by Al Gore
The global spread of industrial agriculture techniques has resulted in the increased reliance on monoculture, which has, in turn, accelerated the spread of resistance to herbicides and pesticides in weeds, insects, and plant diseases. In many countries, including the United States, all of the major commodity crops—corn, soybeans, cotton, and wheat—are grown from a small handful of genetic varieties. As a result, in most fields, virtually all of the plants are genetically identical. Some experts have long expressed concern that the reliance on monocultures makes agriculture highly vulnerable to pests and plant diseases that have too many opportunities to develop mutations that enable them to become more efficient at attacking the particular genetic variety that is planted in such abundance.
MUTATING PLANT DISEASES
In any case, new versions of plant diseases are causing problems for farmers all over the world. In 1999, a new mutated variety of an old fungal disease known as stem rust began attacking wheat fields in Uganda. Spores from the African fields were carried on the wind first to neighboring Kenya, then across the Red Sea to Yemen and the Arabian Peninsula, and from there to Iran. Plant scientists are concerned that it will continue spreading in Africa, Asia, and perhaps beyond. Two scientific experts on the disease, Peter Njao and Ruth Wanyera, expressed concern in 2012 that it could potentially destroy 80 percent of all known wheat varieties. Although this wheat rust was believed to be reduced to a minor threat a half century ago, the new mutation has made it deadlier than ever.
Similarly, cassava (also known as tapioca, manioc, and yucca), the third-largest plant-based source of calories for people (after rice and wheat), is consumed mostly in Africa, South America, and Asia. It developed a new mutation in East Africa in 2005, and since then, according to Claude Fauquet, who is the director of cassava research at the Donald Danforth Plant Science Center in St. Louis, “There has been explosive, pandemic-style spread.… The speed is just unprecedented, and the farmers are really desperate.” Some experts have compared this outbreak to the potato blight in Ireland in the 1840s, which was linked in part to Ireland’s heavy reliance on a monocultured potato strain from the Andes.
Sixty percent of the U.S. corn crop was destroyed in 1970 by a new variety of Southern corn leaf blight, demonstrating clearly, in the words of the Union of Concerned Scientists, “that a genetically uniform crop base is a disaster waiting to happen.” The UCS notes that “U.S. agriculture rests on a narrow genetic base. At the beginning of the 1990s, only six varieties of corn accounted for 46 percent of the crop, nine varieties of wheat made up half of the wheat crop, and two types of peas made up 96 percent of the pea crop. Reflecting the global success of fast food in the age of Earth Inc., more than half the world’s potato acreage is now planted with one variety of potato: the Russet Burbank favored by McDonald’s.”
Although most of the debate over genetically modified plants has focused on crops for food and animal feed, there has been surprisingly little discussion about the robust global work under way to genetically modify trees, including poplar and eucalyptus. Some scientists have expressed concern that the greater height of trees means that the genetically modified varieties will send their pollen into a much wider surrounding area than plants like soybeans, corn, and cotton.
China is already growing an estimated thousands of hectares of poplar trees genetically modified to make the Bt toxin in its leaves in order to protect them against insect infestations. Biotech companies are trying to introduce modified eucalyptus trees in the U.S. and Brazil. Scientists argue that in addition to pest resistance, modifications might be useful in enabling trees to survive droughts and could modify the nature of the wood in ways that will facilitate the production of biofuel.
In addition to plants and trees, genetically modified animals intended for the production of food for humans have also generated considerable controversy. Since the discovery in 1981 of a new technique that allows the transfer of genes from one species into the genome of another species, scientists have genetically engineered several forms of livestock, including cattle, pigs, chickens, sheep, goats, and rabbits. Although earlier experiments that reduced susceptibility to disease in mice generated a great deal of optimism, so far only one of the efforts to reduce livestock susceptibility has succeeded.
However, the ongoing efforts to produce GM animals have already produced, among other results, spider silk from goats (described above) and the production of a synthetic growth hormone in dairy cattle that increases their milk production. Recombinant bovine growth hormone (rBGH), which is injected into dairy cows, has been extremely controversial. Critics do not typically argue that rBGH is directly harmful to human health, but rather, that evidence suggests it causes the increase of a second hormone known as insulin-like growth factor (IGF), which is found in milk from cows treated with bovine growth hormone at levels up to ten times what is found in other milk.
Studies have shown a connection between elevated levels of IGF and a significantly higher risk of prostate cancer and some forms of breast cancer. Although other factors obviously are involved in the development of these cancers, and even though IGF is a natural substance in the human body, the concerns of opponents have been translated into a successful consumer campaign for the labeling of milk with bovine growth hormone, which has significantly decreased its use.
Chinese geneticists have introduced human genes associated with human milk proteins into the embryos of dairy cows, then implanted the embryos into surrogate cows that gave birth to the calves. When these animals began producing milk, it contained many proteins and antibodies that are found in human milk but not in milk from normal cows. Moreover, the genetically engineered animals are capable of reproducing themselves with the introduced genetic traits passed on. At present, there is a herd of 300 such animals at the State Key Laboratory of Agrobiotechnology of the China Agricultural University, producing milk that is much closer to human breast milk than cow milk. Scientists in Argentina, at the National Institute of Agribusiness Technology in Buenos Aires, claim to have improved on this process.
Scientists in the U.S. applied for regulatory approval in 2012 to introduce the first genetically engineered animal intended for direct consumption by human beings—a salmon modified with an extra growth hormone gene and a genetic switch that triggers the making of growth hormone even when the water temperature is colder than the threshold for normal production of growth hormone, resulting in a growth rate twice as fast as a normal salmon, which means it will reach market size in only sixteen months, compared to the normal thirty months.
Opponents of the “super salmon” have expressed concern about the possibility of increased levels of insulin-like growth factor—the same issue they have with milk produced from cattle injected with bovine growth hormone. And they expressed concern about these modified salmon escaping from their pens to breed with wild salmon, changing the species in an unintended way—much as the opponents of GM crops have expressed concern about the crosspollination of non-GM crops. Moreover, as noted in Chapter 4, farmed fish are fed fishmeal made from ocean fish in a pattern that typically requires three pounds of wild fish for each pound of farmed fish.
Scientists in Canada at the University of Guelph attempted to market genetically engineered pigs with a segment of mouse DNA introduced into their genome in order to reduce the amount of phosphorus in their feces. They called their creation Enviropigs because phosphorus is a source of algae blooms when dumped into rivers and creates dead zones where the rivers flow into the sea. They later abandoned their project and euthanized the pigs, in part because of opposition to what some critics have taken to calling “Frankenfood”—that is, food from genetically modified animals—but also because scientists elsewhere engineered an enzyme, phytase, which, when added to pig feed, accomplishes the same result hoped for with the ill-fated Enviropig.
In addition to the efforts to modify livestock and fish, there have also been initiatives over the last fifteen years to genetically engineer insects, in
cluding bollworms and mosquitoes. Most recently, a British biotechnology company, Oxford Insect Technologies (or Oxitec), has launched a project to modify the principal (though not the only) species of mosquito that carries dengue fever, in order to create mutant male mosquitoes engineered to produce offspring that require the antibiotic tetracycline in order to survive.
The larvae, having no access to tetracycline, die before they can take flight. The idea is that the male mosquitoes, which, unlike females, do not bite, will monopolize the females and impregnate them with doomed embryos, thereby sharply reducing the overall population. Although field trials in the Cayman Islands, Malaysia, and Juazeiro, Brazil, produced impressive results, there was vigorous public opposition when Oxitec proposed the release of large numbers of their mosquitoes in Key West, Florida, after an outbreak of dengue fever there in 2010.
Opponents of this project have expressed concern that the transgenic mosquitoes may have unpredictable and potentially disruptive effects on the ecosystem into which they are released. They argue that since laboratory tests have already shown that a small number of the offspring do in fact survive, there is an obvious potential for those that survive in the wild to spread their adaptation to the rest of the mosquito population over time.
Further studies may show that this project is a useful and worthwhile strategy for limiting the spread of dengue fever, but the focus on genetically modifying the principal mosquito that carries the disease poses a sharp contrast to the complete lack of focus on the principal cause of the rapid spread of dengue. The disruption of the Earth’s climate balance and the consequent increase in average global temperatures is making areas of the world that used to be inhospitable to the mosquitoes carrying dengue part of their expanding range.
According to a 2012 Texas Tech University research study of dengue’s spread, “Shifts in temperature and precipitation patterns caused by global climate change may have profound impacts on the ecology of certain infectious diseases.” Noting that dengue is one of those diseases, the researchers projected that even though Mexico has been the main location of dengue fever in North America, with only occasional small outbreaks in South Texas and South Florida, it is spreading northward because of global warming.
Dengue, which now afflicts up to 100 million people each year and causes thousands of fatalities, is also known as “breakbone fever” because of the extreme joint pain that is one of its worst symptoms. Simultaneous outbreaks emerged in Asia, the Americas, and Africa in the eighteenth century but the disease was largely contained until World War II; scientists believe it was inadvertently spread by people during and after the war to other continents. In 2012, there were an estimated 37 million cases in India alone.
After it was spread by humans to the Americas, dengue’s range was still limited to tropical and subtropical regions. But now, as its habitat expands, researchers predict that dengue is likely to spread throughout the Southern United States and that even northern areas of the U.S. are likely to experience outbreaks during summer months.
THIS CHAPTER BEGAN with a discussion of how we are, for the first time, changing the “being” in human being. We are also changing the other beings to which we are ecologically connected. When we disrupt the ecological system in which we have evolved and radically change the climate and environmental balance to which our civilization has been carefully configured, we should expect biological consequences larger than what we can fix with technologies like genetic engineering.
After all, human encroachment into wild areas is responsible for 40 percent of the new emerging infectious diseases that endanger humans, including HIV/AIDS, the bird flu, and the Ebola virus, all of which originated in wild animals forced out of their natural habitat by human encroachment, or brought into close proximity with livestock when farming expanded into previously wild regions. Veterinary epidemiologist Jonathan Epstein said recently, “When you disrupt the balance, you are precipitating the spillover of pathogens from wildlife to livestock to humans.” Overall, 60 percent of the new infectious diseases endangering humans came originally from animals.
THE MICROBIOME
We also risk disrupting the ecological system within our bodies. New research shows the key role played by microbial communities within (and on) every person. Indeed, all of us have a microbiome of bacteria (and a much smaller number of viruses, yeasts, and amoebas) that outnumber the cells of our bodies by a ratio of ten to one. In other words, every individual shares his or her body with approximately 100 trillion microbes that carry 3 million nonhuman genes. They live and work synergistically with our bodies in an adaptive community of which we are part.
Early in 2012, 200 scientists who make up the Human Microbiome Project published the genetic sequencing of this community of bacteria and found that there are three basic enterotypes—much like blood types—that exist in all races and ethnicities, and are distributed in all populations without any link to gender, age, body mass, or any other discernible markers. All told, the team identified eight million protein-coding genes in the organisms, and said that half of them have a function that the scientists still do not understand.
One of the functions performed by this microbiome is the “tutoring” of the acquired immune system, particularly during infancy and childhood. According to Gary Huffnagle, of the University of Michigan, “The microbial gut flora is an arm of the immune system.” Many scientists have long suspected that the repeated heavy use of antibiotics interferes with this tutoring process and may do damage to the process by which the adaptive immune system learns precision in discriminating between invaders and healthy cells. What all autoimmune diseases have in common is the inappropriate attack of healthy cells by the immune system, which needs to learn to distinguish invaders from cells of the body itself. “Autoimmune” means immunity against oneself.
There is mounting evidence that inappropriate and repeated use of antibiotics in young children may be impairing the development and “learning” of their immune systems—thereby contributing to the apparent rapid rise of numerous diseases of the immune system, such as type 1 diabetes, multiple sclerosis, Crohn’s disease, and ulcerative colitis.
The human immune system is not fully developed at birth. Like the human brain, it develops and matures after passage through the birth canal. (Humans have the longest period of infancy and helplessness of any animal, allowing for rapid growth and development of the brain following birth—with the majority of the development and learning taking place in interaction with the environment.) The immune system has an innate ability at birth to activate white blood cells to destroy invading viruses or bacteria, but it also has an acquired—or adaptive—immune system that learns to remember invaders in order to fight them more effectively if they return. This acquired immune system produces antibodies that attach themselves to the invaders so that specific kinds of white blood cells can recognize the invaders and destroy them.
The essence of the problem is that antibiotics themselves do not discriminate between harmful bacteria and beneficial bacteria. By using antibiotics to wage war on disease, we are inadvertently destroying bacteria that we need in order to remain in a healthy balance. “I would like to lose the language of warfare. It does a disservice to all the bacteria that have co-evolved with us and are maintaining the health of our bodies,” said Julie Segre, a senior investigator at the National Human Genome Research Institute.
One important bacterium in the human microbiome, Helicobacter pylori (or H. pylori), affects the regulation of two key hormones in the human stomach that are involved in energy balance and appetite. According to genetic studies, H. pylori has lived inside us in large numbers for 58,000 years. Up to 100 years ago, it was the single most common microbe in the stomachs of most human beings. As reported in an important 2011 essay in Nature by Martin Blaser, professor of microbiology and chairman of the Department of Medicine at NYU School of Medicine, however, studies have found that “fewer than 6 percent of children in the United States, Sweden a
nd Germany were carrying the organism. Other factors may be at play in this disappearance, but antibiotics may be a culprit. A single course of amoxicillin or a macrolide antibiotic, most commonly used to treat middle-ear or respiratory infections in children, may also eradicate H. pylori in 20–50% of cases.”
It is important to note that H. pylori has been found to play a role in both gastritis and ulcers; the Australian biologist who won the 2005 Nobel Prize in Medicine for discovering H. pylori, Dr. Barry Marshall, noted, “People have been killed who didn’t get antibiotics to get rid of it.” Still, several studies have found strong evidence that people who lack H. pylori “are more likely to develop asthma, hay fever or skin allergies in childhood.” Its absence is also associated with increased acid reflux and esophageal cancer. Scientists in Germany and Switzerland have found that the introduction of H. pylori into the guts of mice serves to protect them against asthma. Among people, for reasons that are not yet fully understood, asthma has increased by approximately 160 percent throughout the world in the last two decades.
One of the hormones regulated by H. pylori, ghrelin, is one of the keys to appetite. Normally, the levels of ghrelin fall significantly after someone eats a meal, thus signaling to the brain that it’s time to stop eating. However, in people missing H. pylori in their guts, the ghrelin levels do not fall after a meal—so the signal to stop eating is not sent. In the laboratory run by Martin Blaser, mice given antibiotics sufficient to kill the H. pylori gained significant body fat on an unchanged diet. Interestingly, while scientists have long said that they cannot explain the reason why subtherapeutic doses of antibiotics in livestock feed increase the animals’ weight gain, there is now new evidence that it may be due to changes in their microbiome.
