means that overall, in terms of emissions and pollution, organic agriculture is usually worse than conventional for the environment.
Since you need more land for similar yield, you have higher rates of habitat and land conversion. This means that in order to meet food demand, you have higher rates of local and global deforestation, encroachment on marginal lands or sensitive habitats, which can further harm wildlife and ecology. Organic farms may actually accelerate habitat loss, deforestation, and biodiversity decline.
Organic farming results in higher greenhouse gas emissions per unit of output
Organic practices rely heavily on organic amendments, such as compost and manure, which release methane and nitrous oxide—a potent greenhouse gas—during decomposition. Organic farming may necessitate more frequent soil tillage, contributing to soil carbon loss and exacerbating climate change. That’s especially the case when comparing to GE conventional crops, which often don’t require tilling and can minimize soil runoff and nutrient retention.A meta-analysis inclusive of 71 peer-reviewed studies demonstrated that organic products are worse for the environment. Organic milk, cereals, and pork generated higher greenhouse gas emissions per product than conventional counterparts. A 2018 Nature study confirmed that organic farming leads to higher emissions than conventional farming. This study found that organic peas resulted in a 50% increase in climate impact due to lower yields. To produce the same amount of organic food, you therefore need a much bigger area of land. The greater land-use in organic farming leads indirectly to higher carbon dioxide emissions, thanks to deforestation.Organic farming generally consumes more water per unit of yield compared to conventional agriculture
Organic practices rely on natural irrigation methods, such as rainwater harvesting and drip irrigation, which may be less efficient than conventional irrigation systems. Moreover, organic farms often require more intensive manual labor for weed control and crop management, leading to higher water demand for irrigation.
Demonizing affordable and nutritious conventional produce is harmfulThe false dichotomy between conventional and organic isn’t just misleading, it’s dangerous. Our constant attention on natural versus synthetic only causes fear and distrust, when in actuality, our food has never been safer.Eating fewer fruits and vegetables due to fear of pesticides or the high price of organic food does far more harm to our health. Conventional produce has the same nutritional content and is as safe to consume as ‘organic’ produce. Most of Americans already don’t eat enough fruits and vegetables, and produce contains important nutrients, fiber, and other substances that are extremely important to our health.
From a scientific point of view, organic foods are not superior. If you want to spend more money on them, go for it. But don’t buy organic because you think it’s better for you or for the planet, because it’s not.
Dr. Andrea Love has a PhD in Immunology and Microbiology. Andrea is a subject-matter expert in infectious disease immunology, cancer immunology, and autoimmunity and is adept at translating complex scientific data and topics for the public and healthcare providers. Follow Andrea on X @dr_andrealove
A version of this article was originally posted at Immunologic and has been reposted here with permission. Any reposting should credit the original author and provide links to both the GLP and the original article.
The adage “Follow the science” when formulating public policy has much to recommend it, but it’s not as straightforward as it sounds. Let us explain.Astrophysicist and science writer Ethan Siegel recently wrote, “Science is a way of thinking about the world, the process of inquiry and investigation, and also the full suite of relevant knowledge that we know, collectively, about an enterprise.” It is based on “the scientific method,” a rigorous process that reveals new information, or knowledge, that enables us to know what we know.
But simply saying that scientific knowledge, not science itself, should guide policy is insufficient. An essential ingredient is missing: value judgments. Knowledge created by science tells us, with ever-increasing accuracy, what the world >is, but it does not tell us what the world >ought to be. This gap between “is” and “ought,” which cannot be filled by logic or reason, was articulated by Scottish philosopher David Hume. It can only be filled by value judgments, be they moral, religious, or political.
Value judgments are needed because of tradeoffs. Decisions can be informed by scientific knowledge, but they are not dispositive because differing values can lead to different decisions based on the same accepted body of scientific knowledge. Consider, for example, California’s High-Speed Rail Project, which would link San Francisco and Los Angeles. Although it is technically achievable, whether the cost is worthwhile is a value judgment, and it has changed over the years. As of March 2023, according to a California High Speed Rail Authority project update report, the price tag for the system had risen to $128 billion. That’s a nearly 22 percent increase from last year’s estimate of $105 billion and a far cry from the $33 billion voters approved in 2008. That massive outlay inevitably diverts government resources from other projects—and from taxpayers’ pockets—and what is cost-effective and societally advantageous is a matter of value judgment.
Follow the latest news and policy debates on sustainable agriculture, biomedicine, and other ‘disruptive’ innovations. Subscribe to our newsletter.SIGN UPGenetic engineering The interplay of scientific knowledge and value judgments also applies to opinions about innovative technologies, from nuclear power and fracking to genetic engineering. Let us focus on the last of these, a particular interest of ours.
When it comes to certain activists’ decades-long objections to societally important advances in “genetic engineering,” or “genetic modification,” we would argue that they have been wrong on both the science and the value judgments.
First, the science. Genetic modification refers to a continuum of techniques that have been used over millennia. These include hybridization, mutagenesis, somaclonal variation, wide-cross hybridization (movement of genes across “natural breeding barriers”), recombinant DNA, and, most recently, gene-editing. The primary distinction between the last two and the others is that they are far more precise and predictable than the earlier techniques, which often introduced off-target mutations. And yet, some organizations such as Greenpeace and Friends of the Earth have singled out the newer, more precise, more predictable techniques for sui generis, excessive regulation that has boosted research and development costs and delayed or prevented important advances.
Credit: Wikimedia Commons (CC BY-SA 2.0)Because of the continuum alluded to above, and the fact that the newer techniques are more precise and predictable, science is against the activists and so, we would argue, are the value judgments. Activists have teamed up with companies that sell organic and “natural” food products to denigrate crops crafted with molecular techniques, which they have dubbed “Frankenfoods.” This anti-genetic-engineering industry and its lobbyists contribute significantly to the public apprehension toward this technology. They then exploit that fear to sell alternative food products to consumers.
Now, this same industry is lobbying globally for stringent regulation of plants and animals that have been modified with state-of-the-art gene editing techniques such as CRISPR–Cas9. One prominent genetic engineering skeptic, North Carolina State University professor Jennifer Kuzma, said about gene editing, “We need a mandatory regulatory process: not just for scientific reasons, but for consumer and public confidence.” The latter claim, especially, is a fallacy: Thirty years of excessive regulation of genetic engineering has neither reduced public anxiety nor quieted the critics. If anything, these gratuitous regulations have fanned public concerns about this safe, superior technology. As Barbara Keating-Edh, representing the consumer group Consumer Alert, testified before the U.S. National Biotechnology Policy Board three decades ago:
For obvious reasons, the consumer views the technologies that are >most regulated to be the >least safe ones. Heavy involvement by government, no matter how well intended, inevitably sends the wrong signals. Rather than ensuring confidence, it raises suspicion and doubt.
Precautionary PrincipleDecades of large-scale use—millions of acres cultivated and trillions of meals consumed without a single mishap—undermine activists’ concerns. However, there remains one particularly resistant formulation of risk analysis that rejects evidence-based considerations of overall benefit and harm. That is the “Precautionary Principle,” which posits that regulatory action should be taken to avoid risks even when there is incomplete scientific evidence as to their magnitude or potential effects. Advocates of the Precautionary Principle portray it as a neutral tool for assessing risks. But it oversimplifies the complex processes of risk analysis and risk management, allowing regulators to assume that new technologies have infinite risks but uncertain benefits. A new technology is thus assumed to be guilty until it can be proven innocent to a safety standard dictated by its antagonists—a practical impossibility. (See “The Paralyzing Principle,” Winter 2002.)
The Precautionary Principle has now been incorporated into legislation in the European Union and elsewhere.
As a tool of public policy, the primary shortcoming of the Precautionary Principle is that it incorporates neither coherent evidentiary standards nor any clear limits. It stipulates that hypothetical risks should take precedence over substantive demonstrated benefits and effectively frees regulators to arbitrarily require any amount and kind of testing they wish. Likewise, it permits them to ignore overwhelming evidence of a product’s (or a technology’s) safety and benefits, and to prevent or delay its use. It functions independently of “what the science says” and penalizes innovation. It ensures that wherever it is applied, progress—especially in agriculture—will be stunted for the foreseeable future.
The Precautionary Principle is especially perverse when it is applied to the genetic engineering of plants and animals because, without any scientific basis, it discriminates against the use of the newest, most precise, and most predictable techniques by subjecting them to the most intense, stultifying regulation. The negative societal effects of such policies are discussed eloquently in a recent >Nature Plants article by Daniel Jenkins et al.:
Regulation based on process will not advance common goals of nutrition, sustainability or consumer preference. On the contrary, process-based regulation will only delay or prevent the achievement of these goals. Differential requirements lead to a confusing system with higher burdens, lower utility and increased time to market. This only creates disincentive to fund research and business investment, and ultimately throws up barriers to reaching consumers and improving diets for even the simplest and most-familiar of characteristics. When science cannot distinguish one seedless grape from another, neither should regulation.
The Precautionary Principle is not the only tool of anti-genetic-engineering activists, who also invoke opposition to certain new products based on resentment of corporate entities’ profits or on the fact that most agricultural innovation comes from industrialized countries and therefore somehow represents “colonialism” when transferred to developing countries. Such factors obviously should have no bearing on regulation to assure safety and efficacy.
If we are to realize the potential of the newest techniques of genetic engineering, we need to fend off the sophistry and mendacity of anti-innovation activists, both within and outside governments. Public policy, including regulation, should be dictated by science and common sense.
David Bertioli studies peanut genetics, genomics and evolution. He works with breeding programs in the USA, Brazil, Senegal and Uganda to produce improved peanut cultivars with pest and disease resistance derived from wild peanut species. Find David on X @BotanyBert
Henry I. Miller, a physician and molecular biologist, is the Glenn Swogger Distinguished Fellow at the American Council on Science and Health. He was the founding director of the Office of Biotechnology at the FDA. Find Henry on X at @henryimiller
A version of this article ran on the GLP site on Novembere 27, 2023.