Is That a Fact?
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Is That a Fact?

Frauds, Quacks, and the Real Science of Everyday Life

Joe Schwarcz

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eBook - ePub

Is That a Fact?

Frauds, Quacks, and the Real Science of Everyday Life

Joe Schwarcz

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About This Book

The bestselling "quackbuster" and "tireless tub-thumper against pseudoscience" fishes for the facts in a flood of misinformation ( Maclean's ). Eat this and live to 100. Don't, and die. Today, hyperboles dominate the media, which makes parsing science from fiction an arduous task when deciding what to eat, what chemicals to avoid, and what's best for the environment. In Is That a Fact?, bestselling author Dr. Joe Schwarcz carefully navigates through the storm of misinformation to help us separate fact from folly and shrewdness from foolishness. Are GMOs really harmful? Or could they help developing countries? Which "miracle weight-loss foods" gained popularity through exuberant data dredging? Is BPA dangerous or just a victim of unforgiving media hype? Is organic better? Schwarcz questions the reliability and motives of "experts" in this "easy-to-understand yet critical look at what's fact and what's plain nonsense. "Takes its readers through the carnival of pseudoscience, the morass of half-truths and, finally, the relatively safe road of reproducible scientific knowledge. This journey is made all the more enjoyable by Dr. Schwarcz's surgical use of words and his mastery of public writing... [He] can always be counted on to write about the chemistry of the world in a way that is both entertaining and educational." — Cracked Science "Written with a light touch and refreshing humor, this book provides a solid, authoritative starting point for anyone beginning to look at the world with a skeptical eye and a refresher for those further along that path." — Library Journal

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Publisher
ECW Press
Year
2014
ISBN
9781770905283
WHITE
It’s in the Can!
It may not be quite on par with the Manhattan Project or with the challenge of beating the Soviets to the moon, but the race to find a substitute for the lacquer used to line food cans is heating up. The canning industry is frantically trying to find a replacement for the epoxy resin currently being used because of concerns that bisphenol A (BPA), the chemical we have already encountered as an “endocrine disruptor,” may be leaching into the contents. BPA is combined with other components to form a polymer that keeps the metal from reacting with the food. Once the BPA has been incorporated into the polymer, it no longer has any hormonal effects, but there are always traces of unreacted BPA left over that can indeed leach out. Before exploring this issue, however, a bit of history is in order.
Napoleon, as many other generals before him, discovered that soldiers do not fight well on empty stomachs. And stomachs were often empty due to the difficulty of supplying food to massive traveling armies. So the emperor offered a prize of 12,000 francs, a healthy amount of money at the time, to anyone who could come up with a viable method of preserving food.
This challenge was taken up by Nicholas Appert, who, as the son of an innkeeper, had learned about brewing and pickling. He knew these “fermentation” methods could be halted by heat, and he began to wonder if food spoilage could also be stopped in this fashion. After all, it was clear that cooked food kept longer than fresh food, although eventually it too would spoil. Years of experimentation led Appert to make a critical discovery: if food was sealed in a glass jar and then heated, it would keep for a remarkably long time. Long enough to please Napoleon, at least, as he awarded the prize to Appert in 1809. The method clearly worked, although nobody at the time understood why. Bacteria were not identified as the cause of food spoilage until another famous Frenchman, Louis Pasteur, came along later in the century.
Appert’s invention came to the attention of Peter Durand in England, who was troubled by the use of glass jars because they often broke. There had to be a better way! Why not a metal container? Iron was the first choice. But it would corrode, especially when exposed to acidic foods. A coating that would protect it from the air and contents had to be found. Tin, concluded Durand, would do the job! The metal had been known since antiquity and could easily be melted and applied to iron as a coating to make tin plate. And, most importantly, tin did not corrode. By 1818, the British Company Donkin and Hall was mass-producing food in tin cans. When Admiral Parry sailed to the Arctic Circle in 1824, he and his crew subsisted on canned food. One can of roast veal apparently was not consumed, because it turned up in a museum 114 years later. Inquisitive scientists opened it and decided to check the effectiveness of the canning process. They were not quite brave enough to try the veal themselves, but the rats and cats that had the pleasure of partaking of the 114-year-old feast not only survived, but thrived!
Although tin did not corrode, small amounts did dissolve, resulting in tainted food. This also meant the possibility of forming microscopic holes through which bacteria could enter and undermine the canning process. Aluminum eventually turned out to be more suitable for cans but still presented the problem of the metal interacting with the food. Chemists now stepped into the picture and found that an epoxy resin made by reacting bisphenol A with epichlorohydrin was excellent for providing a barrier that was stable under the high heat and pressure of sterilization, did not crack if the can was dented, and stood up well to the varying acidity of different foods.
Epoxy resins performed admirably, but cracks, figuratively speaking, began to appear in the early 1990s. By then, analytical techniques had been developed to detect extremely small amounts of BPA, and more importantly, the hormonal effects of this chemical were being demonstrated by its effects on the multiplication of cultured breast cancer cells. In 1995, researchers at the University of Granada in Spain investigated a number of canned foods and found estrogenic activity in peas, artichokes, green beans, corn, and mushrooms, but not in asparagus, palm hearts, peppers, or tomatoes. The authors pointed out that while an estrogenic effect was observed, it was far less than that observed for estradiol, the body’s naturally occurring estrogen.
The significance of the estrogenic effect of canned foods is difficult to estimate given that, on top of the estrogen produced by the body, as we have previously seen, we are exposed to a wide variety of natural estrogenic compounds found in foods that include milk, chickpeas, soybeans, vegetable oils, cabbage, flaxseeds, and oats. It should also be noted that the concentration of pure bisphenol A required to produce maximum proliferation of breast cancer cells in the laboratory is 1,000-fold greater than for estradiol.
Even though no risk from traces of BPA in canned foods has been demonstrated, there is clamor for invoking the “precautionary principle,” which aims to prevent harm even when the evidence is not fully in. For food companies, pleasing consumers is a high priority, whether consumers’ demands are justified or not. So the race is on to find substitutes for epoxy resins. In some cases, for low-acid foods such as beans, plant extracts that harden into a resin have met with success. For other foods, companies are looking into various acrylics, polyesters, polyurethanes, and polyvinyl compounds. These do not match the performance of epoxy resin, nor is it clear that they have a better safety profile. Could we be trading in a perceived but unsubstantiated risk for a possible increased risk of food poisoning?
And one more thing: while you’ve been reading this little piece, hundreds of people have died from hunger, lack of clean water, poor sanitation, and a host of preventable diseases ranging from malaria to AIDS. By contrast, we have the luxury of worrying about traces of chemicals contaminating our ample food supply. A prescription for a dose of perspective is in order.
A Natural Conundrum
The Texas farmer was alarmed. Never before had he heard his cows bellow in this fashion. He rushed out to the pasture to see what was happening, only to be confronted by a horrific scene. The previously healthy animals were either staggering around or writhing on the ground. Eventually, fifteen of the eighteen cattle in the field perished. The veterinarian who conducted the necropsies concluded they had been poisoned by cyanide. The culprit, as it turned out, was the grass the cattle had been grazing on, a hybrid of two other grasses. It contained “cyanogens,” compounds capable of releasing cyanide! So much for the facts. Now for some butchering of the same.
The world first heard about the cattle catastrophe from a CBS correspondent in Elgin, Texas, who, to the obvious delight of the anti-GMO crowd, filed a report under the headline “Genetically Modified Grass Linked to Cattle Deaths.” Before long, a herd of bloggers and journalists piped in with alarmist stories about how “Genetically Modified Grass Kills Cattle by Producing Warfare Chemical Cyanide.” But they were too quick to pull the trigger. They had not done their homework. The grass in question was not genetically modified; at least, not in the fashion that activists worry about. It was a hybrid grass, a product of traditional crossbreeding, and was in no way a novel product, having been around since 1983. It was, however, for some reason, in this particular pasture, producing an unusually large amount of cyanide.
Production of cyanide by plants is not a rare phenomenon. More than 2,600 cyanide-releasing species have been identified. Within the plant, the toxin is stored in an inactive form, bound to a sugar molecule, ready to be released as hydrogen cyanide upon reaction with an enzyme stored separately in the plant’s tissues. The inactive compound and the enzyme are brought together when the plant is damaged, for example, when feasted upon by hungry insects. A whiff of cyanide and the insect is highly motivated to satisfy its hunger elsewhere. It seems these plants have evolved a mechanism to protect themselves from predators. And sometimes cattle, or even humans, can suffer the consequences as the plant unleashes its chemical defense system.
Perhaps the best example of the impact of cyanogens on humans is cassava, a plant we encountered earlier. It’s a staple for millions of people in Africa, South America, and Asia. Like a potato, cassava’s tuber-like roots can be boiled, fried, or processed into flour. The plant is easy to grow, is ­drought-resistant, and grows well without fertilizer. But it harbors a good dose of linamarin, a cyanogen. As discussed earlier, if not properly processed to rid it of cyanide, cassava can cripple or even kill. Thousands of children in Africa are victims of konzo, an irreversible paralysis of the legs caused by ingesting cyanide. Countless others suffer from headaches and dizziness due to low-grade cyanide poisoning. Drying, soaking in water, rinsing, and baking result in the cyanide being released into the air as hydrogen cyanide, but the process requires time. During periods of famine there is a tendency to shortcut procedures, and consumption of the improperly processed cassava can have tragic results.
If linamarin were eliminated from cassava, the time-consuming processing would not be needed. With the aid of genetic engineering, this is a distinct possibility. The gene that codes for the production of linamarin has been identified, and a method to silence it by interfering with the messenger RNA through which it sends out its information has been developed. Silencing cannot be total since some linamarin is needed by the plant to protect it from predators. But studies have shown that most of the linamarin is produced in the leaves from where it is ferried to the roots. Reducing leaf linamarin content by 40 percent still leaves plenty for protection and virtually eliminates the ­cyanide-producing compound from the roots. Further field trials are needed to ensure that inhibition of linimarin formation does not affect crop yields, since cyanide is a source of nitrogen and linamarin may be important in its transport from the leaves to the roots of the growing plant.
Yet another way of genetically modifying cassava may reduce its cyanide content. Cassava is quite low in protein but its content can be boosted by incorporating genes from sweet potatoes or corn that code for the production of a protein called zeolin. Enriching cassava with zeolin could save millions of children from potentially fatal protein-energy malnutrition. Furthermore, it turns out that cassava uses its natural supply of cyanide to produce the amino acids needed to build the new protein, thereby reducing the risk of cyanide toxicity. Again, further testing is required to ensure that the incorporation of the sweet potato or corn genes causes no untoward changes. But the possibility of saving human lives through genetic modification doesn’t get as much play in the press as the demise of a few cows whose deaths were wrongly attributed to genetically modified grass by a bunch of bloggers and reporters when they came across a story that was just too juicy to check properly.
So, what did happen in that Texas field? The hybrid grass does contain dhurrin, a cyanogen. That is a fact. Why this grass that has long been used in cow pastures should all of a sudden produce lethal amounts of cyanide is not clear. Cyanide content is known to vary with growth, with the highest concentrations usually found in seedlings. Stress brought on by drought can lead to cyanide release, as can the use of nitrogen fertilizer at the wrong time, and the grass in the Texas pasture is known to have been heavily fertilized. Curiously, many other farms in the area grow the same kind of grass and have not experienced any problems. At this point, the only thing we can say for sure is that the cattle tragedy had nothing to do with genetically modified organisms. Obviously, nature can do plenty of damage without any help from humans.
Out of the Mouths of Babes
“Water Balz Toy Recalled.” “35,000 Rubber Ducks in Santa, Reindeer Outfits Seized at Los Angeles Port.” Not exactly the kind of headlines you like to see. What gives?
The ducks, it seems, were trying to duck regulations about the maximum amount of plasticizers called phthalates allowed in children’s toys. But, contrary to the headline, they were not rubber ducks, they were polyvinylchloride (PVC) ducks. Had they really been rubber ducks, there would have been no issue, because rubber does not require plasticizers to make it pliable.
PVC is used in numerous items ranging from water pipes to shower curtains and, of course, toy duckies. It is a hard plastic but can be softened by blending in plasticizers. These do not react chemically with the polymer, but serve as sort of internal lubricants. Since they are not chemically bound, plasticizers, which can make up as much as 30 percent of the weight of the plastic, can leach out, albeit in small amounts. Nevertheless, this is an issue since some phthalates exhibit hormone-like properties. Since hormones can have biological effects in incredibly small amounts, there is an understandable concern about any chemical that may mimic the action of natural hormones in the body.
How do we know whether a chemical has hormone-like effects? Obviously it is not possible to purposely expose people to differing doses and watch for outcomes. Even if volunteers could be enlisted, and even if there were no ethical considerations, such a study would be practically impossible to carry out. “Endocrine disrupting effects” are subtle and may take decades to manifest. Evidence therefore comes not from randomized studies in people, but from the laboratory.
But what happens to cells in a petri dish can be very different from what happens in the body in the presence of thousands of other compounds that are either naturally produced or are introduced via eating, drinking, or breathing. Other evidence for the effect of chemicals can be obtained from observational studies that attempt to link exposure, often determined by blood or urine analysis, to measurable properties s...

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