THAT’S THE WAY THE COOKIE CRUMBLES (13 page)

The processed food industry loves salt. Sodium chloride is cheap, allows water to be retained, acts as a preservative, and enhances flavor. As one salt promoter says, “Salt is what makes things taste bad when it isn’t in them.” True enough. We may partially explain our craving for salt by attributing it to our physiological need for sodium. Without it, our nerve cells can’t transmit electrical impulses, our muscles can’t contract properly, and our body fluids go out of kilter. So it shouldn’t come as a surprise that “salty” is one of the basic human tastes. But salt does more than just add saltiness to food; it can also modify the way we perceive the other common tastes — namely, sour, bitter, and sweet.

Salt inhibits bitterness, and it can enhance sweetness. That’s why you’ll find salt in such unlikely foods as chocolate, apple pie, and breakfast cereals. Indeed, studies have shown that consumer acceptance drops dramatically when salt levels in processed foods decline. That would explain the popularity of foods such as dill pickles, hot dogs, sauerkraut, vegetable juices, cottage cheese, olives, canned soups, and pizza, which can have up to a gram of salt per serving. It isn’t hard to see how one can easily exceed the recommended intake of six grams a day.

Salt was the first seasoning our ancestors used. They got it by evaporating seawater or by mining it. We have traced the origin of salt deposits in the ground back to oceans that no longer exist; essentially, all salt is sea salt. People mined salt near Salzburg (“City of Salt”) in Austria as early as 6500 B.C., and the ancient Romans built large evaporation ponds by the sea to collect the stuff. In fact, the Romans valued salt so highly that they gave their soldiers a special allowance, known as the “salarium,” to purchase it. (Our word
salary
derives from this Latin expression.) Salt was so important that many believed the person who spilled it would attract bad luck and malevolent spirits. Tossing a little salt over the shoulder was the antidote: the grains of salt would lodge in the spirit’s eyes and distract it from the evil it was planning. Spilled salt as an omen of bad things to come was an enduring belief. In Da Vinci’s painting
The Last Supper
, we clearly see an overturned salt container in front of Judas, foreshadowing his betrayal of Jesus.

It wasn’t only for its taste that salt was so prized. It was also for its value as a preservative. When the salt concentration outside a bacterial or fungal cell is higher than it is inside, water is drawn out of the cell to reduce the outside salt concentration. This process of osmosis dehydrates the cell and eventually destroys it. That’s why our ancestors rubbed salt into wounds to reduce the risk of bacterial infection. But this would also disturb tissue cells and cause the irritation we associate with “rubbing salt into the wound.” At one time, people also preserved meat by soaking it in a brine solution or by covering it with whole grains of salt (which were known as “corn,” hence the origin of “corned beef”). Perhaps the most unusual use of salt as a preservative was devised by the seventeenth-century British authorities who put the heads of executed villains on public display to deter other criminals. They discovered that the heads would rot quickly and attract birds; the birds would strip off the flesh, leaving behind a clean skull, which was apparently less frightening. The answer to this little problem was to boil the heads in salt water so they would not putrefy.

These rogues were salted after death. But what about the possibility of salt bringing on death? Our bodies try to maintain a certain concentration of sodium in the blood. If the amount of sodium rises, the body will retain more water in order to maintain the same concentration. This increases the blood volume, so there is more blood for the heart to pump around the body. The pressure the blood exerts against the walls of the arteries intensifies, and this can lead to stroke or heart attack. But, if the body takes in less sodium, then it will retain less water, and the blood pressure should go down. “Go easy on the salt” is the advice of the physician who has diagnosed high blood pressure.

Numerous studies have shown us that about fifty percent of those suffering from high blood pressure respond to a low-sodium diet. Why not all of them? Because controlling blood pressure is more complicated than simply striking a balance between sodium and water. Calcium and potassium play important roles as well. In fact, many researchers now believe that increasing potassium and calcium intake is as important as reducing sodium intake for people with high blood pressure. This means more skim milk, more bananas, and more oranges.

While no one disputes that the low-sodium diet is an important treatment for people with high blood pressure, experts bicker when it comes to making recommendations for the public at large. Some say the argument that everyone should reduce their salt intake from about nine to six grams a day is not based on science. I think they are wrong. Many people have undiagnosed high blood pressure and would benefit from a reduced salt intake. Experiments with chimps have indicated that as salt in the diet increases, blood pressure rises. Human epidemiological studies demonstrate the same thing. Populations with low salt intake have lower blood pressure. The Yanomani Indians of Brazil add no salt to their food, and they do not develop hypertension — despite being surrounded by poisonous snakes, bugs, and researchers who constantly want to measure their blood pressure.

By contrast, we North Americans, with our penchant for salty hot dogs, chips, and pizza, are in the midst of a hypertension epidemic. Whether a reduced-salt diet lowers blood pressure in people who do not have high pressure to start with is irrelevant. Eating less salty processed food automatically translates to a healthier diet. I’m sure that spokespeople for the influential Salt Institute, an organization that promotes the use of salt, will dispute this. But I would take their comments with a grain of salt.

The young mother was surprised by the doctor’s question. “What does your little girl eat for breakfast?” “Only hot oatmeal with milk,” she answered. “Does she put any sugar on it?” the doctor queried. Now the lady became indignant. “We eat only whole, natural foods. No meat, no processed food, no sugar. Sugar is poison. We use only natural honey on the oatmeal.” And with those words she confirmed the doctor’s suspicion. The little girl’s baby brother, whom they had brought to the hospital suffering from a mysterious ailment, had botulism poisoning.

It was a bizarre case. The three-month-old baby suddenly stopped nursing, and his body became progressively floppy. Within four days, he was practically lifeless, so they rushed him to emergency. At first, the doctors suspected spinal muscular atrophy, a rare neurological disease that is essentially a death warrant. But this horrific disease doesn’t usually come on so suddenly. Such a rapid onset of symptoms smacks of poisoning. Botulism would explain the muscular flaccidity, but why wasn’t the mother affected? She swore that she’d fed the baby nothing but breast milk. The doctor, however, was not so sure. That’s what prompted him to ask those questions about the boy’s sister. Yes, she did like to help with the baby, the mother divulged. Sometimes she even pretended to feed him with an empty spoon. Now the lights flashed in the physician’s mind. When her parents weren’t watching, the little girl probably did more than pretend, treating her baby brother to a bit of her honey-laced oatmeal. Unfortunately, the honey was likely laced with the poison produced by the
Clostridium botulinum
bacterium.

Laboratory tests confirmed the physician’s suspicions by revealing the presence of the toxin in the baby’s serum and feces, as well as in the jar of honey. The little boy eventually recovered, after spending five weeks on a respirator. That’s what botulinum toxin can do to you — if you’re lucky. Want to know how poisonous the substance is? Picture a grain of salt. Now imagine dividing this grain into roughly a million pieces. Each piece will weigh about one nanogram, the amount of botulinum toxin it takes to kill a human. How did the toxin get into the honey? Easily. Spores of this deadly bacterium are everywhere. They’re in the earth, in the air, and in the pollen and the nectar that the bees gather. Spores are forms of the bacterium that exist in a sort of suspended state of animation. They do not feed, and they don’t reproduce until they encounter the right conditions. Low acidity, moderate temperatures, and the absence of oxygen make them come alive and start spewing venom. Conditions in the gut are favorable to these venomous bugs, but there they encounter a problem: other bugs. The human gastrointestinal tract harbors numerous species of bacteria, which all compete for food; luckily for us, botulinum bacteria do not fare well in this contest, and they cannot establish themselves. Unless, of course, there are relatively few competing bacteria, as is the case with the gastrointestinal tracts of infants. That’s why children younger than twelve months old should not be fed bee regurgitation — that is, honey.

While we adults don’t have to worry about botulinum spores germinating in our digestive tracts, we do have to be concerned about eating food in which the bacteria have multiplied and produced their toxin. In Vancouver, thirty-seven people were poisoned when a restaurant used contaminated garlic to make garlic bread. Dirt that adheres to garlic bulbs commonly contains botulinum spores. If we store the cloves under oil in an anaerobic environment and keep the jar at room temperature, then the bacteria will come alive and produce the toxin. When this toxin enters the bloodstream, it binds irreversibly to nerve endings and prevents the release of acetylcholine, the neurotransmitter that triggers muscle activity. The result is droopy eyelids, double vision, difficulty speaking and swallowing, progressive weakness, and, finally, paralysis of the chest muscles and respiratory failure. If the victim survives the initial onslaught of the toxin, recovery is likely because the affected nerves will eventually sprout new branches capable of acetylcholine release.

Garlic in oil is not the only problem. The first account of botulism — recorded in 1822 by Justinus Kerner, a German physician — focused on sausages, which provide an internal environment conducive to the growth of the bacteria. Indeed, the term
botulism
was coined from the Latin word for sausage. Not to worry, though. Today, food processors add nitrites to sausages and hot dogs to prevent the growth of this nasty microbe. But another concern has cropped up. Oil infusions are now popular offerings in some restaurants. Adventurous chefs use vegetables, herbs, spices, and even lobster meat to flavor oil, which they then use to add a flavor dimension to a variety of dishes. If improperly prepared, these oils can be lethal. The chef must use only well-washed produce, add lemon juice or vinegar to the oil (one tablespoon per cup of oil), shake the mixture vigorously, store the infusion in the refrigerator, and keep it for no longer than a week. We can destroy botulinum toxin by boiling for ten minutes, but spores are resistant to heat. Only by cooking a contaminated food in a pressure cooker for fifteen minutes can we kill them. We are able to subject canned food to these conditions during processing, but not infusions.

Ah, I can practically see you frowning out there. But be careful. Frown too much and those wrinkles between your eyebrows could become permanent. There is a treatment, though. Ask a doctor to inject tiny amounts of botulin into the muscles of your forehead; this will paralyze them, making those wrinkles practically disappear. An ingenious use of a toxin, half a glass of which could kill the entire population of the world.

We are in the jungles of South America. It’s the late sixteenth century. Monkeys are jumping from tree to tree. Suddenly, one of them emits a shrill cry. He manages to jump to another tree and then to one more before falling to the ground, dead, an arrow protruding from his side. The poison was not a particularly potent one. The natives call it a “three tree” poison — as opposed to stronger formulations, which would be termed “two tree” or, the ultimate, “one tree.”

Sir Walter Raleigh himself witnessed such an event, and he was dumbstruck by the quickness of the monkey’s death. He asked to examine the mixture that coated the arrow. Raleigh then took a speck of the “urari,” as the stuff was called, and rubbed it between his fingers. Sir Walter must have had a small, unhealed cut on one of his fingers, because he immediately became dizzy and promptly collapsed as the poison entered his bloodstream. Luckily for him, it was only a three-tree dose.

Raleigh learned the meaning of “urari” the hard way. In the language of the natives, the word meant “he to whom it comes, falls.” He also learned that some tribes put the poison under their fingernails, where it would come in handy during hand-to-hand combat. Stories circulated about how certain tribe members secretly mixed the lethal brews. The tribe’s oldest women would perform the task in closed huts; if, after two days, the fumes had not killed them, the mixture would be judged too weak to use, and the women would begin work on another batch.

The active ingredient in the preparation turned out to be the root or stem of a certain species of climbing vine, known today as
Chondodendron tomentosum
. Sir Walter took a sample back to Europe, where it was given the name “curare,” derived from the Indian word for poison. No one paid much attention to the substance until 1812, when Charles Waterton learned that if he administered the right dose, he could achieve muscle relaxation without death. Doctors began using curare to treat lockjaw, infantile paralysis, and even epilepsy.

It wasn’t until 1844 that scientists started to acquire an understanding of the drug’s mechanism of action. The French physiologist Claude Bernard experimented with frogs. He found that curare blocked nerve impulses from the brain to the muscles and had the effect of relaxing the muscles to the point of limpness. Even the muscles that controlled breathing could be made to relax to the point that the frog appeared to be dead. If the dose was just right, the effect would soon wear off, and recovery was complete. One might say that the frog had experienced a living death.

The concept of living death brought fear to the hearts of nineteenth-century Europeans and Americans. Edgar Allan Poe dramatized this fear in his classic tale “The Premature Burial.” The story was written in 1844, just around the time that stories about curare’s effects began to spread. Various accounts of individuals being mistakenly declared dead and waking up inside their coffins also made the rounds. People were scandalized by stories about unearthed coffins containing skeletons with hands clutching at the lid from the inside. Some went as far as having elaborate safety mechanisms built into their coffins so that they could sound the alarm should they find themselves prematurely buried.

Poe’s tale of premature burial is haunting. The reader shares the protagonist’s panic as he emerges from a condition called “catalepsy” and discovers that he’s enclosed in a wooden container and enveloped in the smell of fresh earth. We hear his terrified screams and feel his horror as he realizes that his worst nightmare has come true. The screams, however, do bring help. Reassuring hands rouse him, and we learn that he has not, in fact, been buried alive; earlier, he’d taken refuge from a storm on a docked boat and fallen asleep in a rather cramped wooden bunk. The boat carried fertilizer, hence the smell. The burial was not real, but the panic was. Did knowledge of curare contribute to Poe’s obsession with death and to his fear of premature burial? Very possibly, since scientists working with curare had recently shown that deathlike states really did exist.

When those scientists isolated the active ingredient in Sir Walter Raleigh’s climbing vine and identified it as tubocuranine, modern medicine soon found applications for the substance. It could counter the effects of some muscle-contracting poisons, such as strychnine and tetanus toxin, and, even more importantly, it could serve as a muscle-relaxant for surgical patients. Curare greatly facilitated abdominal surgery by preventing the muscles from becoming stiff and almost impenetrable. In 1942, Dr. Harold Griffith, chairman of McGill University’s Department of Anesthesia, became the first to attempt this application, using curare during an appendectomy at Montreal’s Homeopathic Hospital (later the Queen Elizabeth Hospital). Dr. Griffith spent his life researching anesthesia, and he probably deserves more credit than anyone else for establishing the field as a medical specialty. He received numerous awards for his work, but his contributions are best encapsulated in his biographer’s comment: “There are only two eras in anesthesia, before Harold Griffith and after.”

We rarely use curare these days because more effective synthetic derivatives have supplanted it. These — including pancuronium, better known as Pavulon — are more potent, have more limited side effects, and can be given in smaller doses. But in larger doses, Pavulon can cause paralysis and death, as illustrated by a notorious 1975 criminal case.

During a six-week period, thirty-five patients suffered fatal or near-fatal cardiopulmonary arrest in a veterans’ hospital in Ann Arbor, Michigan. All of them had been on intravenous lines. The FBI investigated and found Pavulon in the tissues of the five patients who had died. The bureau charged two nurses, both from the Philippines, with murder and attempted murder. The prosecution claimed that the women were trying to dramatize the need for more nurses. Imelda Marcos, the first lady of the Philippines, paid for part of their defense, insisting that the FBI had trumped up the charges in order to keep foreign nurses out of the country. Wherever the truth lay, the nurses eventually served only a few months in jail. They were released when a mysterious judgment was issued claiming that irregularities had occurred during the trial. Some people say that Imelda had threatened to make trouble over American bases in the Philippines. Perhaps, in this case, curare paralyzed the long arm of the law.