A debate has emerged as to why humans mate in private while every other animal – except the Arabian babbler – is willing to do it out in the open. In a paper published in the journal Proceedings of the Royal Society B, Zürich University anthropologist Yitzchak Ben Mocha suggests it’s about the evolution of privacy. Wesley J. Smith writing for the National Review posits it’s what makes us human—not instinct but morality. Here are excerpts from the two perspectives…the first by Bob Yirka of Phys.og representing Mocha.
Ben Mocha retrieved data from 4,572 accounts of cultural studies—ethnographies—and studied them looking for what he describes as normal sexual practices… He found that virtually every known culture practices private mating—even in places where privacy is difficult to find. He also looked for examples of other animals mating in private, and found none, except for the babblers. He also found that there were no explanations for it, and in fact, there were very few other people wondering why humans have such a proclivity. And, not surprisingly, he was unable to find any evolutionary theories on the topic.
Ben Mocha concludes his paper by introducing a theory of his own—he believes that the reason humans (and babblers) began looking for privacy during sex was because the male wanted to prevent other males from seeing his female partner in a state of arousal. Such a state, he suggests, would likely have encouraged other males to attempt to mate with her. Thus, privacy, or perhaps more accurately, seclusion, allowed the male to maintain control over a sexual partner—while also allowing for continued cooperation within a group. He further suggests that the study of the evolution of private mating could lead to a better understanding of how thinking skills in humans matured as they learned to function in groups.
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This approaches the question from the wrong angle. There is much more to human life than biology. We are not just a collection of carbon molecules and the sum of our genes expressing. We are more than intelligent apes. There is a deeper side to us, something that can neither be measured nor fully explained from exclusively materialistic analyses…
Sex is profoundly consequential morally. We are not just animals yielding to an irresistible biological imperative when the female goes into estrus. For us, intimacy isn’t — or ideally, shouldn’t be — mere rutting. Moreover, sex is something we can choose to refuse based on moral considerations. Animals do not have that ability.
Indeed, sexual morality is one of the most important factors in creating culture. That is the reason those who wish to destroy existing paradigms subvert cultural status quos through transgressive sexual advocacy and/or behavior.
Bottom line: Evolution doesn’t explain everything in human nature or the development of culture. It can’t. We have stepped beyond subjugation to the immutable forces of natural selection. We are self-directing, and that includes our approaches to sex.
Abandon human exceptionalism in anthropology, treat us as if we are just another animal in the forest, and the discipline misses the forest for the trees.
In the wake of a highly publicized legal settlement between Bayer, owner of former glyphosate-maker Monsanto, and lawyers representing plaintiffs alleging their cancer was caused by the popular herbicide, the Environmental Working Group (EWG) announced on July 14 that chickpeas and hummus contain “high levels” of glyphosate:
The health-food staple hummus and the chickpeas it is made from can be contaminated with high levels of glyphosate, a weedkilling chemical linked to cancer, according to independent laboratory tests commissioned by EWG.
Like EWG’s earlier claims about glyphosate in breakfast cereals and its annual “Dirty Dozen” list, these safety thresholds for humus are entirely fabricated. And the reported results were not published in a peer-reviewed journal or other scholarly forum, meaning no independent experts were allowed to verify EWG’s analysis.
Credit: EWG
The amounts of glyphosate detected in almost all the sampled items were far below the US Environmental Protection Agency’s (EPA) pesticide tolerances, but the activist group tried to sidestep this criticism, deeming the EPA’s limits “too permissive”:
Of the 43 conventional, or non-organic, chickpea and chickpea-based samples tested, more than 90 percent had detectable levels of glyphosate. Over one-third of the 33 conventional hummus samples exceeded EWG’s health-based benchmark for daily consumption, based on a 60-gram serving of hummus (about four tablespoons). One sample of hummus had nearly 15 times as much glyphosate as EWG’s benchmark, and one of two tests from a sample of conventional dry chickpeas exceeded even the Environmental Protection Agency’s too-permissive legal standard.
EWG also tested 12 organic hummus and six organic chickpea samples. Most of these also contained levels of glyphosate, but at much lower levels than conventional products.
What are these levels?
EWG, thanks to mass spectrometry work by Anresco, an analytical chemistry lab in San Francisco, reported glyphosate levels from “2,379 parts per billion,” down to 6 ppb for conventional hummus, and 13,982 ppb, down to 2 ppb for organic and conventional chickpeas.
While Anresco’s techniques are indeed capable to measuring down to those levels, no regulatory body or scientific study has detected any harm from glyphosate in such minute quantities. It’s also important to note that while “2,379 ppb” or “13, 982 ppb” may sound scary, it’s only 2.4 and 13.98 when expressed in parts per million. That’s important because EPA and other hazard levels are set in parts per million, not in parts per billion.
One part per billion of a trace residue amounts to a drop in a lake or about one second every 32 years.
The EPA sets tolerances for glyphosate use on a host of plants (and some farm animal products) that vary according to product. These range from 0.1 ppm to 300 ppm, depending. EPA tolerances for glyphosate in legumes, lentils and chickpeas before the plant erupts are 5.0 ppm. That means one or two of EWG’s readings would be of concern to the EPA, but most of the readings were well below safe tolerance settings.
For chickpeas, glyphosate is used as a “pre-emergent” herbicide. It is sprayed before the plant sprouts. This prevents the plant itself from being killed by the herbicide, and prevents weed growth that chickpeas are particularly susceptible to.
In fact, when the EPA studied glyphosate for toxicity in animals (it’s not ethical to do this in humans), they found harm at levels starting at 1,000 parts per million, 100 times its own tolerance level, and one million times the “safe” level espoused by EWG. According to the EPA:
Numerous studies are available that evaluated chronic exposure to glyphosate in rats, mice, and dogs. In most instances, effects were only seen at or near the limit dose (1000 mg/kg/day). Developmental effects in rats were only observed at a dose exceeding the limit dose (3500 mg/kg/day) and there were no developmental effects observed in rabbits. Route-specific studies are available that evaluated dermal and inhalation exposures. Dermal irritation effects were only seen at a dose exceeding the limit dose (5000 mg/kg/day), which is well above exposures expected from glyphosate use and not relevant for human health risk assessment.
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As for glyphosate’s cancer hazard, EWG cited only one source: the International Agency for Research on Cancer (IARC), a sub-agency of the World Health Organization (WHO). The activist group also claimed that California identifies glyphosate as a carcinogen under Proposition 65, but the state says it does so only because IARC does. Additionally, a federal judge ruled in June that California could not force glyphosate manufacturers to place a cancer warning on their products, because
It is inherently misleading for a warning to state that a chemical is known to the state of California to cause cancer based on the finding of one organization [International Agency for Research on Cancer (IARC)] . . . when apparently all other regulatory and governmental bodies have found the opposite.
Indeed dozens of health and environment agencies—including WHO (separately from IARC), the European Food Safety Authority, the EPA, European Chemicals Agency, and Germany’s Federal Risk Assessment Institute—have found no harm from the chemical. Only IARC claimed that glyphosate poses a “probable” hazard (which isn’t the same as an exposure risk).
Credit: Reid Middleton
These safety evaluations of the weedkiller are based on a large body of peer-reviewed research, which is typically overlooked by anti-pesticide groups that rely on IARC. The EPA states, for instance, that its risk assessment of glyphosate was more rigorous than IARC’s hazard-based analysis.
EPA considered a significantly more extensive and relevant dataset than the International Agency on the Research for Cancer (IARC). EPA’s database includes studies submitted to support registration of glyphosate and studies EPA identified in the open literature. For instance, IARC only considered eight animal carcinogenicity studies while EPA used 15 acceptable carcinogenicity studies. EPA does not agree with IARC’s conclusion that glyphosate is “probably carcinogenic to humans.”
As in its “killer Cheerios” study, EWG misrepresented IARC’s conclusions on the possible harm caused by consumer exposure to minuscule amounts of glyphosate. In its monograph, IARC specifically reported that the herbicide posed a hazard to farm workers who were chronically exposed, but not to consumers. Of course, a 2017 study of more than 50,000 agricultural workers found no association “between glyphosate and any solid tumors or lymphoid malignancies overall,” thus superseding IARC’s hazard finding.
Quoting dietitian Stefani Sassos, Good Housekeeping appropriately summed up the situation, noting that hummus and chickpeas are safe to eat considering how little glyphosate consumers are actually exposed to.
‘EWG’s prescribed threshold for having ‘too much’ of the agent is very limited… Their limit is practically zero, at 0.01 milligrams per day, so their results shouldn’t be too shocking’ …. Any pull that eating hummus has on your cancer risk is far overshadowed by other lifestyle choices, [Sassos] says, like eating processed meat, drinking alcohol, smoking, or other lifestyle factors. ‘One food component isn’t going to cause or cure cancer.’
Andrew Porterfield is a Contributing Correspondent to the Genetic Literacy Project. He is a writer and editor, and has worked with numerous academic institutions, companies and non-profits in the life sciences. BIO. Follow him on Twitter @AMPorterfield
With the world COVID-19 pandemic in its sixth month, food activists are back to trumpeting locally grown, and even home grown, as a viable option for mass food production, but for most of the world how realistic is that? It’s fine if Michael Pollan claims it is from his walled Berkeley back yard, but even most New York Times subscribers can’t afford that.
To make it suitably ironic, environmentalists who have spent decades and $40 billion on campaigns saying single-family homes in suburbia are a blight on nature and we should all live in urban apartments are now claiming we should be growing vegetables and trading them with each other to create a more sustainable future.
Former Flinders University nutritionist Professor Kaye Mehta, for example, advocates community gardening, home gardening, and also resulting food swap groups as ways to reduce plastic packaging and, of course, meat eating, but commercial agriculture would never have come into existence if growing food at home were equally viable for all. Australia is a world leader in science approaches to agriculture, and in a ‘land of plenty’ it is easy to forget how bad it once was, and perhaps even believe The Ancients knew what they were doing instead of having no choice.
Credit: Shutterstock
But Utopia is a mythical place, and idylls to nomadic life are not written by actual shepherds. Most of Africa wants science, and they want Europe to stop penalizing competition by poor countries who use science. They don’t want idylls from industrialized nation residents saying how lucky they are to not have centralized energy and clean water or enough food to sell it in packages.
Activists have an answer for those farmers that don’t want Western idylls. If you don’t embrace their ways, you lack “literacy” about food systems. And their ‘scientific’ conclusion that this was valid came from teaching a course to people already in their tribe; actual staff and students at the same university who unsurprisingly, after taking a two week course they got paid to attend, agreed that fairness and sustainability are important and that farmers need to get with the program.
Such “literacy” framing is insulting. It is western academics and staff and students insisting that developing world farmers are literally illiterate about farming if they don’t do what white people in rich countries tell them to do.
I grew up on a subsistence farm, before organic farming was cool, and I have to tell you from the experience of someone who lived it rather than wrote about it, it is a lot of work and you are likely to be poor. Farming is always a campaign issue in America—former US Vice-President Al Gore even lauded ethanol as a viable approach to greenhouse gas reduction to get Iowa votes in the 2000 election—and it was again an issue in 2016. But that last time it was about estate taxes, even though only 153 farms out of 38,328 farm estates paid them. Instead of there being “factory” farms, as organic industry trade groups and sympathetic allies in journalism claim, 2.1 million farms make just $10,000 a year or less—as my family did. Maybe enough to cover their real estate taxes, which means they are also working outside jobs.
Farming is not an issue in the US election this year because there is a much bigger concern; 50 million unemployed Americans and concern about a second wave of COVID-19 deaths. Activists who would ordinarily be off in the minutiae weeds arguing for their candidates by manufacturing concern about invisible pollution (PM2.5 in epidemiology), quasi-homeopathic effects (endocrine disruption in rats) or other things where only more big government can supposedly save us are instead scrambling for relevance in a culture that suddenly wants Clorox, Lysol, and Purell. And that wants government to get out of the way of scientists racing to create a vaccine.
During all this the one thing no one is worried about is food.
Yet instead of praising how agricultural science has saved us during this pandemic, Mehta and others want the world to get back to thinking about food in terms of ill-defined environmental populism rhetoric like “sustainability” and “fairness”, without recognizing it is not environmentally sustainable to have a wave of new amateurs spraying pesticides they bought on Amazon in their vegetable gardens, and it is not fair that people who are not wealthy elites and lack a large backyard and money for equipment should starve.
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COVID-19 has made it cool to embrace science again. The same elites who once opposed vaccines now want them. And that includes Whole Foods shoppers, who on surveys share common cause with food “fairness” rhetoric but in reality stockpiled regular old non-recycled toilet paper.
Instead of it being environmentally responsible to go back to old, inefficient ways, the evidence is on the side of progress. Since GMOs became commercialized, for example, the emissions savings have been equal to removing 15,000,000 cars from the road. All while keeping food affordable. Even solar panels, another idyll of rich elites that leaves out the poor, don’t come close to that.
We can thank science for getting us through this so far, just like science will get us to the other side. All while being environmentally terrific in ways that academics with no experience in farming just can’t understand.
Hank Campbell is the founder of Science 2.0 and co-author of the book Science Left Behind. Follow him on Twitter @HankCampbell
This article originally ran at Science 2.0 and has been republished here with permission. Science 2.0 can be found on Twitter @science2_0
The fate of society rests in part on how humans navigate their complicated relationship with insects – trying to save “good” insects and control “bad” ones. Some insects, like mosquitoes, bite people and make them sick – remember Zika? Now the U.S. mosquito season is already in full swing, with over 10 cases of Dengue fever reported in the Florida Keys this year. Some insects, like bees, are pollinators that help produce our food. Others, like locusts, currently threaten cropsin East Africa and Asia, preferring to eat our food instead.
Insects have proven themselves extremely capable at evolving strategies to get around control methods, such as chemical insecticides and habitat modification, and current pest control technologies are simply not keeping up.
Moratoriums on gene drive technology have been called for and rejected at the last two United Nations Conventions on Biological Diversity. But there is a new push for a moratorium.
What is a gene drive?
Gene drive is a technology that could allow society to control insects in a more targeted manner.
The general underlying principle of all gene drives is an organism that will produce offspring similar to themselves.
Some characteristics are randomly passed on from parents to the next generation. However, gene drive forces a different type of inheritance that ensures a specific characteristic is always present in the next generation. Scientists engineer gene drive using various molecular tools.
In insects with a gene drive, a trait is passed to almost all progeny. Credit: Entomological Society of America
Gene drive is not just a human invention; some occur naturally in insects. For example, in stalk-eyed flies, a gene on a sex-related chromosome causes any male fly to die without a certain gene “cargo,” including a gene that results in longer eyestalks. This type of genetic phenomenon has been well studied by scientists.
To date, gene drive has been discussed in the media primarily in order to eradicate malaria. This may give you the impression that gene drive can be used only to drive mosquitoes to extinction. However, gene drive technologies are highly versatile and can be designed to bring about different outcomes. They can also be applied in most insect species that scientists can study in the laboratory.
Why insects?
Insects reproduce quickly and produce lots of offspring, which makes them obvious candidates for a technology that relies on inheritance like gene drive. This is why insects are at the leading edge of gene drive research. Gene drive is a new technology that could provide a solution to a variety of insect issues society faces today.
Gene drive could also be a more targeted approach to stopping invasive insects, such as the infamous fire ant, from destroying native ecosystems. In the United States, millions of dollars have been spent on removing fire ants using techniques including chemical insecticides, but if these persistent ants are not completely eradicated, they invade again.
Aside from how good insects are at circumventing our strategies to control them, another major struggle for controlling insects is finding them. Insects have evolved to quickly find the opposite sex to mate, and gene drives, which are passed on by mating, can take advantage of this fact of insect life. This also means this technology targets only the intended species, which is not the case for chemical insecticides currently in use.
The first gene drive in insects were developed by nature: for example, in stalk-eyed flies. Credit: Gbohne/WikimediaCommons
Insect scientists, inspired by natural examples of gene drive, have wanted to design gene drive in insects for decades. Only recently have new molecular tools, such as the gene editing tool CRISPR-Cas, made the gene drive dream a reality. For now, gene drive insects live in laboratories and none has been released into the wild. Still, a lot can be learned about how gene drive works while it is safely contained in a laboratory.
Criticisms of gene drive
Using gene drive is not a universally popular idea. Criticisms tend to fall into three categories: ethical concerns, mistrust of technology and unintended ecological consequences.
Ethical concerns about gene drive are often motivated by larger issues, such as how to stop gene drive from being used in biological weapons by engineering insects that are more dangerous. Then there is the question of who should decide which gene drive projects move forward and what types of insects with gene drive can be released into the environment. These questions can’t be answered by scientists alone.
Societal mistrust of technology is a hurdle that some powerful, innovative technologies must overcome for public acceptance. The issue of technological mistrust often stems from disagreements about who should be developing technology to control insects and for what purposes.
The third common argument against gene drive technologies is that they might cause unintended consequences in the ecosystem because gene drive is designed by humans and unnatural. What will happen to the natural ecosystem if a population, even of mosquitoes that make people sick, is driven to extinction? Will this cause threats to natural biodiversity and the security of food? These questions are ultimately asking the consequences of intervening in the natural order of the world. But who defines what is the natural state of an ecosystem? Ecosystems are already constantly in flux.
Preparing for a future that may include gene drive insects
When a gene drive is developed, it is tailored to the needs of a particular situation. This means the anticipated risks posed by each gene drive are project-specific and should be considered and regulated on a case-by-case basis. A responsible way to protect society from these risks is to advocate for continued research that enables scientists to describe and find solutions to them. Beyond the science, regulatory and accountability systems are needed so that regulations are adhered to and public safety is protected.
Researchers are also still exploring the science underlying the gene drive. Can gene drive be designed to be reversible or more efficient? Can the effect of a gene drive on an ecosystem be predicted? Such important unanswered questions are why even the most ardent supporters of this technology say more research is needed. Society needs new tools to control insect pests and protect ecosystems, and gene drive promises to augment our toolbox.
Isobel Ronai is an Endeavour Postdoctoral Research Fellow at Columbia University. Follow her on Twitter @IsobelRonai
Brian Lovett is a postdoctoral researcher at the Division of Plant and Soil Sciences at West Virginia University working on fungal biology and biotechnology. Follow him on Twitter @lovettbr
This article was originally published at the Conversation and has been republished here with permission. Follow the Conversation on Twitter @ConversationUS
The latest statistics, as of July 10, show COVID-19-related deaths in U.S. are just under 1,000 per day nationally, which is down from a peak average of about 2,000 deaths per day in April. However, cases are once again rising very substantially, which is worrisome as it may indicate that substantial increases in COVID-19 deaths could follow. How do these numbers compare to deaths of other causes? Ron Fricker, statistician and disease surveillance expert from Virginia Tech, explains how to understand the magnitude of deaths from COVID-19.
As a disease surveillance expert, what are some of the tools you have to understand the deaths caused by a disease?
Disease surveillance is the process by which we try to understand the incidence and prevalence of diseases across the country, often with the particular goal of looking for increases in disease incidence. The challenge is separating signal from noise, by which I mean trying to discern an increase in disease incidence (the signal) from the day-to-day fluctuations in that disease (the noise). The hope is to identify any increase as quickly as possible so that medical and public health professionals can intervene and try to mitigate the disease’s effects on the population.
A critical tool in this effort is data. Often disease data is collected and aggregated by local and state public health departments and the Centers for Disease Control and Prevention from data that is reported by doctors and medical facilities. Surveillance systems then use this data and a variety of algorithms to attempt to find a signal amidst the noise.
Early on, many people pointed out that the flu has tens of thousands of deaths a year, and so COVID-19 didn’t seem so bad. What’s wrong with that comparison?
The CDC estimates the average number of flu-related deaths since 2010-11 is around 36,000 per year. This varies from a low of 12,000 deaths in 2011-12 to a high of 61,000 deaths in 2017-18. Thus, the number of COVID-19 deaths to date is three to four times greater than the annual average number of flu-related deaths over the past decade; it is 10 times larger when compared to the 2010-11 flu season but only about twice as large compared to 2017-18.
To make this a fair comparison, note that seasonal influenza mostly occurs over a few months, usually in late fall or early winter. So, the time periods are roughly comparable, with most of the COVID-19-related deaths occurring since late March. However, COVID-19 does not appear to be seasonal, and fatalities are a lagging measure because the time from infection to death is weeks if not months in duration, so the multiples in the previous paragraph will be greater by the end of the year.
Furthermore, while death rates have been coming down from a peak of more than 2,700 on April 21, 2020, the United States is now averaging just under 1,000 deaths per day as of July 10, and given the dramatic increase in cases of late, we should expect the fatality rate to further rise. For example, the University of Washington’s IHME model currently predicts slightly more than 208,000 COVID-19-related deaths by November 1.
So, by any comparison, the COVID-19 death rate is significantly higher than the seasonal influenza death rate.
What are some comparisons that could provide some context in understanding the scale of deaths caused by COVID-19?
As of this writing, more than 130,000 people have died of COVID-19, and that total could grow to 200,000 or more by fall. Those numbers are so big, they’re hard to grasp.
Michigan Stadium in Ann Arbor is the largest football stadium in the United States. It holds 107,420 people, so no football stadium in the country is large enough to hold everyone who has died from COVID-19 thus far. By the time bowl season comes along, assuming we have a football season this year, the number of COVID-19 fatalities will likely exceed the capacity of the Rose and Cotton bowl stadiums combined.
The state of Wyoming has a population of slightly less than 600,000 people, so it’s the equivalent of one out of every five people in that state dying in the last four months. By this fall, the COVID-19 death total will be the equivalent of fully one-third of the people in Wyoming dying.
The populations of Grand Rapids, Michigan; Huntsville, Alabama; and Salt Lake City, Utah are each just over 200,000 people. Imagine if everyone in one of those cities died over the course of six months. That’s what COVID-19 may look like by fall.
How do COVID-19 deaths compare to chronic diseases like cancer or heart disease?
Today, COVID-19 ranks as the sixth leading cause of death in the United States, following heart disease, cancer, accidents, lower chronic respiratory diseases and stroke. Heart disease is the leading cause, with just over 647,000 Americans dying from it each year. Alzheimer’s disease, formerly the sixth largest cause of death, kills just over 121,000 people per year. If the University of Washington IHME model’s current prediction of COVID-19-related deaths comes to pass, COVID-19 will be the third leading cause of death in the United States by the end of the year.
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The American Cancer Society estimates that in 2020 there will be an estimated 1.8 million new cancer cases diagnosed and 606,520 cancer deaths in the United States. Lung cancer is estimated to kill about 135,000 people in the US in 2020, so the number of COVID-19 deaths is currently equivalent and will exceed it soon. Of course, it is important to note that the COVID-19 deaths have occurred in about the past four months while the number of lung cancer deaths is for a year. So, COVID-19 deaths are occurring at roughly three times the rate of lung cancer deaths.
What are some historical comparisons that you think are useful in understanding the scale of deaths from COVID-19?
The 1918 influenza pandemic was similar in some ways to the current pandemic and different in other ways. One key difference is the age distribution of deaths, where COVID-19 is concentrated among older adults while the the 1918 pandemic affected all ages. In my state of Virginia, only 8% of the people who died in the 1918 pandemic were more than 50 years old, compared to more than 97% for COVID-19.
The CDC estimates that the 1918 pandemic resulted in about 675,000 deaths in the United States, so slightly more than five times the current number of COVID-19 deaths. In October of 1918, the worst month for the influenza pandemic, about 195,000 people died – well more than all who have died so far from COVID-19.
As with any historical comparison, there are important qualifiers. In this case, the influenza pandemic started in early 1918 and continued well into 1919, whereas COVID-19 deaths are for about one-third of a year (March through June). However, today the United States’ population is about three times the size of the population in 1918. These two factors roughly “cancel out,” and so it is reasonable to think about the 1918 epidemic being about five times worse than COVID-19, at least thus far.
In comparison to past wars, the U.S. has now had more deaths from COVID-19 than all the combat-related deaths in all the wars since the Korean War, including the Vietnam War and Operations Desert Shield and Desert Storm. In World War II there were 291,557 combat casualties. So the number of people who have died from COVID-19 thus far is about 45% of the WWII combat casualties. By the fall, it could be more than 70%.
Finally, note that the number of confirmed and probable deaths from COVID-19 in New York City (23,247 on July 10, 2020) is more than eight times the number who died in the 9/11 attack (2,753).
Ronald D. Fricker, Jr. is a Professor of Statistics and an Associate Dean in the Virginia Tech College of Science. Dr. Fricker’s research is focused on studying the performance of various statistical methods for use in disease surveillance and statistical process control methodologies. Find him on Twitter @RonFricker
This article was originally published on July 23, 2020.
A version of this article was originally published at the Conversation and has been republished here with permission. The Conversation can be found on Twitter @ConversationUS
Cancer treatments have always been linked to a specific part of the body — these drugs for breast cancer, and those for lung cancer. Or at least they used to be.
The situation changed in May 2017, when the US Food and Drug Administration issued its first approval for a cancer drug that’s “site-agnostic.” The drug, Keytruda, had previously been approved for advanced melanoma and a few other cancers. But the new approval was remarkable because it meant that anyone with a specific genetic biomarker — no matter the initial cancer site — may use the drug.
Making treatment decisions based on a tumor’s genetic variations signifies a landmark shift in thinking about cancer. That shift has forced researchers to rethink their approach to studying new treatments. Keytruda’s approval was one of the first to follow from an emerging kind of clinical trial, called a basket trial, that evaluates a drug with a specific molecular target across many different types of cancer. These trials group patients in “baskets” according to where their tumors are located, so a single trial might include one basket for lung cancer, another for thyroid cancer and a third for breast cancer.
Basket trials are one of the first designs customized to test the idea of using genetic profiles to match patients to the drugs most likely to help them. Along the way, the trials have begun to answer questions about how rare genetic mutations contribute to cancer, says medical oncologist Gary Doherty at Cambridge University Hospitals in the United Kingdom.
Although the vision of targeted cancer therapy has remained largely out of reach, a growing number of researchers see basket trials as a way to improve the odds of success. Some early basket trials have led to some remarkable treatments, such as Keytruda, for some patients. Others have failed to find new treatments, but Doherty and others say even those trials have bolstered our knowledge about the stunning complexity of cancer, reemphasizing the diversity of its molecular underpinnings and its often dogged resistance to treatment.
New breed of trials
Mutations in more than 700 culprit genes have been implicated in the onset or growth of cancer. In any one tumor, four or five these genetic variations may turn it down a malignant path. Some mutations drive the growth of a tumor; others cripple the body’s natural defenses. There could be millions of mutation combinations — possibly even billions — behind cancerous growth. That complexity may help explain why survival rates for people with many types of advanced cancers have barely changed in the last 50 years. But at the same time, those hundreds of genes offer a tantalizing solution: more opportunities for targeted drugs to home in on vulnerabilities in a patient’s tumor.
Conventional clinical trials investigate the effects of a new treatment on patients with cancer in a specific organ or tissue. Some scientists worry that such trials can mask the benefits of targeted drugs if the majority of patients don’t have the genetic mutation targeted by the drug and so don’t respond to it. One possible solution, recruiting only patients who harbor the targeted — but often rare — mutation in a particular tissue, ends up being inefficient and costly.
Using that approach, “it’s hard to enroll a clinical trial with enough patients to draw a conclusion,” says Robert Beckman, an oncologist and biostatistician at Georgetown University Medical Center. “If there are only 15 patients in the world with a disease, how can you tell with statistical significance that a therapy is working?” Beckman leads an international group of about 200 researchers focused on creating new clinical trial designs that improve the efficiency of drug development.
A basket trial gives researchers the opportunity to directly study the effect of a drug by grouping patients with cancers at a variety of sites, not just one site, based on the genetics of their tumor. “When you undertake a basket trial, you’re essentially saying that the genetic information is more fundamental than the organ site,” says Beckman.
Another advantage of basket trials is the prospect of building on the success of a therapy in one cancer type to address other malignancies. The BRAF gene, for example, is mutated in about half of all melanoma cases — and in about 5 to 10 percent of colon cancers. BRAF mutations have also been found in some lung cancers, brain cancers and non-Hodgkin’s lymphoma. (A planned phase II clinical trial is now investigating a targeted drug combination in multiple cancers with a rare BRAF mutation.)
“If you have a drug for one cancer type with a certain molecular feature, can it be used to treat other cancer types?” says oncologist Keith Flaherty at the Harvard Medical School and Dana-Farber Cancer Center in Boston, who has helped design clinical trials to answer this question.
Signals and noise
Experts point to the trial that focused on Keytruda — the first site-agnostic drug approved in 2017 — as a rousing success. Keytruda dismantles the brakes of the body’s immune cells, empowering the body’s defenses to detect and attack cancer cells. In 2013, after promising results suggesting that the drug could extend the lives of people with melanoma, an-often deadly skin cancer with few treatment options, researchers were eager to test it on other cancers. Their efforts paid off: Subsequent studies suggested that patients with some lung cancers, kidney cancers and bladder cancers might live longer with the therapy.
That evidence led to a basket trial that involved 149 patients with a total of 15 different cancer types. Patients qualified as long as they had mutations associated with a mismatch-repair (MMR) deficiency, a condition in which a cell’s repair shop can’t adequately fix DNA mutations connected to cancer’s growth. About 40 percent of the patients benefited from Keytruda, providing enough evidence for the FDA to grant accelerated approval — a process by which a drug can be made available to patients before all the survival data has been analyzed.
“That drug is so spectacular, and the unmet need was so great, that the FDA didn’t really require the same rigor as they demand for other drugs,” says Beckman. “It was just so evident that these drugs were very useful.”
Another success soon followed. In late 2018, the FDA approved a second site-agnostic drug, Vitrakvi, for patients who have exhausted other treatment options and whose solid tumors have what’s called an NTRK gene fusion, where a gene called NTRK breaks off one chromosome and attaches to another. The process produces what are called TRK proteins, which can promote cancer growth. That approval was based on results from 55 patients, representing 12 different types of cancer, from three small, ongoing basket trials. By eight weeks, in 12 patients, all observable signs of cancer disappeared entirely; in another 29 patients, the tumors decreased in size.
However, not all basket trials have led to effective drugs, says oncologist Aaron Mansfield at the Mayo Clinic in Rochester, Minnesota. In fact, there have been some frustrating failures.
In 2012, French researchers launched the SHIVA trial, a randomized basket trial designed to measure whether targeted cancer drugs, when used off-label, could extend progression-free survival (the amount of time after treatment until cancer gets worse). More than 700 patients were enrolled and had their tumors sequenced. About 200 patients with mutations that were targets of existing drugs were divided into two groups. About half received standard care, and the rest received a drug that wasn’t approved for their type of disease but was designed to target one of their identified genetic mutations.
The results of this large, high-profile trial were dismal. After 11 months, patients who had been prescribed targeted drugs were just as likely as the others to have cancer-related symptoms recur, and more likely to experience serious or even life-threatening side effects. That led study investigators to discourage the off-label use of targeted therapies in general.
“It didn’t move the needle” on any of the tested drugs, says Flaherty.
However, SHIVA wasn’t a total loss, says Doherty, who recently coauthored an article in the Annual Review of Biochemistry on treating cancer in the age of genomics. “The results told us that even if the same genomic biomarker in one tissue is present in another, it doesn’t mean they are both actionable,” he says. In other words, a mutation in one tumor might be driving the growth and spread of the disease, while the same mutation in another might not play as significant a role.
Mixed results have also come out of the largest basket study to date, more appropriately described as a basket-of-baskets: the National Cancer Institute’s Molecular Analysis for Therapy Choice trial, or NCI-MATCH. Flaherty is the lead investigator, and the study was designed to find promising drugs for a variety of tumor sites.
Launched in 2015, it has since enrolled more than 6,000 patients, who have each had their tumors genetically sequenced. As of early 2020, nearly a dozen separate treatment groups were still being formed, each arm of the study probing the effect of a targeted drug on a specific mutation. Where SHIVA randomly assigned targeted drugs to patients based only on a common mutation, in the MATCH trial drugs were given to patients only if previous studies in the lab and on animals suggested that they might be beneficial.
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In November 2018, investigators reported that treatment with capivasertib, a drug that interferes with a cellular signaling pathway that promotes cancer growth, had so far led to tumor shrinkage in 8 of 35 patients who took it — findings promising enough to warrant future studies. But in another arm of the study, none of the 65 patients saw their tumors shrink when they took taselisib, an experimental drug that looked promising in lab and animal studies against a mutation in a gene called PIK3Ca. Other arms have had similarly weak results.
“Certainly, I’d say I’m disappointed,” says Flaherty. Knowing that taselisib doesn’t work suggests that PIK3Ca may not be the Achilles’ heel that pre-clinical trials suggested it would be, but “even a zero percent response rate tells you something,” Flaherty says.
Mixed basket
Researchers disagree about how to interpret these mixed results. One possibility is that some early basket trials suffered from flaws in their design. Many experts blame the SHIVA findings on a failure to compile enough evidence from pre-clinical animal studies to justify using the drugs tested.
More broadly, because of the way data from different treatment arms is often pooled, basket trials may not be as statistically robust as phase II conventional trials. They may also be more vulnerable to false positives, or erroneously inflating benefits. And they don’t reveal the biological significance of mutations or show why participants in one basket respond while those in another don’t.
But Doherty believes many of the obstacles can be overcome. He says that past experiences have shown that a good basket trial needs to have enough participants to make the findings reliable, a clear trial design that includes well-defined goals, and pre-clinical evidence suggesting that the drug will work for patients harboring a particular mutation.
Flaherty says basket trials, coupled with information from other genetic analyses, can fill important gaps in researchers’ understanding of which mutations do what, and when, and in which cancer types. And these pieces, he hopes, will reveal the optimal ways to get new treatments to as many patients as possible.
Stephen Ornes is a science and medical writer who lives in Nashville, Tennessee. Follow him on Twitter @StephenOrnes
A version of this article was originally published at Knowable Magazineand has been republished here with permission. Newsletter signup. Find Knowable on Twitter @KnowableMag
As the days unfold with a seeming sameness in this odd summer of the pandemic, news of vaccine clinical trials begins to trickle in, and another buzzword from epidemiology is entering the everyday lexicon: durability.
To be successful, a vaccine’s protection must last or booster shots periodically restore it. Some vaccines lose efficacy over time, including those for yellow fever, pertussis, and of course influenza.
For some vaccines, antibodies and the B cells that make them persist and protect for a long time. For other infectious diseases, like TB and malaria, T cells are needed in vaccines too. B and T cells (lymphocytes) are types of white blood cells, which are part of the immune system.
Antibody response may be ephemeral
“Give a man a fish and you feed him for a day. Teach him how to fish and you feed him for a lifetime,” said Chinese philosopher Lao Tzu, founder of Taoism.
Tzu might have been referring metaphorically to the immune system’s response to viral infection: an initial rush of antibodies that fades as a longer-lasting cell-based memory builds that primes the body to rapidly release antibodies upon a future encounter with the pathogen.
Credit: Matthieu Louis
Antibodies are proteins, so they don’t make more of themselves as cells might. That’s why antibodies collected from plasma from a person who’s recovered from COVID-19 lasts a few weeks. It’s also why an “antibody medicine” like Regeneron’s dual-antibody REGN-COV2 provides only short-term protection, a bridge until a vaccine becomes available.
To remain effective over a reasonable period of time, a vaccine must mimic the memory component of an immune response, which arises from B and T cells and is therefore called the “cellular” immune response. The shorter-term release of antibodies into the bloodstream is the “humoral” immune response (“humor” means fluid).
A strong antibody response to a vaccine may be a harbinger of lasting B and T cell protection, but vaccines may be marketed before their durability is known – a complete understanding of how long a vaccine’s protection lasts can take years. The vaccine against the mumps, for example, went on the market in 1967, but in 2006, several colleges had outbreaks, among students whose childhood mumps vaccine had worn off. A booster extends the coverage.
Clues to a COVID-19 vaccine’s durability come from natural immunity from past coronavirus infections. The antibody response to SARS and MERS persisted less than a year. But so far, the cellular immune response to SARS, the older of the two, has lasted eleven years.
Clinical trials to evaluate COVID-19 vaccines in people consider both antibody production and the building of cellular immunity. And a vaccine can be even more protective than natural immunity.
“A vaccine elicits memory B and T cells so the immune system remembers how to fight the disease in the future. Natural infection is not likely to produce durable immunity and vaccination will be essential to produce herd immunity to reduce the probability of viral transmission,” said Arlene Sharpe MD PhD co-director of the Evergrande Center for Immunologic Diseases at Harvard Medical School and Brigham and Women’s Hospital on a recent zoom that MassCPR, a group of Boston-area institutions that formed in early March in response to the pandemic, held.
Making antibodies
The immune system isn’t as easy to visualize as a skeleton splayed out in a Halloween decoration, the flattened entrails of a roadkill, or the circulatory system, which even Groucho Marx in the film Horse Feathers could easily explain. (“Let us follow a corpuscle on its journey through the body.”)
Credit: iStock
Instead, the immune system is an army of billions of cells and their secretions that stand ready to attack newly encountered pathogens, remember old ones, and at the same time recognize “self,” protecting the body’s own tissues. The cells travel in clear lymph fluid, passing through lymph nodes that filter out debris.
The immune system reacts in three stages. First, physical barriers keep pathogens out: skin, earwax, waving cilia in the throat, stomach acid, diarrhea. Next, innate immunity unleashes a bath of inflammatory molecules that are a generalized response to infection.
Finally comes adaptive immunity, which is specific and provides the ‘memory’ that a vaccine emulates. In addition to T and B cells, innate immunity includes the wandering, blobby macrophages, which engulf pathogens and are festooned with bits of a pathogen’s surface – antigens – that alert other immune defenses.
Antibody production begins when a stimulated B cell divides in the bone marrow, giving rise to two types of cells. One, a plasma cell, has a clear oblong area that is a ginormous Golgi apparatus, which processes 2,000 antibodies per second that enter the circulation.
The second “daughter cell” of a dividing B cell is a memory B cell. Like the name suggests, a memory B cell hangs around, and if the pathogen shows up again, jumps into action and pumps out more antibodies, cutting off the new infection fast.
An important part of the antibody response is that it’s “polyclonal” – differently-shaped antibodies are produced, each recognizing and binding to a different part of a pathogen, like using different weapons to tackle different parts of an enemy’s body.
Some antibodies just bind to a pathogen, but others “neutralize” it, and those are the ones that make a vaccine or immune response effective. Yet certain other antibodies actually enhance infection; vaccines are designed to block this from happening.
T cells call the shots
T cells come in several varieties and exert complex effects.
Helper (aka CD4) T cells activate B cells and release interleukins, which also stimulate B cells.
Killer (aka cytotoxic or CD8) T cells directly attack cells stuffed with viruses, which antibodies can’t do.
Regulatory T cells (T regs) check the entire response so it doesn’t destroy healthy cells.
Tracking T cells is important in evaluating potential vaccine durability. And although we only have a half-year of data, the natural infection suggests that antibody responses may be short-lived or not strong enough.
“Investigators are reporting the antibody response in humans infected with COVID who recover tends to drop relatively quickly. To some people that’s an alarm bell and they guess that a vaccine will show little durability. But following recovery from an acute infection, a decline in antibodies is normal B cell biology and is exactly what we predict,” said Daniel Barouch, MD, PhD, professor of medicine, Harvard Medical School and director, Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center.
One of the first reports showed antibodies decreasing by half in just 37 days among a small sample of people who had mild cases. That’s similar to SARS and MERS, in which antibodies fade away within a year. But so far, reports of phase 1 clinical trial results for two COVID vaccines are encouraging.
Moderna’s and Oxford’s vaccine candidates boost antibodies and T cells
The first interim report, published in The New England Journal of Medicine July 14, found that all 45 participants who received one of three doses of Moderna’s mRNA-1273 vaccine made antibodies, more with the higher dose. Binding antibodies appeared by day 15 and neutralizing antibodies after a second dose on day 28. Neutralizing antibodies are a biomarker of vaccine protection for other respiratory viruses, so that’s good news.
“Responses are comparable to what occurs with natural infection, and perhaps a little higher. Data are encouraging; the strategy elicits immune responses that are targeted against the virus,” said Lindsey R. Baden, MD, associate professor of medicine, Harvard Medical School and director of clinical research, Brigham and Women’s Hospital. The study used antibodies in plasma from recovered patients as a control for the natural immune response, and the vaccine exceeded that comparison.
Even better news: participants made T cells. Helpers appear first, which pump out a specific soup of cytokines, and then after the second dose of vaccine, killers appear, making sure that any remaining viruses can’t replicate.
The phase 1 trial showed that the middle of three doses is best for tempering efficacy with side effects. Phase 2 began in May and phase 3, began on July 27. Overall, depending on the number of trials that progress, hundreds of thousands of people may participate.
Credit: Sarah Grillo/Axios
Moderna’s vaccine (mRNA-1273) is designed to enhance visibility to the immune system. The target cell translates it into an engineered version of the virus’s spike protein that tames the inflammatory response. The spike is also tweaked to be more stable than the natural one.
On July 20 the second clinical trial report came from the Oxford COVID Vaccine Trial Group’s candidate ChAdOx1, in The Lancet. That vaccine consists of the genetic instructions for the spike protein delivered in a chimpanzee virus.
Like the mRNA vaccine, Oxford’s candidate is given in doses 28 days apart. And it, too, evokes both a humoral (antibody) and cellular (T cell) response.
So far, the numbers of vaccinated people are small, but the reports are optimistic.
You can’t rush science: Potential dangers to fast rolling out of a vaccine
With clever variations on the clinical trial theme, like overlapping phases and designing spike proteins to be more visible to the immune system, it may indeed be possible to barrel through phase 3 clinical trials that test a statistically significant number of people. But post-marketing surveillance, a normal part of drug development, is going to be critical.
The participants in the MassCPR zoom marveled that vaccine development for COVID-19 is so far taking 5 to 10 months, compared to the historical 5 to 10 years.
“We are only months into knowing about this virus, so any longevity of the immune response we have to interpret with care because our understanding of the biology and durability of the biology will take time. The virus will evolve and we have to take that into consideration,” said Baden. He showed data from monkeys that suggest a long-lasting effect is possible.
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Practically speaking, the phase 3 trials will take time because the participants aren’t being injected with virus, for ethical reasons. Instead, investigators must wait for the volunteers to encounter the virus in their communities, to see if a smaller percentage of vaccinated people become infected than the unvaccinated control groups. And that’s why a vaccine “by the end of the year would be quite a surprise for many of us,” said Ken Mayer, MD, of the Fenway Institute.
“We’ll have increasing clarity as the next 3 to 6 months proceed with a suite of clinical trials underway or soon to be. Most optimistic is late fall for first availability for an Emergency Use Authorization. But a tremendous number of things would have to go perfectly to achieve that. Early 2021 is more realistic,” said Barouch. An “EUA” brought COVID-19 treatment remdesivir to patients before the official FDA approval.
Baden agreed that early 2021 is more feasible. He points out the potential savings of 6 to 12 months from beginning to manufacture candidate vaccines before their clinical trials conclude, well before. “Financial risks are acceptable, safety not, and that’s why it will take at least 3 to 6 months more.”
Credit: Aspioneer
Once a vaccine is out there, attention will turn to epidemiology. What percentage of the population must be vaccinated or have natural immunity to induce herd immunity? And how many people will actually take a vaccine?
If several vaccines make it to the finish line, how will people be assigned to them? People over age 65, for example, would benefit most from a vaccine that includes an adjuvant, which is a chemical that affects the immune response. A vaccine candidate from Australian biotech company Vaxine Pty Limited, for example, includes a complex sugar that lowers the risk of the vaccine triggering an excessive immune response. The sugar adjuvant has worked well in vaccines against influenza, hepatitis B, and West Nile virus, according to Nikolai Petrovsky, PhD, research director at the company.
Assessing the all-important T cell response will take time, too, because that’s the way the cellular immune response unfurls in nature. Gradually. A full immune response is a finely-tuned process that is a consequence of millennia of evolution – not of politics, PR, potential profits, or wishful thinking.
Ricki Lewis has a PhD in genetics and is a genetics counselor, science writer and author of Human Genetics: The Basics. Follow her at her website or Twitter @rickilewis.
Geneticist Dr Kat Arney takes a look at the ancient war between our genes and the pathogens that infect us, looking back thousands of years to the Black Death and before, all the way through to our very latest foe.
One of the most curious things about COVID-19 – the disease caused by the novel SARS-CoV-2 coronavirus that’s causing so much trouble – is the wide variation in how it affects different people, from being a very serious or even fatal illness, through a range of strange symptoms like skin rashes or diarrhea as well as the cough, fever and loss of smell, which vary in their severity. And there are some lucky people who seem to catch the virus but have no symptoms at all. So, do these differences lie in our genetics? Or are their other factors at play?
To find out, Kat speaks with consultant geriatrician Dr Claire Steves from King’s College London. She’s part of a team of researchers analysing data from the COVID Symptom Study app, originally built by health science company ZOE to survey some of the thousands of identical and non-identical twins involved in the TwinsUK cohort study. The app now has more than 4 million users in the UK, US and Sweden, and is providing valuable insights into the key symptoms of COVID-19 and how they affect different people.
COVID-19 is just the latest in a long string of outbreaks, epidemics and pandemics that have ravaged humanity over the years. Christiana Scheib, head of the ancient DNA research facility at the University of Tartu, Estonia, is looking at much older plagues – including the Black Death – to discover how underlying genetic variations may have contributed to susceptibility to disease. By studying ancient remains from many burial sites in the Cambridge area, she’s piecing together a picture of the past to understand how these people lived and died.
Finally, Kat talks to Lucy Van Dorp from University College London, who is studying how the human genome has co-evolved over millennia alongside the pathogens that infect us. Although it may seem strange to be studying ancient diseases in today’s modern era, particularly when we’ve got a brand new pandemic to worry about, her work to trace the spread, movement and migration of humans and their pathogens is essential for understanding the spread of outbreaks today, including COVID-19.
Full transcript, links and references available online at GeneticsUnzipped.com
When a mother gives birth to twins, the offspring are not always identical or even the same gender. Known as fraternal twins, they represent a longstanding evolutionary puzzle.
Identical twins arise from a single fertilised egg that accidentally splits in two, but fraternal twins arise when two eggs are released and fertilised. Why this would happen was the puzzle.
In research published [May 11] in Nature Ecology & Evolution we used computer simulations and modelling to try to explain why natural selection favours releasing two eggs, despite the low survival of twins and the risks of twin births for mothers.
Why twins?
Since Michael Bulmer’s landmark 1970 book on the biology of twinning in humans, biologists have questioned whether double ovulation was favoured by natural selection or, like identical twins, was the result of an accident.
At first glance, this seems unlikely. The embryo splitting that produces identical twins is not heritable and the incidence of identical twinning does not vary with other aspects of human biology. It seems accidental in every sense of the word.
In contrast, the incidence of fraternal twinning changes with maternal age and is heritable.
Those do not sound like the characteristics of something accidental.
The twin disadvantage
In human populations without access to medical care there seems little benefit to having twins. Twins are more likely to die in childhood than single births. Mothers of twins also have an increased risk of dying in childbirth.
In common with other great apes, women seem to be built to give birth to one child at a time. So if twinning is costly, why has evolution not removed it?
Paradoxically, in high-fertility populations, the mothers of twins often have more offspring by the end of their lives than other mothers. This suggests having twins might have an evolutionary benefit, at least for mothers.
But, if this is the case, why are twins so rare?
Modelling mothers
To resolve these questions, together with colleagues Bob Black and Rick Smock, we constructed simulations and mathematical models fed with data on maternal, child and fetal survival from real populations.
This allowed us to do something otherwise impossible: control in the simulations and modelling whether women ovulated one or two eggs during their cycles. We also modelled different strategies, where we switched women from ovulating one egg to ovulating two at different ages.
We could then compare the number of surviving children for women with different patterns of ovulation.
Women who switched from single to double ovulation in their mid-20s had the most children survive in our models – more than those who always released a single egg, or always released two eggs.
This suggests natural selection favours an unconscious switch from single to double ovulation with increasing age.
Strategy for prolonging fertility
The reason a switch is beneficial is fetal survival – the chance that a fertilised egg will result in a liveborn child – decreases rapidly as women age
So switching to releasing two eggs increases the chance at least one will result in a successful birth.
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But what about twinning? Is it a side effect of selection favouring fertility in older women? To answer this question, we ran the simulations again, except now when women double ovulated the simulation removed one offspring before birth.
In these simulations, women who double ovulated throughout their lives, but never gave birth to twins, had more children survive than those who did have twins and switched from single to double ovulating.
This suggests the ideal strategy would be to always double ovulate but never produce twins, so fraternal twins are an accidental side effect of a beneficial strategy of double ovulating.
Joseph L. Tomkins is Associate Professor in Evolutionary Biology at the University of Western Australia studying sexual selection and threshold trait evolution
Rebecca Sear is the Head of the Department of Population Health a the London School of Hygiene & Tropical Medicine. Follow her on Twitter @RebeccaSear
Wade Hazel is a Professor of Biology at DePauw University. He specializes in evolutionary analysis of decision-making in organisms.
This article was originally published at the Conversation and has been republished here with permission. Follow the Conversation on Twitter @ConversationUS
Europe has suspended some of its oppressive GMO regulations to speed development of a COVID-19 vaccine, drawing accusations of hypocrisy from the scientific community. A growing body of research suggests very low-carb diets could treat Alzheimer’s, ALS and even cancer. Your risk of coronavirus infection and death may be heavily influenced by your genetics—but how big of an influence are we talking about?
Join geneticist Kevin Folta and GLP editor Cameron English on this episode of Science Facts and Fallacies as they break down these latest news stories:
For decades, Europe has so tightly regulated biotech crops that they’re effectively banned on the continent. A single variety of insect-resistant corn is the only GMO plant grown commercially in the EU. Despite these restrictions, ostensibly motivated by concerns for public health and the environment, Europe has suspended some of its rules governing genetic engineering to quickly develop a vaccine for the novel coronavirus. Why would the EU so rapidly drop its rules if biotech plants really pose a serious risk?
The scientific community is always debating the merits of low-carb diets, but these discussions typically center around carbohydrate restriction as a treatment for obesity and diabetes. However, ongoing research suggests that very high-fat, low-carb ketogenic diets may also be viable treatments for a variety of debilitating diseases, most notably cancer. Is this more hype than science, or does such an extreme way of eating really hold promise?
Everybody knows that age and pre-existing conditions boost your risk for severe coronavirus infection. What remains less clear is why some seemingly healthy individuals appear immune to COVID-19 while others quickly succumb to the disease. The answer to this perplexing question may lie in genetics. Dramatic advances in DNA sequencing technology are helping scientists zero in on particular variables—say, blood type or mutations in genes that influence immune function—that may help explain why there are such wide-ranging reactions to coronavirus. Knowledge of these genetic factors could also help fine tune efforts to trace and control the spread of SARS-COV-2, or even develop targeted treatments for the resulting infection.
Subscribe to the Science Facts and Fallacies Podcast on iTunes and Spotify.
Kevin M. Folta is a professor in the Horticultural Sciences Department at the University of Florida. Follow Professor Folta on Twitter @kevinfolta
Cameron J. English is the GLP’s managing editor. BIO. Follow him on Twitter @camjenglish
Their target remains GMOs—a range of agricultural products made with modern techniques of genetic engineering, from eggplant grown mostly in Bangladesh and modified to resist insects to corn, soybeans and cotton that tolerate exposure to weed-killing herbicides. Anti-biotech advocacy groups are waging a battle against GMOs in America’s courtrooms, and they’ve been emboldened by a string of recent successes, as the pro-organic Center for Food Safety (CFS) brags on its website:
CFS is preventing the mass approval of GMO crops and foods! We’re in court fighting some of our earth’s biggest polluters: Monsanto, Dow Chemical, and the agency that gives a green light to these polluters—the U.S. Environmental Protection Agency (EPA) …. Our team is here to stop the use of dangerous pesticides that threaten our health and the health of our planet. If we work together, we can stop the next generation of dangerous GMO crops!
Bayer’s decision in June to settle some 95,000 lawsuits alleging its Roundup weedkiller causes cancer for $10.9 billion is perhaps the best indicator of how effective this litigation strategy is. The settlement, one of the largest in US history, was Bayer’s way of putting the breaks on a legal fight that was crippling it financially, though it appears the biotech giant may still have to defend its flagship weedkiller against many more plaintiffs after part of the deal fell through. In mid-July, the company also lost an appeal in the first Roundup case that went to trial, a 2018 suit brought by a California groundskeeper.
What’s emerging from the chaos of years of litigation targeting Monsanto (now owned by Bayer) and other makers of agricultural chemicals is that industry antagonists are not finished. Advocacy anti-GMO groups, now partnered with the tort industry, are poised to go after other chemicals in the conventional agricultural toolbox, including other herbicides, insecticides and synthetic fertilizers.
Credit: Walsh Family, father and son
Just last week, the Pennsylvania Supreme Court ruled that the family of golf course groundskeeper Thomas Walsh could proceed with its civil case against a dozen major chemical manufacturers for allegedly causing his leukemia and eventual death. Glyphosate is technically not on trial here, as it has not been linked in any studies to leukemia. But a handful of studies have shown some correlation between glyphosate and non-Hodgkin’s lymphoma in long-term users, while the vast majority of studies have not confirmed any links. Rather, the focus will be on a range of other chemicals used to control pests.
Beyond glyphosate
Success breeds copycats, and the windfall generated by anti-biotechnology activism has primed the litigation pump. Since many popular weedkillers are paired with genetically engineered crops that resist their herbicidal effects, activist groups or trial lawyers they work with are filing a slew of lawsuits alleging that other pesticides pose serious risks to human health or the environment. Their goal is to force the manufacturers to pull their products off the market or get the EPA to ban them. Eliminate the pesticides and farmers have no incentive to plant the herbicide-resistant seeds.
Dicamba drift damage
Environmental groups led by CFS have recently convinced a federal court to ban another popular herbicide, drift-prone dicamba, and are trying to get the same circuit court to vacate the registration for Enlist weedkillers sold by Corteva Agriscience. Activist groups are also agitating to block EPA approval of Bayer’s new corn variety that withstands exposure to five different herbicides. True to form, CFS executive director Andrew Kimbrell said victory in these suits could “massively reduce” the use of GMO crops.
Europe exemplifies where US anti-GMO activists want to take America. Cultivating biotech plants is tightly restricted and thus effectively banned across the Atlantic (although they are widely imported for animal feed). A single variety of insect-resistant corn is only the such crop grown in Europe today. The EU could also ban the use of glyphosate as soon as 2022 and mandate that 25 percent of its farmland be converted to organic production by 2030. European regulators have already banned a class of pesticides known as neonicotinoids because they allegedly are responsible for a swath of bee deaths, though the evidence doesn’t support this conclusion.
If successful, activist efforts to push the US in Europe’s direction could leave American farmers with access to only subpar pest-control tools. The problem is compounded because consumers watch the courtroom drama play out on social media and demand access to “more sustainable” food options. Such developments prompt an obvious question: will the US follow in Europe’s footsteps?
New technologies on the horizon
The answer appears to be no, for two reasons. While anti-GMO groups have been successful in court recently, the American public is far less ‘precautionary’ in its view of chemicals, seeking a more evidence-based balance of risks and rewards. But there’s another twist to the story. The drumbeat of legal actions in recent years has begun spurring the development of a new generation of sustainable pest-control tools that will just be harder to ban.
Striking evidence of this trend surfaced in early July. “Conventional pesticide makers, including Syngenta and Bayer AG, have been under pressure in recent years over their products’ impact on the environment and biodiversity,” Bloomberg reported, “as more and more consumers grow more …. distrustful of pesticides used to produce their food.” In response, these biotech giants, alongside smaller startups and university research groups, have taken a variety of approaches to develop products that address sustainability concerns—everything from new seeds and pesticides to genetic technologies that reverse herbicide resistance in weeds and protect crops from pest attacks.
Gene-editing technology, which allows scientists to make specific changes to DNA, is one of the best tools researchers can use to tackle farm sustainability issues, and some early results are promising. With the help of tools like CRISPR, researchers are devising new combinations of herbicides and resistant crops that will give farmers options beyond the pest-control systems currently in the activist crosshairs. An herbicide-resistant canola variety developed through gene editing has been available in the US and Canada since 2016. And other crops, including corn, rice, wheat, soy and even watermelon, are also being engineered to withstand exposure to a variety of weedkillers.
Image: iStock/monsitj
Gene editing can also be used to immunize plants against attacks from insects and deadly pathogens. Significantly, these crops possess insect resistance that isn’t dependent on chemical spraying. That makes them more akin to transgenic (GMO) Bt crops already grown by farmers all over the world, such as eggplant in Bangladesh and cotton in India and the US. The resistance trait is bred into the plants themselves, so spraying is often cut to near zero. As they become available, these new plant varieties will rob anti-GMO activists of their current favorite line of attack: banning synthetic pesticides meant to be used in concert with biotech crops.
Natural biopesticides, typically developed from plants and microbes, are another important part of this effort to make farming more sustainable. GLP reported on the dramatic growth of biopesticides last summer, including a weedkiller known for now as MBI-014. The bacteria-based herbicide is effective against weeds that glyphosate and dicamba can’t control. In field trials completed last fall, the bioherbicide
… demonstrated control of a target weed approaching that of a current post-emergent chemical herbicide. At commercial rates across multiple trial locations that used uniform protocols, control of palmer amaranth was evaluated at three stages of growth, 7-to-10 days after MBI-015 was applied. Control ranged from the mid-70s to the high-80s percent ranges.
Palmer amaranth: Credit: Howard Schwartz/Colorado State University)
Gene-edited crops and biopesticides may prove to be especially important because they’re generally easier to get through the US regulatory system than transgenic plants and synthetic chemicals. In Europe, where gene-edited plants are regulated just like GMOs, biological pest controls may be the only novel technology capable of navigating the EU’s byzantine regulatory system.
But activists are not expected to suddenly drop their opposition, even though the environmental and health effects of these technologies are minimal. They will warn of “unintended consequences,” of course. They are wont to complain, for example, that developing new pesticides, natural or otherwise, and resistant crops fuels the so-called pesticide treadmill. “Patented GE seeds are designed for use with specific pesticides, leading to increased use of these chemicals,” warns Pesticide Action Network (PAN), another plaintiff in the lawsuits alongside CFS. “And widespread application of these pesticides leads to the emergence of herbicide-resistant ‘superweeds,’ which facilitates the need for more herbicides and GMO seeds resistant to them.” Yet many of these products are designed specifically to address the threat of pesticide resistance.
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Farmers do rely on pesticides season after season, but utilizing a variety of weedkillers and insecticides alongside non-chemical strategies can help mitigate the risk of resistant weeds and bugs. That’s a key reason why the activist lawsuits to ban effective pesticides are counterproductive. The fewer chemistries farmers have access to, the more likely it is that resistance issues will arise. Moreover, two decades of research show that biotech crops have cut pesticide use by 776 million kilograms since their introduction in 1996. Despite these important qualifications often overlooked by activists, pesticide resistance remains a real concern for many farmers. Fortunately, biotechnology may yield a more direct solution in the coming years.
Reversing pesticide resistance
Beyond introducing more pesticides, it may be possible to re-sensitize weeds to chemical treatments they’ve become resistant to using modern genetic engineering techniques. Two approaches called virus-induced gene silencing (VIGS) and Virus-mediated overexpression (VOX), for example, would allow scientists to turn off herbicide resistance in weeds. A team of scientists at UK-based Rothamsted Research demonstrated how these techniques work in an April 2020 study:
The team first inserted their gene of interest into a virus, and then infected the weed with it. During VIGS, the plant tries to defend itself and in the process shuts down production of all genes coming from the virus – including the weed’s own copies of the inserted gene – whereas during VOX, both the virus’ and the inserted gene’s copies manufacture proteins for the plant …. This made previously resistance plants susceptible
A similar technology, developed by Monsanto several years ago, involves treating herbicide-tolerant weeds with glyphosate and an RNA-based substance that shuts down their tolerance to the herbicide. Gene drives, which can be used to spread specific genetic alterations through targeted wild populations (of, say, weeds and crop pests), could also be used to eliminate pesticide resistance.
Center for Food Safety, Pesticide Action Network and their ideological allies won’t have a sudden change of heart on biotechnology. As they readily acknowledge, they’re on a campaign to promote organic farming, and that won’t end because we devise a long-term solution to herbicide resistance, especially given their recent success in court. What’s more interesting is that this extremist wing of the environmental movement has been gradually pushing itself into irrelevancy by attacking the technologies that make farming more sustainable; these recent biotech-fueled innovations are just the latest example of that process in action. As science writer Matt Ridley has pointed out:
Far from starving, the seven billion people who now inhabit the planet are far better fed than the four billion of 1980 …. Remarkably, this …. has happened without taking much new land under the plow and the cow …. Nor have these agricultural improvements on the whole brought new problems of pollution in their wake. Quite the reverse …. I was wrong to be pessimistic about the environment in 1980, and it would be wrong to give young people a counsel of despair today. Much has improved since then, and …. much improvement from here is not only possible, but likely.
Cameron J. English is the GLP’s managing editor. BIO. Follow him on Twitter @camjenglish
In a few months, the first transgenic (GMO) salmon will be sold in the US, produced in an AquaBounty farms facility in Indiana. The story will go unnoticed, buried by the infodemic related to COVID-19. However, it is an announcement that the biotech community has been awaiting for 31 years.
Aquaculture operations produce 2.5 million tons of salmon annually and the main producers are Norway, Chile, the United Kingdom and Canada. In general, fish farms are responsible for producing more than 50% of all the fish we consume. Imagine you have an idea to double the growth rate of farm-raised salmon through a simple genetic modification, getting it to market size in half the time (18 months vs. 36) while consuming fewer resources.
Imagine doing all possible tests, for more than 20 years, to show that the only difference between transgenic and non-transgenic salmon is the intended difference: their growth rate. There are no organoleptic differences (flavor, texture) or variations in the composition of the meat, nor is there any problem when consuming it.
Suppose you also do all the necessary biosecurity testing to confirm that production is sustainable and safe for the environment, making an escape into the wild practically impossible. This is achieved through the introduction of multiple geographical barriers: farms on land, far from the sea or any river or lake; redundant physical security measures; and facilities that only produce sterile, female salmon. Even assuming there were any leaks, multiple studies and the FDA review itself indicate that there would be no significant impact on the environment.
Imagine that you finally get official authorization to produce and sell these GM salmon. Now imagine that all this started in 1989 and you’ve had to wait 31 years to bring this biotech product to US consumers, which looks like it is going to happen this fall. What company is capable of waiting 30 years without being able to place its product on the market? How many rounds of investors will it have to organize to keep confidence alive and contain the impatience of successive boards of directors? This is what AquAbounty has had to face.
Europe will have to wait
In Europe, with regulations that usually limit biotechnological advances, we are still much further from achieving this. We will have to content ourselves with reading this news in the papers and waiting to make a trip to the US to taste the first transgenic animal authorized by the FDA—quite possibly the most analyzed food to ever be sold in grocery stores.
The history of transgenic salmon (which now have the trade name AquAdvantage) dates back to 1989. It was then that the first specimens were born using a very ingenious gene construction, all fish. This means that all their genetic elements came from similar fish, without including segments from unrelated animals. The publication of these results would not take place until 1992 , 28 years ago. The researchers reported very significant increases in growth rates, between 2 and 13 times faster than normal. The initial authorization to produce these fish for food was not granted until November 2015.
How to make a transgenic salmon
The transgene that was microinjected into Atlantic salmon embryos ( Salmo salar ) in 1989 was called opAFP-GHc2 and consisted of three DNA fragments, all derived from other fish.
First, the promoter of the gene encoding the antifreeze protein (AFP) was obtained from a benthic fish from the Atlantic Ocean called Macrozoarces americanus. This promoter directed the expression of a cDNA (complete copy of the RNA of a gene converted to DNA thanks to reverse transcriptase) of the gene that encodes the growth block of the Pacific salmon ( Oncorhynchus tshawytscha ). Finally, this gene construct included a transcriptional terminator similarly derived from Macrozoarces americanus.
The gene for the AFP antifreeze protein turns on in the cold and allows these fish to survive in icy waters below freezing temperature. It acts as a natural antifreeze for these animals. Here, only the regulatory elements of the AFP gene are used to activate the expression of the Pacific salmon growth hormone gene in cold weather.
The idea is to take advantage of this genetic trick to maintain a constant supply of growth hormone throughout the year. In general, Atlantic salmon only grow in the warm spring and summer months, when they activate their own growth hormone gene. But in the fall and winter this gene is turned off and the animals stop growing. With this transgene, the production of this second source of growth hormone is activated during the cold months.
This ensures that there is enough growth hormone throughout the year to allow a sustained increase in size. This reduces the time it takes to reach commercial size from 36 to 18 months, half the time, with lower feeding costs (25% of what it would cost to feed non-GMO salmon).
Frankenfish accusations
Naturally, these salmon have had to face terrifying smear campaigns referring to them as “frankenfish.” The FDA received more than 1.8 million letters opposing its approval of the GMO salmon. Politicians were influenced, for example, by traditional Alaskan salmon farms that saw their business model threatened by a company able to put salmon on the market in half the time and with considerable savings in production costs. Many lies have been told to negatively influence the opinion of Americans, despite initiatives that debunk such fears with scientific evidence and corroborate the safety, for consumers and the environment, of the production of these transgenic salmon.
After approval by the FDA , Canada also approved the marketing of these salmon, and as early as 2017, it was announced that AquaBounty had sold the first 4.5 tons of salmon in the country. These first salmon came from the fish farm that AquaBounty established in Panama, which was authorized by the FDA after the company produced the sterile (triploid) eggs at a facility on Prince Edward Island, Canada. A production facility in Indiana was approved by the FDA in 2018. It is from this fish farm that the first genetically engineered salmon will come, which can now be sold in US supermarkets.
A very profitable food
Salmon offers one of the best food conversion factors. For every kilogram of food consumed, one kilogram of salmon is obtained. In comparison, two kilograms of food are needed for every kilogram of chicken, and no less than ten kilos of food for every kilogram of beef, one of the animal species with the worst conversion factor. Salmon farming also consumes relatively little fresh water; 900 liters of water are needed per kilogram of salmon, but 3,500 liters are required for one kilogram of rice, or up to 15,000 liters of water per kilogram of beef.
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Finally, the carbon footprint left by salmon farming is ten times lower than that derived from beef production (2.9 kg of CO₂ per kg of salmon produced compared to 30 kg of CO₂ per kg of meat cow). The need to produce food for a growing world population will double by 2050, when it is expected that there will be nine billion people on the planet, according to the FAO. Traditional agriculture, livestock and fish farming will be unable to produce all the necessary food. That is why it is necessary to utilize biotechnology, both for animals and plants.
It would have been nice if transgenic salmon could have reached consumers sooner than 31 years after it was developed. Hopefully, the next genetically modified ( or gene-edited ) product intended for consumption doesn’t have to wait that long to hit American tables.
In the meantime, Europeans will continue to read the news from across the Atlantic and watch, once again, as the trains of innovation and progress go by—trains that go at full speed and, for the moment, still have no stop in Europe.
Lluís Montoliuis a molecular biologist at the National Center for Biotechnology in Spain. Visit his website. Find Lluís on Twitter @LluisMontoliu
This article originally ran at The Conversation and has been republished here with permission. It has been translated from Spanish and lightly edited for clarity. Find the Conversation on Twitter @ConversationUS
For more than three decades Michael Koob has been working out complicated puzzles using the tools of molecular biology and genetics. Today his deliberative labors are paying off—with untold implications for the study of human disease and the development of drug therapies and vaccines. Koob has figured out how to replace entire genes of laboratory mice with their human counterparts, transporting huge segments of human DNA to their proper corresponding location in mouse chromosomes. Now he is applying his genetic puzzle-solving ingenuity to the scourge of the COVID-19 pandemic.
Michael Koob. Credit: University of Minnesota
An LMP associate professor, Koob launched his molecular investigations while a graduate student at the University of Wisconsin in Madison, where he earned a PhD in molecular and cellular biology in 1990. His graduate adviser was the legendary molecular geneticist Waclaw Szybalski. Koob and Szybalski pioneered a technique they called “Achilles’ heel cleavage” that cuts DNA in a single targeted location, which enabled them to create large DNA segments. Koob joined the LMP faculty in 1995. He brought with him those early insights about how to use molecular tools to manipulate DNA in human and animal cells and thereby answer questions about health and disease.
Now Koob has set his sights on COVID-19, the disease caused by coronavirus SARS-CoV-2 infection. SARS-CoV-2 respiratory viruses enter human lung tissue via a cell-surface receptor molecule called angiotensin-converting enzyme 2 or ACE2. Once in the lung the virus multiplies and travels throughout the organ, in some patients causing Acute Respiratory Distress Syndrome (ARDS), which can be fatal.
But there’s a problem in using mice to understand SARS-CoV-2 infection and COVID-19 disease progression. “In the mouse, the ACE2 receptor doesn’t bind the virus, so mice don’t get infected and show the respiratory symptoms we see in people,” Koob said. But what if mice expressed the human gene for the ACE2 receptor instead of their own? That would potentially enable investigators to track COVID-19 pathology beginning with infection and viral replication in airway epithelial cells all the way to lower lung zones where the virus often settles, consolidates, and can cause viral pneumonia. That mouse model is under construction in Koob’s laboratory.
Coronavirus attaching to a human ACE2 receptor on the outside of a cell. Credit: Shutterstock
Infection at the entry point would make the mouse model work for COVID-19, and full human ACE2 receptor gene substitution for the mouse version should make infection possible, Koob said. “The internal viral replication will be maintained between the mouse and humans. So this should model the infection route, disease progression in the lungs, everything like that. It’s really just basic cell biology. If you want to mimic what happens in a person the most important thing really is to get the cell types correct. If the right cells are ACE2 receptor-positive, then you can mimic what happens in people.”
Other research groups have transferred only a small part of the ACE2 receptor DNA gene sequence into mice, creating transgenic animals but ones that do not mimic the potentially lethal lung pathology of a SARS-CoV-2 infection and COVID-19, such as ARDS. Koob’s team will replace the entire mouse ACE2 receptor gene with the entire human ACE2 receptor gene plus associate regulatory sequences—transferring in all some 70,000 DNA sequences to the precise location on the mouse chromosome where its own ACE2 receptor gene once resided. “The mouse gene will be gone, and the human gene will be there,” Koob said. “It now becomes a human ACE2 receptor gene in a true sense. The sequence of tissues that become positive for ACE2 receptor expression should be recapitulated.”
When a human gene is put in the same spot where the mouse gene once resided, genomic regulatory factors come into play that are appropriate for that gene, Koob said. “There’s a global regulatory context to take into account in animals that have a common ancestor, which all mammals do. Mice and humans are fairly close on the evolutionary tree. So there’s global regulation if we put it in the right spot.” The “right spot” transfer of the human gene construct is into a mouse embryonic stem cell, which Koob then puts into a blastocyst or early mouse embryo. Selective breeding yields mice with the human gene in all cells and tissues.
A search of the database ClinicalTrials.gov yields more than 400 studies when the terms “COVID-19” and “lung therapy” are combined. Small molecule drugs, therapeutic antibodies and antivirals, immunotherapies, stem cells and natural killer cells, steroids, and laser and radiotherapies are among the lung injury therapies currently being investigated. A validated, reliable, and clinically informative mouse model for testing COVID-19 lung injury therapies would be invaluable, as it would be for future coronavirus vaccine trials.
Koob anticipates his human ACE2 receptor gene mouse strain will be ready by this fall. He will send it by courier to Jackson Laboratory (JAX) in Bar Harbor, Maine to join more than 11,000 strains of mice that JAX distributes to researchers around the world. JAX will breed the mice over several months while Koob and LMP professors Steve Jameson and Kris Hogquist and Department of Medicine assistant professor Tyler Bold, all at the Center for Immunology, conduct characterization and SARS-CoV-2 infection studies of the mice in a Level 3 biosafety facility. JAX is currently distributing Koob’s full gene replacement mouse strain that carries the human microtubule-associated protein tau, which is responsible for the neurofibrillary tangles in the brain associated with Alzheimer’s disease and other dementias. Koob is making full gene replacement mouse models of other neurodegenerative diseases.
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“Our philosophy is to make our mouse strains available to the research community in an expedited way,” Koob said. “I contacted JAX about this ACE2 receptor gene replacement mouse. They’re very happy to collaborate with us because they don’t have anything like this. And we’re making it available to researchers without restrictions.”
It’s been a long time since Koob collaborated with his graduate adviser Waclaw Szybalski, now a 98-year-old professor emeritus. Together their research careers encompass the history of molecular biology going back to the early 1950s with the discovery of the DNA double helix. Szybalski was born in 1921 just after a pandemic virus infected an estimated one-third of the Earth’s population and killed tens of millions of people. A century later, with another pandemic raging, the timing couldn’t be better for his student to exercise his manifest molecular inventiveness.
William Hoffman is a writer and editor at the University of Minnesota. He has worked closely with faculty in genetics and bioengineering, medical technology and bioscience industries, and the science policy and ethics communities. He is author with Leo Furcht of “Divergence, Convergence, and Innovation: East-West Bioscience in an Anxious Age,” Asian Biotechnology and Development Review, Nov. 2014.
A version of this article was originally published at the University of Minnesota website and has been republished here with permission. The University of Minnesota can be found on Twitter @UMNews
When you think of a typical meal in the US South, you will likely recall the rich, hearty dishes that have immortalized themselves in the food culture of the Southern States. Fried chicken, mashed potatoes, gravy, macaroni and cheese; it’s all mouth-watering stuff, but of course there is a catch. Foods like these are loaded with fats and, as a result, calories. A diet heavy in such dishes can have a detrimental impact on your health and wreak havoc on your heart and circulatory system.
The CDC has highlighted the fact that, as a result of such diets, various forms of heart disease kill more Southerners than any other disease. One such example can be found in the fact that Southern Counties record a much higher death rate for diseases such as strokes than the rest of America. Strokes are fast acting and deadly, occurring every 40 seconds in the United States, claiming a life every four minutes. That’s 140,000 deaths a year, the third highest total from any disease. Globally, strokes are an epidemic and the second highest cause of death.
While a satisfying cure remains elusive, advances in biotechnology are offering new hope to the millions of people who experience strokes.
What is a stroke?
A stroke is triggered when a blood vessel in the brain gets blocked or bursts. Striking when the blood supply to part of the brain is cut off, a stroke deprives brain cells (neurons) of their critical supply of oxygen. If neurons go without oxygen for more than a few minutes, they start to die by the millions, so it is critical to act fast if you see any signs of onset. Typically a patient will exhibit distinct physical symptoms such as facial drooping, inability to raise arms and slurred speech, and the stroke usually occurs in one of two ways. During an ischemic stroke, the blood supply is stopped by a clot in a blood vessel, which accounts for roughly 85 percent of cases. A hemorrhagic stroke, in contrast, occurs when a blood vessel within the brain becomes weak and bursts.
Regardless of which scenario occurs, a stroke poses a serious threat to the health of a patient. A constant blood supply is the single most essential component in keeping the brain operational. Every cell within the body relies on oxygen from the blood in order to make energy and function, and the brain is a very “oxygen-hungry” organ. Despite its relatively small size, your brain requires 20 percent of your total oxygen supply. The damage can, therefore, be severe and irreversible if the blood supply to the brain is cut off for more than 10 minutes. For this reason, it is essential that current stroke therapies are administered quickly, but many stroke victims are still likely to suffer long-term consequences that can take years to correct. Consequently, scientists work tirelessly to find better therapies for stroke patients.
Treatment shortfalls and arduous recovery
The need for new and innovative therapies for stroke patients is driven by limitations in currently approved medical interventions. There are two current drug regimens used to treat strokes. Anticoagulants such as warfarin break up existing bloodclots, preventing the most common types of strokes. Antiplatelets such as clopidogrel (Plavix) can be used to help prevent blood clots from forming altogether. But neither one of these drug types repairs the brain damage often associated with strokes.
Mechanical thrombectomy for treating strokes. Image: Penumbra
Additionally, surgery can be performed to treat brain swelling and help prevent further bleeding, but the lingering problem is that patients are still often left with long-term issues after suffering a stroke. Recovery can be a long and arduous process because of the difficulty the brain has in replacing the cellular connections that are lost when neurons die as a result of a stroke. When the cells die, the functions they are responsible for are lost. Regaining those functions often involves a long course of “reablement” therapies aimed at teaching the brain to build new connections and re-learn skills that were lost after a stroke.
Why gene therapy provides promise
Research indicates that in many instances, a brain can heal itself after a stroke. Cells that are damaged are not beyond repair. They can regenerate. Researchers in the field are pushing for pharmaceutical options to help speed up this regeneration of the lost network of brain cells. This is where gene therapy could make a real difference. Gene therapy offers scientists the tools required to genetically reprogram cells to help speed up the regeneration process during stroke recovery.
The use of gene therapy is still very much in its infancy, with a lot of research underway to ensure the technology can be implemented safely and effectively. Direct administration of DNA into the brain offers the advantage of producing high concentrations of therapeutic agents in a relatively localized environment. Gene transfer also provides longer duration of effect than traditional drug therapy. Recent studies have shown a lot of promise.
In one such study, researchers at Penn State University developed a gene therapy platform using a gene called neurogenic differentiation 1 (NeuroD1). The study, which was conducted on mice, investigated the potential of using a retrovirus to deliver NeuroD1 directly into the brains of mice that had suffered from a stroke. Researchers found that the therapy converted glial cells into the neuronal cells that are critical to regenerating lost brain tissue. Mice treated with this novel gene therapy not only lost less brain tissue but also showed a significant improvement in motor function. According to the leader of the research team, Prof Gong Chen:
The biggest obstacle for brain repair is that neurons cannot regenerate themselves. Many clinical trials for stroke have failed over the past several decades, largely because none of them can regenerate enough new neurons to replenish the lost neurons. I believe that turning glial cells that are already present in the brain into new neurons is the best way to replenish the lost neurons.
In another study from Florida Atlantic University, a research team explored the potential of using a protein called granulocyte-colony stimulating factor (G-CSF) to give cells in the brains of mice the “genetic push” they needed to trigger regeneration after stroke. The results were, once again, very positive, with treated mice showing an improvement in prognosis after stroke. The cells were more resistant to damage-induced death and this significantly improved behavioral functions in treated mice.
This therapy provides another promising avenue, but study co-author Prof Howard Prentice emphasized the need for further investigation:
Future research will need to focus on uncovering the complete mechanisms by which GCSF retains the ER and mitochondrial homeostasis.
While Prentice underscored the preliminary nature of this research, the data generated so far indicate gene therapies are extremely promising avenues for improving the lives of stroke patients. And just last month, a team at the University of San Diego Medical School released a study showing that just a single treatment that inhibits a gene known as PTB resulted in the disappearance of symptoms associated with Parkinson’s disease and other neurodegenerative impairments.
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“It’s my dream to see this through to clinical trials, to test this approach as a treatment for Parkinson’s disease, but also many other diseases where neurons are lost, such as Alzheimer’s and Huntington’s diseases and stroke,” said Xiang-Dong Fu, head of the research team. “And dreaming even bigger — what if we could target PTB to correct defects in other parts of the brain, to treat things like inherited brain defects?”
The positive nature of Xiang-Dong Fu’s outlook is something we can all feel inspired by. At present, the road to recovery for stroke patients is long and their quality of life can suffer. But we have the potential to kick-start that recovery and help the brain rebuild the precious connections that enable stroke victims to lead healthier lives. For now, there’s no easy answer; preventing a stroke remains a better option than treating and recovering from one. But the constant influx of advances in gene therapy could provide a quicker route to repairing the severe damage when it does occur—dramatically boosting the quality of life for millions of people.
Sam Moxon has a PhD in regenerative medicine and is currently involved in dementia research. He is a freelance writer with an interest in the development of new technologies to diagnose and treat degenerative diseases. Follow him on Twitter@DrSamMoxon
Research validating a homeopathic ‘drug’ for erectile function was published in a peer-reviewed science journal. Europe’s Green Party opposes genetic engineering in agriculture but approves of it in medicine. Why the double standard? The wine industry is embracing gene editing to cut down on pesticide use and battle crop disease.
Join geneticist Kevin Folta and GLP editor Cameron English on this episode of Science Facts and Fallacies as they break down these latest news stories:
“There’s little evidence to support homeopathy as an effective treatment for any specific health condition,” the NIH says, and mainstream medicine has roundly rejected the alternative health movement. So how did a study backing the use of a homeopathic compound to boost erectile function pass peer review? Though the paper was ultimately retracted, it raises important questions about the integrity of the peer-review process.
Europe’s Green Party is beginning to divide on the efficacy of crop biotechnology, with the next generation of members arguing that gene editing could help the EU sustainably produce food long into the future. But this small faction of pro-science environmentalists was overruled by the party’s older leadership, which contends that genetic engineering in medicine is acceptable while the same technology used in agriculture poses a serious threat. Is Europe finally progressing past its fear of GMOs?
Winegrowers around the world are even more excited about gene editing than the next generation of environmentalists. The industry faces a handful of deadly diseases that threaten to wipe out the most prized wine grape varieties—Cabernet Sauvignon, Merlot, Chardonnay and Pinot Noir, among several others—that for now can only be controlled with pesticides.
While consumers only want certain kinds of wine, they’ve also grown wary of the chemicals (even the organic ones) used to protect grapes from disease. Tackling these plant pests with CRISPR may be the solution that satisfies consumers without disrupting the wine industry’s business model.
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Kevin M. Folta is a professor in the Horticultural Sciences Department at the University of Florida. Follow Professor Folta on Twitter @kevinfolta
Cameron J. English is the GLP’s managing editor. BIO. Follow him on Twitter @camjenglish
Biotech giant Bayer is currently in the fight of its life against more than 100,000 lawsuits alleging its flagship weedkiller Roundup (glyphosate) causes cancer. There is no sound scientific evidence to support such allegations, and every relevant research and regulatory authority in the world has concluded the herbicide poses no cancer risk when used appropriately by farmers. But Bayer, fearing for its financial well being, has opted to settle the bulk of the lawsuits (roughly 95,000) and is working to resolve the remaining cases, though the future of the litigation is uncertain.
This epic legal battle in the US tends to dominate the headlines, but the debate over glyphosate is an international affair. Multiple nations have attempted to institute glyphosate restrictions as a means of limiting the use of herbicide-resistant GMO crops, designed to be utilized with glyphosate. India recently proposed such a policy. And Mexico, building on earlier efforts to restrict GMOs, is moving perilously close to an outright glyphosate ban.
Simply put, Mexico’s proposed nationwide glyphosate ban is motivated by extremist ideology and utterly devoid of scientific justification. More importantly, it would be disastrous for Mexican farmers and consumers.
An activist-occupied government
The current administration led by President Andrés Manuel López Obrador (AMLO) has created uncertainty about the future of genetically engineered crops in Mexico by refusing to approve any new biotech crop authorizations in over two years, since May 2018.
The president has also given important regulatory positions to former activists that have led anti-GMO campaigns, and to former leaders from environmental groups. The most prominent of these figures are the current science minister Elena Alvarez-Buylla and the head of SEMARNAT (Secretariat of Environment and Natural Resources) Victor M. Toledo. Both officials are former leaders of the Union of Concerned Scientists (UCS). Adelita San Vicente Tello, the director-general of the Primary Sector and Renewable Natural Resources at SEMARNAT—also linked to UCCS—is the former director of Seeds of Life (Semillas de Vida), an anti-biotechnology NGO that agitated to ban GMO corn in Mexico and invited Vandana Shiva, a darling of the anti-biotech movement, to speak several times.
With the help of environmental groups like Greenpeace, this alliance of activist-regulators has launched a new effort to ban glyphosate-based herbicides at the national level, linking the weedkiller with the use of GMOs in the country. Glyphosate is often paired with biotech crops, but the reality is that this herbicide was introduced to Mexico long before GMOs were ever planted in the country. It has also been used to control unwanted vegetation in parks and gardens for many years.
Credit: GMO Free USA
SEMARNAT announced on November 25, 2019 that Mexico had turned away a 1,000-ton cargo ship carrying glyphosate, citing “the precautionary principle of risk prevention” and making reference to scientific studies alleging glyphosate harms pollinators and damages the environment. The agency’s press release didn’t reference the large body of evidence showing that glyphosate poses minimal risk to the environment, pollinators included. According to Toledo, the head of SEMARNAT, the decision fulfilled “an urgent need to promote an agroecological public policy and reduce the harmful environmental, social and cultural effects of modern agriculture.” Toledo made strikingly similar pronouncements as an activist before joining SEMARNAT. He once declared , for example, that modern agriculture relies on “products harmful to human health, produces less nutritious food, and is responsible for global warming.”
As part of the government strategy to gradually reduce the use of glyphosate-based herbicides in the country, Adelita San Vicente said that the National Council of Science and Technology (CONACyT), is analyzing possible alternatives to replace the popular weedkiller. However, CONACyT’s budget has been cut and shifted to funding mostly social science research, thus eliminating support for basic scientific studies that could lead to new herbicides. The only other “alternatives” on the table are the techniques that have been applied by farmers and indigenous communities for thousands of years, mainly massive amounts of manual labor in the fields to remove weeds. There are other options for some growers, but none are very good, as we’ll see.
The impact on farmers
According to experienced Mexican agricultural scientists, glyphosate is the only effective option that most farmers can afford. Although Monsanto (now owned by Bayer) initially developed and sold glyphosate exclusively, its patent has expired and 56 companies in Mexico use the herbicide in their weed-control products, which are widely distributed to small and large farms.
Alfredo Gutierrez, an agronomist and fifth-generation dairy farmer in the central region of Mexico, recently reported that if he and his colleagues lose access to glyphosate (which they use while growing feed for their milking cows), they will replace it with several other herbicides, which are more expensive and potentially more toxic. Gutierrez also mentioned that controlling weeds manually is not viable due to the higher associated labor costs. Some farmers might therefore turn to controlled burns as a weed-management strategy, a practice that carries a variety of risks including wildfires.
Farmers have rapidly adopted glyphosate and resistant crop technology for three main reasons: cost savings, better weed management, and simplicity of use. As has been reported by national newspapers in Mexico, 73 percent of farmers have used glyphosate over the last 40 years to control more than 100 types of weeds that affect crops such as corn, sorghum, beans, citrus, coffee, sugar cane, avocado, and tomato.
If the remaining herbicide reserves run out, these crops are going to suffer because they’ll have to compete with once easily controlled weeds for nutrients, water, and sunshine—reducing their production between 30 and 40 percent, according to Cristian García de Paz, executive director of the Crop Protection, Science and Technology Organization (PROCCYT). Just like higher production costs, lower yields affect not only the seven million farmers and producers who utilize glyphosate, but also the public, who will pay more for foods that are widely consumed in Mexico.
Illegal—and maybe dangerous—alternatives
The illegal market for agrochemicals in Mexico is going to get a shot in the arm when a glyphosate ban takes effect, representing a real threat to farmers, consumers, and the environment. Regulatory oversight would normally ensure the composition, concentration, and efficacy of the product. But black-market pesticides aren’t subject to rigorous review by independent experts. Farmers won’t know if these chemicals are dangerous to human health or how they’ll impact soil health, pollinators and other wildlife.
Broken promises
There is a general feeling in Mexico’s farming community that this decision is rooted in ideological thinking rather than real scientific concern regarding the safety of glyphosate. Officials who support the ban have discarded a lot of evidence that supports the safe use of glyphosate and considered only the research that justifies their desire to ban the weedkiller. The activists in key positions at SEMARNAT and the Secretariat of Agriculture are taking advantage of the bad publicity glyphosate and Bayer have received from the mainstream media, pushing this ban to serve an agenda to ban GMOs instead of looking out for the common good of farmers. This is the administration’s first step in a long-term plan to promote agroecology, a term often used to describe organic farming practices.
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Currently, the discussion about a glyphosate ban in the country is being had by the National Agricultural Council (CNA) and SEMARNAT. It will be crucial to focus the dialogue on the scientific evidence, because more than 130 million Mexicans rely on farmers for sustenance. If their productivity is stifled by this arbitrary decision, Mexico will be obligated to import food that is usually produced locally, moving the country further away from food security—one of the strongest campaign promises made by the current government.
Luis Ventura is a biologist with expertise in biotechnology, biosafety and science communication, born and raised in a small town near Mexico City. He is a Plant Genetic Resources International Platform Fellow at the Swedish University of Agricultural Sciences. Follow him on Twitter @luisventura
As ethicists specializing in how technology alters human-nature relations, we can understand why advocates see the ethics this way. If “crossing species lines” is the measure of whether a technique counts as “natural” or not, then genome editing appears to have the potential to pass a naturalness test.
Genome editing, its boosters say, can make changes that look almost evolutionary. Arguably, these changes could have happened by themselves through the natural course of events, if anyone had the patience to wait for them. Conventional breeding for potatoes resistant to late blight is theoretically possible, for example, but it would take a lot of time.
Although we understand the potential advantages of speed, we don’t think an ethics hinging on the idea of “cisgenesis” is adequate. We propose a better ethical lens to use in its place.
Naturalness and species lines
Our work is part of a four-year project funded by the Norwegian Research Council scrutinizing how gene editing could change how we think about food. The work brings together researchers from universities and scientific institutes in Norway, the U.K. and the U.S. to compare a range of techniques for producing useful new crops.
Our project is not focused on the safety of the crops under development, something that obviously requires concerted scientific investigation of its own. Although the safety of humans and the health of the environment is ethically crucial when developing new foods, other ethical issues must also be considered.
To see this, consider how objections against genetically modified organisms go far beyond safety. Ethical issues around food sovereignty range broadly across farmer choice, excess corporate power, economic security and other concerns. Ethical acceptability requires a much higher bar than safety alone.
Although we believe gene editing may have promise for addressing the agricultural challenges caused by rising global populations, climate change and the overuse of chemical pesticides, we don’t think an ethical analysis based entirely on “crossing species lines” and “naturalness” is adequate.
It is already clear that arguing gene-edited food is ethical based on species lines has not satisfied all of gene editing’s critics. As Ricarda Steinbrecher, a molecular biologist cautious about gene editing, has said, “Whether or not the DNA sequences come from closely related species is irrelevant, the process of genetic engineering is the same, involving the same risks and unpredictabilities, as with transgenesis.”
Charles Darwin in a 1881 oil painting by John Collier. Credit: National Portrait Gallery
Comments of this kind suggest talking about species lines is an unreliable guide. Species and subspecies boundaries are notoriously infirm. Charles Darwin himself conceded in “Origin of Species,” “I look at the term species, as one arbitrarily given for the sake of convenience to a set of individuals closely resembling each other.”
The 2005 edition of the Mammal Species of the World demonstrated this arbitrariness by collapsing all 12 subspecies of American cougars down to one Puma concolor cougar overnight. In 2017, the Cat Classification Task Force revised the Felidae family again.
If species lines are not clear, claiming “naturalness” based on not crossing species lines is, in our view, a shaky guide. The lack of clarity matters because a premature ethical green light could mean a premature regulatory green light, with broad implications for both agricultural producers and consumers.
The integrity lens
We think a more reliable ethical measure is to ask about how a technique for crop breeding interferes with the integrity of the organism being altered.
A unifying theme in all these domains is that integrity points toward some kind of functional wholeness of an organism, a cell, a genome or an ecological system. The idea of maintaining integrity tracks a central intuition about being cautious before interfering too much with living systems and their components.
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The integrity lens makes it clear why the ethics of gene editing may not be radically different from the ethics of genetic modification using transgenes. The cell wall is still penetrated by the gene-editing components. The genome of the organism is cut at a site chosen by the scientist, and a repair is initiated which (it is hoped) will result in a desired change to the organism. When it comes to the techniques involved with gene editing a crop or other food for a desired trait, integrity is compromised at several levels and none has anything to do with crossing species lines. The integrity lens makes it clear the ethics is not resolved by debating naturalness or species boundaries.
Negotiation of each other’s integrity is a necessary part of human-to-human relations. Adopted as an ethical practice in the field of biotechnology, it might provide a better guide in attempts to accommodate different ethical, ecological and cultural priorities in policymaking. An ethic with a central place for discussion of integrity promises a framework that is both more flexible and discerning.
As new breeding techniques create new ethical debates over food, we think the ethical toolbox needs updating. Talking about crossing species lines simply isn’t enough. If Darwin had known about gene editing, we think he would have agreed.
Christopher J. Preston is a Professor of Philosophy at the The University of Montana. Dr. Preston’s areas of interest include: Environmental Ethics in the Anthropocene, Feminist Epistemology, and the ethics of emerging technologies. Find Christopher on Twitter @SyntheticAge
Trine Antonsen is a Resarch Scientist at GenØk Centre for Biosafety and Associate Professor at the University of Tromsø. Trine holds a Ph.D. in Philosophy from the Department of Philosophy, Classics, History of Art and Ideas at the University of Oslo.
This article was originally published at the Conversation and has been republished here with permission. Follow the Conversation on Twitter @ConversationUS
While coronavirus is obviously concerning and a very real threat to some people (namely, the elderly and immunocompromised), these data also show that the risk for the rest of the population is quite low.
Credit: Public Domain/Wikipedia
Public health officials and the media have been warning us that coronavirus kills not just old or immunocompromised people but young people too. While this is true, it remains relatively uncommon.
The CDC has accumulated mortality data about the COVID-19 pandemic from February 1 to June 17. Using this, it is easy to summarize how the disease has impacted Americans differentially based on age and race. Bear in mind, that the CDC’s mortality data often lags behind other sources. (For example, the death toll in the United States according to Johns Hopkins is over 120k, but the CDC’s most recent data only shows roughly 103k.) Still, this shouldn’t impact the age and race analysis.
U.S. Coronavirus Deaths by Age
Here’s the coronavirus mortality data by age group:
As shown, deaths in young people (from babies to college students) are almost non-existent. The first age group to provide a substantial contribution to the death toll is 45-54 years, who contribute nearly 5% of all coronavirus deaths. More than 80% of deaths occur in people aged 65 and over. That increases to over 92% if the 55-64 age group is included.
One thing that is often forgotten is that people of all ages are dying all the time. Each year, about 2.8 million Americans pass away. The following chart shows the percentage of deaths in each age group that were due to coronavirus:
Of the roughly 1.2 million American deaths that occurred between February 1 and June 17, almost 9% were due to coronavirus. The proportion of deaths due to coronavirus were about the same for each age group above 45 years. Below that, the proportion of deaths due to coronavirus fell dramatically. Thirteen children of primary and middle school age (5-14 years) died from COVID-19, but this represented only 0.7% of all deaths in this age group; 1,742 kids died of other things during this same time period.
U.S. Coronavirus Deaths by Race
The following chart depicts U.S. coronavirus deaths by race.
The number that stands out here is the percentage of COVID deaths that occurred among Black Americans. Blacks constitute about 13% of the U.S. population but suffered 23% of all COVID deaths.
Risk of Death from Coronavirus: COVID-19 Infection Fatality Rate (IFR)
None of the above data answers the question, “What is my risk of dying from coronavirus if I get infected?” For that, we need to look at the infection fatality rate (IFR), which is the percentage of people who die given that they are infected. (This includes people with asymptomatic infections or those who are infected but never get tested.) One group believes the range is 0.1% to 0.41% (with a point estimate of 0.28%). Another group, which examined deaths in Geneva, Switzerland, concluded that the overall IFR is 0.38% to 0.98% (with a point estimate of 0.64%.)
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Of course, IFR varies depending on age. Young people are far less likely to die than older people. The Swiss study estimated IFR’s by age group:
While coronavirus is obviously concerning and a very real threat to some people (namely, the elderly and immunocompromised), these data also show that the risk for the rest of the population is quite low.
Dr. Alex Berezow is a PhD microbiologist, science writer, and public speaker who specializes in the debunking of junk science for the American Council on Science and Health. Find Alex on Twitter @AlexBerezow
A version of this article was originally published at the American Council on Science and Health and has been republished here with permission. The American Council on Science and Health can be found on Twitter @ACSHorg
COVID-19 threatens to slow or halt agricultural innovation in the US by exacerbating the decline in public R&D and threatening private sector R&D as well. Research at universities, government labs, and companies has slowed down as labs have closed or downsized. In addition, venture capital funding for startups is falling, though lab, salary, and other expenses remain.
To ensure that promising research efforts, companies, and infant industries do not fail, it is critical to increase public R&D funding as well as incentives for private R&D investments.
Summary
American agricultural innovation, which generates tens of thousands of jobs, is threatened by COVID-19, the economic downturn, and longstanding public underinvestment in research and development.
Research labs and companies developing novel crop varieties, fertilizers, livestock feeds, alternative proteins, and other technologies are also essential to mitigating climate change and ensuring American leadership in emerging industries.
Government support for basic and applied research efforts and early-stage startups at risk of failure, would accelerate innovation, protect existing jobs, and lead to new job growth.
$300M for ongoing publicly funded R&D to cover COVID-related costs: 3.6+ thousand jobs
$9.4B to cover the agricultural R&D facility maintenance backlog: 140+ thousand jobs
$190M for new interagency research initiatives: 3.7+ thousand jobs
$50M+ for mission-driven research at AGARDA: 600+ jobs
$74M to incentivize private sector R&D through FFAR and SBIR: 650+ jobs
COVID-19 threatens to slow or halt agricultural innovation in the US.
Agricultural Research and Development (R&D) has improved the productivity, global competitiveness, and environmental sustainability of American farms. For example, since the 1960s, productivity advances have enabled farmers to reduce land use by 9% and cut the carbon footprint per pound of milk and chicken over 50%.1 There are many opportunities for innovation to further reduce agricultural emissions. Beef production, nitrogen fertilizer, and dairy production — the largest sources of agricultural emissions — account for 2.1%, 2.1%, and 1.2% of total US greenhouse emissions, respectively.2
Yet state and federal funding for agricultural R&D has recently been stagnant or, by some measures, declining. On average, annual funding grew 2% between 1970 and 1995, but has since fallen about 1% annually.3 While privately funded R&D is also key for innovation and has grown enough to compensate for the decline in public funding, private R&D is not a substitute for public R&D.4 The private sector focuses on shorter-term, lower-risk R&D and on different topics than the public sector.5
COVID-19 is exacerbating the decline in public R&D and threatening private sector R&D as well. Research at universities, government labs, and companies has slowed down as labs have closed or downsized. In addition, venture capital funding for startups is falling, though lab, salary, and other expenses remain.
To ensure that promising research efforts, companies, and infant industries do not fail, it is critical to increase public R&D funding as well as incentives for private R&D investments.
ECONOMIC AND ENVIRONMENTAL IMPORTANCE OF AGRICULTURAL INNOVATION
Recent years have seen a boom in food and agricultural startups and research contributing to sustainable intensification — aiming to raise agricultural productivity while reducing environmental impacts. Particularly promising efforts have developed or seek to develop:
Crops and livestock varieties that are higher yielding6 and more resilient to extreme weather.7
Crop varieties that sequester at least 50% more carbon in soils than current varieties.8
Microbial seed treatments and soil amendments that can increase yields on the order of 10%,9 reduce fertilizer application rates,10 and reduce both nitrate leaching and greenhouse gas emissions.11
Fertilizers made from clean energy12 and fertilizer products that reduce fertilizer greenhouse gas emissions as much as 44%.13
Alternative proteins such as plant-based and cell-cultured meat that pose less zoonotic disease, antibiotic-resistant bacteria, and food safety risks than conventional meat products, while also reducing greenhouse gas emissions.14
Cattle feed supplements that could cut US beef and dairy methane emissions as much as 23% and 19%, respectively, while increasing animal yields.15
Genetically modified soybean plants in a petri dish. Credit: Bayer CropScience.
Startups working on these and other production-focused technologies attracted over $1.5 bil-lion (B) in investment in the US in 2019,16,17 contributing to the creation of tens of thousands of science and technology jobs related to agriculture and food.18 The sector is anticipated to continue growing. The agricultural biotechnology market, for instance, is projected to grow about 7-11% annually in coming years,19 while the precision farming industry is expected to nearly double in size.20
COVID-19 IMPACT ON AGRICULTURAL INNOVATION
R&D, innovation, and industry growth related to sustainable intensification is slowing due to the pandemic.21
Research efforts at universities, government agencies, and companies have stalled, and some com-panies have laid off large shares of their employees.22
Many labs, ranging from those that develop microbe-based fertilizers to those breeding crops to sequester more carbon, have reduced staffing or shut down.23
Shortages of research equipment that are also used for healthcare have further delayed research projects.
Startups are facing new difficulties in raising funds,24 and Venture Capital (VC) funding is anticipated to further fall.25,26
If US VC funding drops as much as seed stage funding has globally,27 it could wipe out $550 million in investment for startups that are making products critical for sustainable intensification such as seeds, alternative proteins, fertilizers, farm software, and sensors.28,29
Unless R&D funding and support is expanded labs may need to cancel research projects that could otherwise have given rise to innovative new technologies and companies. In addition, without expanding support for the private sector, including for R&D, companies may shut down and would-be entrepreneurs may not start new businesses. There are several ways the federal government should support agricultural R&D in order to continue rapid innovation and growth in areas with large financial and environmental potential.
STABILIZE AND STRENGTHEN EXISTING PUBLIC RESEARCH CAPACITY
Spend: $9.7B
Jobs: 143,600-144,70030
Publicly funded extramural research efforts were hamstrung by stagnant funding levels and deteriorating facilities before the crisis. Without additional funding, COVID-related research delays and shutdowns are further undermining research.
Providing supplemental appropriations of at least $300M to USDA research agencies would enable grant and contract-funded researchers to cover current expenses and restart projects. Multi-month lab closures have led to delays and potential cost-overruns in projects with a fixed amount of funding. Supplemental funds should be used to extend grant and contract funding, covering additional personnel and lab costs. Funds should also provide emergency relief to core facilities to maintain base operations, particularly in regions expected to re-open more slowly.31 This level of funding could support about 3,600-4,700 jobs in research and related roles. Many research efforts, such as those funded by AFRI’s Plant and Livestock Production and Protection programs, are also key to enhancing agricultural productivity and environmental sustainability.
It is also important to fund the $9.4B maintenance backlog for USDA Agricultural Research Service (ARS) facilities and agricultural schools at land-grant universities.32 Funding the backlog would:
Reduce future research delays.
Increase the effectiveness of other public R&D
Create over 140,000 jobs.33
DEVELOP NEW INTERAGENCY RESEARCH INITIATIVES
Spend: $190M
Jobs: 3,700-4,200
Developing new R&D initiatives focused on individual technologies would address long-standing research shortfalls, mitigate new COVID-related research slowdowns, and advance long-term sustainable intensification. New R&D efforts should target fields with long-standing research gaps that have been exacerbated recently, and that have high long-term economic and environmental potential.
Interagency research is necessary to effectively fund research in many fields given the wide range of scientific disciplines involved. Many agencies — particularly USDA, DOE, and NSF — fund and conduct active research on sustainable intensification. Coordinated interagency efforts, as the successful National Nanotechnology Initiative has shown, could reduce redundancy, cut costs, and improve agency productivity, while targeting research capacity toward promising industries.34
Image: Victor de Schwanberg/Science Photo Library
New initiatives could include, among others:
A $50M “Alternative Protein Initiative” to build and maintain US leadership in the rap-idly growing alternative protein industry. By 2030 the industry could grow nearly ten-fold,, generating as many as 1 million jobs globally. Public R&D investment would help ensure that nascent research efforts in the US continue, that a large portion of industry job growth occurs in the US, and that farmers who grow the crops used in new products benefit. Canada recently invested nearly $110M USD, with a 1-to-1 private sector match, into a university-industry consortium focused on plant-based proteins. If a $50M US effort had the same economic impact per dollar invested as the Canadian effort is projected to have, it would create over 2,000 jobs and add nearly $1.5 billion to the US economy over 10 years.35
A $50M “Cow of the Future Initiative” to establish US leadership in the nascent industry of products that can increase livestock productivity and reduce GHG emissions. Many of the technologies are still under research, receive little public or private funding, and now are receiving less private funding due to the economic downturn.36 Congress has previously appropriated funding for one particular cattle feed supplement — it should dramatically expand funding to explore additional feed and other livestock mitigation technologies. In addition to ensuring the nascent industry survives and substantially expands in the long-term, this would generate about 600-800 jobs in the near-term.37
A $40M “Agricultural Nitrogen Initiative” to bring down the cost of new technologies that increase crop yields, reduce farmers’ fertilizer costs, and reduce nitrogen pollution. Despite promising advances and increasing demand from farmers for products that will help them cut fertilizer costs and more easily comply with environmental regulations, the fertilizer industry only spends about 0.2% of its $20.5B revenue on R&D, orders of magnitude less than the seed industry’s 10-20%.38 While there is currently relevant federal research funding, it is minimal and potentially duplicative.39 For example, NSF, DARPA, and USDA have funded overlapping research on microbes that can deliver more nutrients to crops, and crops that fix their own nitrogen from the air, among other topics. Increasing annual federal R&D funding to $40M, approximately matching current industry spending, would support foundational research in emerging fields. Besides benefits to farmers and the environment, this would generate about 500-600 jobs in the near term40 and help position the US as a leader in the specialty fertilizer market, which is expected to grow globally by 50% from $23B in 2018 to over $38B in 2026.41
A $50M “Enhanced Root Systems Initiative” to enhance crop productivity and soil carbon sequestration. New research efforts to enhance crop roots, if successful, could increase farmers’ soil quality and sequester hundreds of millions of tons of carbon dioxide-equivalent, enough to offset the majority of greenhouse gas emissions from US agriculture. A 2019 National Academies of Sciences, Engineering, and Medicine report estimated that $40 to $50M in additional funding is needed annually for approximately 20 years. This funding is all the more important now after COVID-19 has stalled efforts and threatened funding to private sector efforts. In addition to establishing the US as a leader in a potentially multi-billion industry, $50M in funding would generate about 600-800 jobs in the near-term.42
PURSUE MISSION-DRIVEN RESEARCH THROUGH AGARDA
Spend:$50-400M, part of or in addition to new interagency initiatives
Jobs:600-6,300, part of or in addition to new interagency initiatives
In addition to, or as part of, any large-scale in-ter-agency R&D initiative, Congress should appro-priate at least $50M for the Agriculture Advanced Research and Development Authority (AGARDA). The 2018 Farm Bill established AGARDA and authorized appropriations of $50M per year between 2019 and 2023. AGARDA can fund grants and col-laborative research between private and public entities, with the goal of spurring long-term, high-risk R&D that the private sector is unlikely to undertake.
Credit: KRVN
The success of R&D efforts similar to AGARDA illustrate why a new agency is necessary. The Defense Advanced Research Projects Agency (DARPA) and the Advanced Research Projects Agency-Energy (ARPA-E), after which AGARDA is modeled, have been credited with laying the groundwork for the internet, GPS, systems for advanced nuclear reactors, and other innovative technologies. Like these agencies, AGARDA should be administered to be mission-driven — focused on achieving specific advances that require broader coordination and longer-term support than other agencies can support.43
AGARDA’s targets for R&D could include, among others:
Developing carbon-neutral beef and dairy production systems that achieve cost parity with conventional systems.
Developing crops that sequester 50% more carbon in the soil.
Halving the average amount of nitrogen lost through crop nutrient management.
Achieving price parity between conventional meats and plant-based products developed to be similar in taste, texture, and other characteristics.
To offset the slowdown in research at universities and private labs due to COVID-19 and to stimulate creation of new companies and jobs, Congress should consider providing additional one-time funding on the order of $400M for AGARDA. In 2009, in the wake of the financial crisis, Congress appropriated one-time funding of $400M to ARPA-E, infusing new funds into the clean energy industry when private capital availability had declined.
Congress could address the current drop in financing for R&D similarly, but should consider one adjustment: retaining equity in companies that receive particularly large support for R&D. This not only would help the government recoup spending, but also ensure that the public benefits from companies’ success.44
While the payoff from agricultural research investments today is unpredictable, past experience suggests funding AGARDA would have outsized job-created benefits. Government investment in mission-oriented innovation increases GDP approximately ten times more than non-R&D government spending, creating about $9 in GDP per dollar spent.45 Ultimately, funding of $400M would generate about at least 4,900-6,300 new jobs for researchers, support staff, suppliers of scientific equipment, and others — a short-term estimate not accounting for the long-run economic benefits from R&D investment.46
INCENTIVIZE PRIVATE SECTOR RESEARCH
Spend: $74 M
Jobs: 650-750
To further restore and stimulate R&D spending, Congress should also create stronger incentives for the private sector to invest in R&D. Private sector spending on agricultural input R&D typically exceeds public agricultural R&D spending, making it key to spurring innovation that in turn helps achieve many societal goals including agricultural decarbonization.47
An effective way to incent greater private investment would be to authorize additional funding for the Foundation for Food and Agriculture Research (FFAR). FFAR, created in the 2014 Farm Bill, spurs development of public-private partnerships and consortia. By requiring at least a 1-to-1 match for all funding, FFAR leverages substantial non-federal funding — about 1.2 non-federal dollars for every 1 federal dollar — and ensures that R&D activities are commercially relevant.48 Its funding has spurred the development of four new public-private consortia working on key long-term challenges livestock antibiotic use and has supported cutting-edge research demonstrating how to improve crop photosynthesis.49 While FFAR was authorized $185M in the 2018 Farm Bill, many agricultural economists argue that the country should double agricultural R&D funding in general.50 Doubling FFAR funding would raise its average annual funding from $37M to $74M, generating 450-600 jobs in the short-term, and more if it induced new non-federal funding.51
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In addition, doubling funding for food and agriculture companies through the National Food and Agriculture Initiative (NIFA) Small Business Innovation Research (SBIR) program, an increase of $37M, would spur innovation and market expansion for the small businesses most impacted by COVID-19. SBIR acts as the federal government’s seed fund for technology-intensive companies, providing early-stage grants through NIFA and other R&D agencies to small businesses to conduct R&D that has high potential for commercialization.
SBIR is highly effective in spurring innovation. Across NIFA and the other agencies that provide SBIR grants, grantees file about 10 patents per day,52 about 70% of projects likely would not have started without SBIR funding,53 and 40-70% of projects reach the market.54 The programs have a high ROI — upwards of $19.50 in economic activity per $1 invested.55 There is good reason to increase program funding for all industries given the general downturn in seed funding and the program’s high oversubscription rate — only 17% of Phase I grants are funded for instance. But doubling agriculture-related SBIR funding alone could address the R&D financing gap for nearly 100 startups that might otherwise shutter,56 and protect or create about 200 jobs in the near-term.57 Related legislation proposed to increase small business R&D funding is the Small Business Innovation Voucher Act (S. 3289, H.R. 5348).58
Dan Blaustein-Rejto is the Associate Director of the Food and Agriculture program at Breakthrough. Follow him on Twitter @danrejto
This article originally ran at The Breakthrough Institute and has been republished here with permission. Follow them on Twitter @TheBTI
Estimates for beef, dairy, and total US emissions drawn from EPA. “Inventory of U.S. Greenhouse Gas Emissions and Sinks: 1990-2018,” 2020. https://www.epa.gov/ghgemissions/inventory-us-greenhouse-gas-emissions-and-sinks. Fertilizer application emissions estimated using 2018 nitrogen usage of 11.67 MMT N, a fertilizer N emissions factor of 2.54%, and a GWP100 of 298 for N2O. Roberto Mosheim. Fertilizer Use and Price. USDA ERS, 2018. https://www.ers.usda.gov/data-products/fertilizer-use-and-price.aspx; Davidson in Joseph Fargione, Steven Bassett, Timothy Boucher, Scott Bridgham, Richard Conant, Susan Cook-Patton, Peter. Ellis, et al. “Natural Climate Solutions for the United States.” Science Advances 4, no. 11 (2018). https://doi.org/10.1126/sciadv.aat1869.
“Agricultural Research Funding in the Public and Private Sectors,” USDA ERS, 2019, https://www.ers.usda.gov/data-products/ agricultural-research-funding-in-the-public-and-private-sectors/.
“Agricultural Research Funding in the Public and Private Sectors.”
Sun Ling Wang et al., “Agricultural Productivity Growth in the United States: Measurement, Trends, and Drivers,” 2015, www. ers.usda.
“Scientists Engineer Shortcut for Photosynthetic Glitch, Boost Crop Growth by 40 Percent,” accessed May 6, 2020, https:// ripe.illinois.edu/press/press-releases/scientists-engineer-shortcut-photosynthetic-glitch-boost-crop-growth-40.
“Scientists Take a Step Closer to Heat-Tolerant Wheat,” accessed May 6, 2020, https://ripe.illinois.edu/press/press-releases/ scientists-take-step-closer-heat-tolerant-wheat.
“Rhizosphere Observations Optimizing Terrestrial Sequestration (ROOTS) Program Overview” (ARPA-E), accessed November 12, 2019, https://arpa-e-foa.energy.gov/Default.aspx#FoaId40aa63a7-689b-4307-90b2-c1b98a2148a3.
“Pivot Bio PROVENTM Creates Sustainably Self-Fertilizing Corn,” 2020, https://blog.pivotbio.com/press-releases/pivot-bio-proven-creates-sustainably-self-fertilizing-corn.
“Pivot Bio PROVEN Outperforms Chemical Fertilizer,” 2019, https://blog.pivotbio.com/press-releases/pivot-bio-proven-out-performs-fertilizer.
Leigh Boerner, “Industrial Ammonia Production Emits More CO2 than Any Other Chemical-Making Reaction. Chemists Want to Change That,” Chemical & Engineering News 97, no. 24 (2019).
Jeanette Norton and Yang Ouyang, “Controls and Adaptive Management of Nitrification in Agricultural Soils,” Frontiers in Microbiology (Frontiers Media S.A., 2019), https://doi.org/10.3389/fmicb.2019.01931.
Daniel Blaustein-Rejto, “Where’s the Fake Beef?,” | The Breakthrough Institute, 2017, https://thebreakthrough.org/issues/food/wheres-the-fake-beef.
Pablo S. Alvarez-Hess et al., “A Partial Life Cycle Assessment of the Greenhouse Gas Mitigation Potential of Feeding 3-Ni-trooxypropanol and Nitrate to Cattle,” Agricultural Systems 169, no. November 2018 (2019): 14-23, https://doi.org/10.1016/j. agsy.2018.11.008; “Summary of Scientific Research on How 3-NOP Effectively Reduces Enteric Methane Emissions from Cows,” accessed January 27, 2020, https://www.dsm.com/content/dam/dsm/corporate/en_US/documents/summary-scientific-pa-pers-3nop-booklet.pdf.
Assuming the US comprises the same 44% share of global VC deals for agricultural biotechnology, innovative food, farm management software, sensor, IoT, novel farming systems, and robotics companies as it does for all AgTech deals.
“AgFunder Agri-FoodTech: Year Review 2019,” 2020.
Allan Goecker et al., “USDA 2015-2020 Employment Opportunities in Food, Agriculture, Renewable Natural Resources, and the Environment,” 2015, https://www.purdue.edu/usda/employment/.
“AgFunder Digitalk: What’s in Store for Agrifood Investing in the Wake of Covid-19?,” accessed April 24, 2020, https://agfun-dernews.com/agfunder-digitalk-1-whats-in-store-for-agrifood-investing-in-the-wake-of-covid-19.html.
“Boston-Based ‘Unicorn’ Indigo Ag Sheds 150 Jobs – Boston Business Journal,” accessed April 24, 2020, https://www.bizjour-nals.com/boston/news/2020/02/28/boston-based-unicorn-sheds-150-jobs.html.
“Joyn Bio,” accessed April 24, 2020, https://joynbio.com/; “Salk Minimizes On-Site Staff and Takes Additional Steps around Coronavirus (COVID-19) – Salk Institute for Biological Studies,” accessed April 24, 2020, https://www.salk.edu/news-release/salk-minimizes-on-site-staff-and-takes-additional-steps-around-coronavirus-covid-19/.
“Agri-Foodtech VCs Assess Covid-19’s Impact on the Sector and Portfolios,” accessed April 24, 2020, https://agfundernews. com/agri-foodtech-vcs-assess-covid-19s-impact-on-the-sector-and-portfolios.html.
“AgFunder Digitalk: What’s in Store for Agrifood Investing in the Wake of Covid-19?”
“Agri-Foodtech VCs Assess Covid-19’s Impact on the Sector and Portfolios.”
Angus Loten, “Startup Funding Dwindles Due to Coronavirus Slowdown,” Wall Street Journal, March 25, 2020, https://www. wsj.com/articles/startup-funding-dwindles-due-to-coronavirus-slowdown-11585175702.
Assuming upstream US AgTech seed funding falls by the same 22% that global seed funding fell from January to March, and assuming that seed funding for upstream AgTech accounts for the same share of total AgTech funding in the US as it does globally.
Loten; “AgFunder Agri-FoodTech: Year Review 2019.”
Unless otherwise noted, jobs estimates are based on employment multipliers per $1 million in final demand for the private-sector, from Josh Bivens, “Updated Employment Multipliers for the U.S. Economy,” 2019. The low estimate uses the multiplier for “Scientific research and development services.” The high estimate uses the multiplier for “Management, scientific, and technical consulting services”. Both multipliers include direct, indirect, and induced jobs.
Peter McPherson, “APLU Urges Congress to Provide Additional Emergency Aid for Students, Universities, and Research” (APLU, 2020), https://www.aplu.org/news-and-media/News/aplu-urges-congress-to-provide-additional-emergency-aid-for-stu-dents-universities-and-research.
Sightlines, “A National Study of Capital Infrastructure & Deferred Maintenance at Schools of Agriculture,” 2015; “King Announces Support for Legislation to Clear Maintenance Backlog, Improve Agricultural Research Facilities,” accessed April 30, 2020, https://www.king.senate.gov/newsroom/press-releases/king-announces-support-for-legislation-to-clear-mainte-nance-backlog-improve-agricultural-research-facilities.
Dan Blaustein-Rejto and Alex Smith, “Economic Recovery for Rural Communities and Agricultural Sustainability: Funding Maintenance and Facility Upgrades for Agricultural Research Infrastructure,” April 2020, https://s3.us-east-2.amazonaws.com/uploads.thebreakthrough.org/RD_Maintenance_Memo_final.pdf.
Frederick M Kaiser, “Interagency Collaborative Arrangements and Activities: Types, Rationales, Considerations,” 2011, www.crs.gov.
“Protein Industries Canada Supercluster Kicks into High Gear,” 2018, https://www.canada.ca/en/innovation-science-eco-nomic-development/news/2018/11/protein-industries-canada-supercluster-kicks-into-high-gear.html.
Adam Satariano, “The Business of Burps: Scientists Smell Profit in Cow Emissions,” The New York Times, May 2020, https:// nytimes.com/2020/05/01/business/cow-methane-climate-change.html.
Bivens, “Updated Employment Multipliers for the U.S. Economy.”
David R. Kanter, Xin Zhang, and Denise L. Mauzerall, “Reducing Nitrogen Pollution While Decreasing Farmers’ Costs and Increasing Fertilizer Industry Profits,” Journal of Environmental Quality 44, no. 2 (March 2014): 325-35, https://doi. org/10.2134/jeq2014.04.0173; “Fertilizer Manufacturing Industry in the US – Market Research Report,” IBISWorld, 2019, https:// www.ibisworld.com/united-states/market-research-reports/fertilizer-manufacturing-industry/.
In total, the US federal government likely funds between $145 and $220 million of soil science and microbiome research, with a fraction of that allocated for research related to crop fertilization. This value is based on NIFA, FFAR, and ARPA-E re-porting data, and assumes ARS funding is roughly similar.
Bivens, “Updated Employment Multipliers for the U.S. Economy.”
“Specialty Fertilizers Market Size to Hit USD 38.66 Billion by 2026,” Fortune Business Insights, March 2020, https://www.glo-benewswire.com/news-release/2020/03/09/1996828/0/en/Specialty-Fertilizers-Market-Size-to-Hit-USD-38-66-Billion-by-2026-Rising-Affordability-of-Superior-Crop-Nutrition-Products-to-Fuel-Market-Expansion-Fortune-Business-Insights.html.
Bivens, “Updated Employment Multipliers for the U.S. Economy.”
Mariana Mazzucato, The Entrepreneurial State : Debunking Public vs. Private Sector Myths (Anthem Press, 2013).
Mazzucato.
Mariana Mazzucato, “The Macroeconomic Impact of Government Innovation Policies: A Quantitative Assessment,” ac-cessed April 29, 2020, www.innovateuk.ukri.org; Bivens, “Updated Employment Multipliers for the U.S. Economy.”
Josh Bivens, “Updated Employment Multipliers for the U.S. Economy,” 2019.
“Agricultural Research Funding in the Public and Private Sectors,” USDA ERS, 2019, https://www.ers.usda.gov/data-prod-ucts/agricultural-research-funding-in-the-public-and-private-sectors/.
Foundation for Food and Agriculture Research, “2018 Annual Report: Transforming Agriculture’s Future,” 2018, https://foundationfar.org/.
Foundation for Food and Agriculture Research; “ICASA – The International Consortium for Antimicrobial Stewardship in Agriculture,” Foundation for Food and Agriculture Research, 2020, https://foundationfar.org/icasa/.
Philip G Pardey and Jason M Beddow, “Revitalizing Agricultural Research and Development to Sustain US Competitive-ness,” 2017, www.instepp.umn.edu.
Bivens, “Updated Employment Multipliers for the U.S. Economy.”
“SBIR Overview” (Small Business Administration, 2016).
Robin Gaster, “Impacts of the SBIR/STTR Programs: Summary and Analysis,” 2017, https://sbtc.org/wp-content/up-loads/2018/02/Impacts-of-the-SBIR-program.pdf.
Gaster
Gaster
Calculation assumes that average grant size for new SBIR grants is $383,610, the same as for 2017, the most recent year data is reported. are the same average are $150,000, the minimum amount provided through its Phase I grants. SBIR Dash-board Available at: https://www.sbir.gov/awards/annual-reports. (Accessed: 30th April 2020)
Gaster
“S.3289 – 116th Congress (2019-2020): Small Business Innovation Voucher Act of 2020,” 2020.
Dan Blaustein-Rejto is the Director of Food and Agriculture at the Breakthrough Institute. Dan analyzes the economics and potential of sustainable agriculture policies and practices. He has conducted research with the Environmental Defense Fund, International Center for Tropical Agriculture, and Farmers Market Coalition. Dan can be found on Twitter @danrejto
Reversing pesticide resistance
