High Seas and Hi-C

[W]hat is the function of these vitamines? 

If fats and carbohydates provide the fuel, and proteins the material 

for tissue supply, and mineral salts are needed for bone construction, etc.,

just what do the vitamines supply? We do not know.

— Benjamin Harrow, The Vitamines: Essential Food Factors, 1922

The first time I saw a vitamin in pure form—as opposed to just gulping one down in a pill—was in Parsippany, New Jersey. It was a drizzly November day, and I was visiting the Nutrition Innovation Center, a product-?development facility run by the world’s largest synthetic vitamin producer, the Dutch company DSM.

Companies come to the center to brainstorm and create new products, harnessing the expertise of DSM’s chemists and flavor technicians to add vitamins and other so-called functional ingredients to their foods. But I hadn’t come to develop a new fortified beverage or cereal or snack bar. My goal was more basic: after more than three decades of eating and taking vitamins, I had come to the center to learn what vitamins actually are.

My host for the day was DSM’s senior director of global technical marketing, a French-?born pharmacist and PhD named Jean-?Claude Tritsch, who had ear-?length graying hair and wore a pink V-neck sweater. We were in the room where product concepts are shared and sampled with food and supplement companies, and Tritsch was explaining the basics of vitamins from behind a wet bar as I sat perched on a high stool at a granite countertop, a selection of product prototypes arranged in front of me.

When we hear the word “vitamin,” many of us immediately think of pills; we also tend to mistakenly apply the term to all dietary supplements, and often lump vitamins and minerals together. But as Tritsch explained, there are actually only thirteen human vitamins, all of which are organic compounds that occur naturally in food. Four are fat-?soluble, meaning they dissolve in fat and need fat to be absorbed: A (retinol), D (cholecalciferol), E (tocopherol), and K (phylloquinone). The other nine are water-?soluble: C (ascorbic acid) and the eight substances grouped together in what’s called the B complex— B1 (thiamin), B2 (riboflavin), B3 (niacin), B5 (pantothenic acid), B6 (pyridoxine), B7 (biotin, also sometimes referred to as vitamin H), B9 (folate/folic acid), and B12 (cobalamin). Sometimes choline is counted as a fourteenth vitamin, but usually the roster ends at thirteen. (Some vitamins come in more than one chemical form— the parentheticals refer to the most common or the most relevant.)

Unlike the macronutrients (fat, protein, and carbohydrate), vitamins are not burned as fuel; instead, their primary role is to facilitate chemical reactions in our bodies that keep us alive. Vitamins, Tritsch told me, are thus considered essential micronutrients— essential because our bodies require them but can’t make sufficient quantities, which means we need to get them from outside sources, and micro because we only need them in really small amounts, typically fewer than 100 milligrams a day.

Indeed, we need vitamins in amounts so tiny that it’s difficult to visualize them, let alone to believe that our lives depend on them. The amount of folic acid that pregnant women are told to take to prevent devastating neurological defects in their babies is 240 micrograms a day, less than the weight of two grains of Morton salt. The Recommended Dietary Allowance for vitamin D, without which you won’t be able to properly absorb calcium and your bones will soften, is 15 micrograms (600 IU), one-?sixteenth of that for folic acid. And the RDA for B12, a vitamin whose deficiency can cause depression, delusions, memory loss, incontinence, nerve damage, and in extreme cases life-?threatening anemia, is smaller still, just 2.4 micrograms—0.0000024 grams. That’s 1/ 100th of the weight of the requirement for folic acid, the equivalent of 1/ 67th of one grain of salt.

Searching for a way to make those tiny numbers tangible, Tritsch let me taste and smell several samples of pure vitamins that were kept on hand at the lab. Vitamin C was a talc-?like white powder, tart like a Super Lemon candy and very irritating, I discovered with the help of a paper cut, if rubbed into an open wound. Thiamin was bitter and white. Powdered riboflavin was the color of butternut squash. Folic acid was yellow and tasted chalky. A and D were clear, sticky, meltable crystals, so concentrated and unstable that they’re usually dissolved in oil. E was a tasteless, viscous clear fluid. Vitamin B12 was bright pink.

By the time I left the Innovation Center, I’d seen diagrams of vitamins’ chemical structures and magnified photographs of individual molecules, colorful crystals that sparkled in the light. But even after I’d touched them, tasted them, and smelled them, I still couldn’t wrap my head around what I was experiencing. It seemed somehow impossible that these odorless, unassuming substances could be essential for keeping me—and every one of us—alive.

The problem, I realized, was that I still didn’t understand what vitamins do in our bodies—which is a necessary concept to grasp if you want to understand why a deficiency could kill you. So I decided to look for an explanation in the vitamin I thought I knew the best: vitamin C.

Most people know that if you don’t have enough vitamin C, you’ll develop a vitamin deficiency disease called scurvy, and you have probably heard tales of sailors on long sea voyages whose teeth fell out as a result. But having loose teeth, while certainly unpleasant, doesn’t sound life-threatening. And besides, scurvy can be cured by drinking orange juice. How serious could it really be?

Really serious, it turns out. Far from just affecting their gums, scurvy killed more than two million sailors between Columbus’s 1492 transatlantic voyage and the rise of steam engines in the mid-?nineteenth century. It was such a problem that ship owners and governments counted on a 50 percent death rate from scurvy for their sailors on any major voyage; according to historian Stephen Bown, scurvy was responsible for more deaths at sea than storms, shipwrecks, combat, and all other diseases combined.

Scurvy starts with lethargy so intense that people once believed laziness was a cause, rather than a symptom, of the disease. Your body feels weak. Your joints ache. Your arms and legs swell, and your skin bruises at the slightest touch. As the disease progresses, your gums become spongy and your breath fetid; your teeth loosen and internal hemorrhaging makes splotches on your skin. Old wounds open; mucous membranes bleed. Left untreated, you will die, likely as the result of a sudden hemorrhage near your heart or brain.

Bown quotes a survival story written by an unknown surgeon on a sixteenth-?century English voyage that illustrates scurvy’s horror. “It rotted all my gums, which gave out a black and putrid blood,” he wrote. “My thighs and lower legs were black and gangrenous, and I was forced to use my knife each day to cut into the flesh in order to release this black and foul blood. I also used my knife on my gums, which were livid and growing over my teeth. . . . When I had cut away this dead flesh and caused much black blood to flow, I rinsed my mouth and teeth with my urine, rubbing them very hard. . . . And the unfortunate thing was that I could not eat, desiring more to swallow than to chew. . . . Many of our people died of it every day, and we saw bodies thrown into the sea constantly, three or four at a time.”

Scurvy affected many of the explorers we learned about in grade school—Vasco da Gama lost his brother to it; Ferdinand Magellan watched it kill many of his men, who had been reduced, he wrote, to existing on “old biscuit reduced to powder, and full of grubs, and stinking from the dirt which the rats had made on it when eating the good biscuit.” Scurvy killed so many men on the 1740–1744 voyage commanded by a British captain named George Anson that it is considered one of history’s worst medical disasters at sea.

When reading about such experiences, it’s difficult not to want to travel back in time, grab these men by the shoulders, and beg them to eat some lemons. The idea that certain foods can cure scurvy wouldn’t even have been a new idea—in 1535, French explorer Jacques Cartier reported that after his ships had become frozen in the St. Lawrence River, his men were saved from scurvy by a special tea, prepared by the local Native Americans from the bark and leaves of a particular tree. In the 1500s and 1600s, several ships’ captains suggested that there might be a connection between produce and scurvy. In 1734, a Dutch physician named Johannes Bachstrom came up with the term “antiscorbutic”—against scurvy— and used it to describe fresh vegetables.

Even Anson—captain of the aforementioned disastrous voyage—made a point of loading up on oranges whenever possible, and his chaplain, Richard Walter, described certain vegetables as being “esteemed to be particularly adapted to the cure of those scorbutic disorders which are contracted by salt diet and long voyages.” But while many mariners recognized that there was a connection between sailors’ diets and their susceptibility, no one knew the true cause of scurvy, or what made certain foods antiscorbutic.

Today, scientists understand the connection, and it has to do with what vitamins are actually doing in our bodies. Despite their chemical differences, all vitamins play crucial roles in our metabolism, a term that refers to the series of chemical reactions that occur in our cells. Though we are rarely aware of these metabolic chemical reactions, our lives depend on them. Walking down the street requires them. Reading a book requires them. So does forming scar tissue, developing a baby, or creating any type of new cell. Chemical reactions build and break down muscle, regulate body temperature, filter toxins, excrete waste, support our immune systems, and affect (or indeed cause) our moods. They generate the energy we need in order to breathe, and use the oxygen that we breathe to pull energy from food. They allow us to feel and see and taste and touch and hear. Our metabolisms aren’t just a facet of our lives— they are our lives. Without these metabolic chemical reactions, we would be as inert and inanimate as stone.

The problem with many of these reactions, however, is that they’re way too slow—if they were left to run at their own speed, life would grind to a halt. Our bodies get around this issue with the help of enzymes, which are large protein molecules that kick-start and speed up specific chemical reactions, often making them occur millions of times faster than they would on their own. But our bodies sometimes need help making enzymes, and enzymes sometimes need help doing their jobs. That’s where vitamins come in: two of their primary functions are to help our bodies create enzymes and to aid enzymes in their work. While enzymes speed up chemical reactions without being destroyed, most of the chemical reactions that depend on vitamins actually use up the vitamins. That’s why we need a continuous external supply.

It makes sense, then, that vitamin deficiencies cause problems, because without adequate vitamins, every enzymatic process that depends on those vitamins will come screeching to a stop. In the case of scurvy, the issue is collagen, a primary structural protein in our muscles, skin, bones, blood vessels, cartilage, scars, and other connective tissues that makes up some 30 percent of the protein in the human body. Collagen holds our tissues together; the word itself is derived from the Greek word for “glue.” Without collagen, our bodies would come apart from within—hence the hemorrhaging, broken bones, and loose teeth of scurvy. We make collagen from its precursor, procollagen, with the help of enzymes. But those enzymatic reactions can’t happen—and thus collagen cannot be formed—without vitamin C.

With that said, scientists still don’t fully understand all the nuances of what vitamins do in our bodies, how they do it, or what the long-?term effects of moderate deficiencies might be. That, in turn, makes it extremely difficult to create precise nutritional recommendations. In the words of a 2003 report from the nongovernmental Food and Nutrition Board at the National Academy of Sciences’ Institute of Medicine, “[s]cientific data have not identified an optimum level for any nutrient for any life stage or gender group, and [today’s nutritional recommendations] are not presented as such.” Instead, the same report explains that “a continuum of benefits may be ascribed to various levels of intake of the same nutrient.”

In fact, the RDAs themselves—which many of us use as personalized scorecards for our diets—are actually not meant to be personal at all. Instead, they’re designed to meet the nutritional needs of 97 to 98 percent of all people, which means that the majority of us could get by just fine on less. (There’s also no need to get 100 percent of your RDA every day—what’s important is your consumption over time, since our bodies maintain stores of most micronutrients.) And even with that generous built-in margin for error, the Food and Nutrition Board, which is responsible for updating the country’s RDAs, still has not established adult RDAs for biotin, pantothenic acid, or vitamin K, and there are no RDAs for infants up to one year old for any vitamin.

It’s also still surprisingly difficult to measure vitamins, whether in our bodies or in foods. Blood tests exist for several, but there are often problems with standardization (that is, results from the same sample can vary from one lab to the next), and there’s continued controversy over what the cut off for “deficiency” should be. Adding to the challenge, some vitamins are stored in inaccessible places in the body—the most accurate way to measure vitamin A would be a liver biopsy—and our vitamin levels can vary considerably by day or by season depending on what we eat. If you eat a lot of pink grapefruit, for example, your vitamin C level will spike within hours. If you smoke a cigarette, it will drop (as will that of folate). If it’s summertime, your vitamin D level will likely be higher than it is in the winter, when you’re less likely to be out in the sun and usually cover more of your skin with clothing. And as if that’s not enough, the vitamin information on food labels is often based on composites, meaning that even if you knew your body’s precise vitamin requirements, you wouldn’t be able to calculate exactly what percentage of those requirements were represented by the food on your plate.

But despite these continued uncertainties, we definitely know more than early explorers, who weren’t aware of vitamins at all. As for the era’s doctors and scientific thinkers, they not only lacked the analytical tools and chemical knowledge necessary to even conceive of a nutritional deficiency disease, but many popular hypotheses about scurvy’s cause were still related to the ancient theory of the humors, which assumed that people’s innate constitutions influenced their likelihood of getting sick, and that disease should be treated by balancing four “humors” that flowed through the body: black bile, yellow bile, blood, and phlegm. Supposed triggers were even more haphazard. According to author Frances Rachel Frankenburg, they ranged from fatigue and depression to homesickness, contagion, seawater, damp air, copper pans, tobacco, hot climate, cold climate, rats, heredity, contagion, fresh fruit (whoops), too much exercise, too little exercise, sea air, salted meat, poor morals, and filth.

And even if the concept of vitamins had been familiar, vitamin C would have been a tough one to figure out. Humans and several other simians— along with guinea pigs and fruit bats— are the only mammals that can’t make their own vitamin C. In other creatures, it’s referred to as “ascorbic acid” (shorthand for antiscorbutic) and, since their bodies can produce it in sufficient quantities, isn’t considered a vitamin at all.

It’s also not obvious where to find vitamin C. There are large amounts in liver and kidneys, but not in muscle meat. Eggs and cheese don’t have any. Cabbage and broccoli have a lot. A half cup of pears will give a woman about 4 percent of her 75 mg/ day RDA, but the same amount of kiwifruit will give her 111 percent. Once the connection between citrus fruit and scurvy had been recognized and accepted, Britain often supplied its sailors with limes— which it chose instead of lemons because it controlled colonies that grew them (hence the nickname “limey” for British sailors). But this thriftiness came at a price: limes have only half as much vitamin C as lemons and oranges. Preparation matters, too. The proponents of “rob,” a popular treatment made from boiled-?down citrus juice, had the right idea, except guess what? Vitamin C is destroyed by heat—not to mention cutting, bruising, exposure to air, and being cooked in copper pots.

As a result, the confusion over scurvy was so great that even James Lind, the person who gets the most credit for establishing that citrus fruit cures scurvy, overlooked his own discovery—making vitamin C an early example of how complicated the overall process of discovering vitamins turned out to be.

Lind was a Scottish physician who served as a naval surgeon on the British HMS Salisbury in 1747, and devised what is considered to be one of the world’s first controlled experiments. First, he took twelve sailors who were sick with scurvy and divided them into six pairs. All the men ate the same food and lived in the same quarters on the ship; the only difference was their treatment. Lind gave each pair daily doses of one of six different supposed scurvy cures: a quart of hard cider, twenty-five drops of vitriol (a mixture of sulfuric acid and alcohol), two spoonfuls of vinegar, a half pint of seawater, two oranges and one lemon, and last, an “electuary”— a creative mix of garlic, mustard seed, balsam of Peru, dried radish root, and gum myrrh, shaped into a pasty concoction the size of a nutmeg. Lest that treatment not sound random enough, those sailors also got barley water treated with tamarinds and an occasional laxative dose of cream of tartar. With the exception of the citrus fruit, which ran out in less than a week, Lind administered the treatments for fourteen days.

As the diversity of treatments indicates, Lind’s experiment had no foregone conclusion. Nonetheless, it didn’t take long for one intervention to emerge as better than the others: the men treated with citrus fruits recovered so thoroughly and rapidly that they were able to help Lind care for the others. Because of this experiment, Lind is often given historical credit for recognizing citrus as a definitive cure for scurvy. But that’s not actually what happened.

Instead, when Lind retired from the navy in 1748, he got to work on the first edition of a massive book called A Treatise of the Scurvy: Containing an Inquiry into the Nature, Causes, and Cure, of That Disease Together with a Critical and Chronological View of What Has Been Published on the Subject. True to its sweeping title, it ended up being some four hundred pages long. Lind described his crucial experiment in five paragraphs about two hundred pages into the book, and condensed the key result into one seriously downplayed sentence: “As I shall have occasion elsewhere to take notice of the effects of other medicines in this disease, I shall here only observe that the results of all my experiments was, that oranges and lemons were the most effectual remedies for this distemper at sea.”

Lind wasn’t trying to bury the lead; he just didn’t recognize the significance of his results. Sure, the oranges and lemons had cured scurvy, but the sailors who got the cider seemed a little better, too. This is plausible, since the unrefined hard cider Lind distributed might have contained a little of the vitamin. And so rather than dwell on citrus, Lind moved on to describe his own humors-?inspired explanation of scurvy: it was actually a digestive disease caused by blocked sweat glands.

By the time Lind published the third edition of his book in 1772, he had completely lost sight of what we now consider his most important observations. While he did still think lemon juice might be effective against scurvy—he thought it might clear out those blocked sweat glands, especially if mixed with wine and sugar— he included so many disclaimers that his argument was hardly convincing. “I do not mean to say that lemon juice and wine are the only remedy for the scurvy,” he wrote. “This disease, like many others, may be cured by medicines of very different, and opposite qualities to each other, and to that of lemons.”

Nonetheless, progress was gradually made. It had to be: as the size of the world’s navies increased, the problem of scurvy only grew worse—and it

wasn’t long before the search for a cure for scurvy became what Stephen Bown describes as “a vital factor determining the destiny of nations.” In 1795, a physician named Gilbert Blane convinced the British navy to issue some form of lemon juice to its sailors. His order likely changed the course of history when it helped Great Britain to successfully defend itself from a Napoleon-?led invasion by setting up a blockade of the English Channel. This blockade, during which many ships spent months on the water without coming to port, went on for twenty years—a feat that scurvy would never have allowed.

Yet no matter how many times the connection between scurvy and produce was demonstrated, people kept forgetting it; cures for scurvy— like those for many of the other vitamin deficiency diseases— continued to be lost and found and lost again. Scurvy appeared in Arctic explorations of the 1820s and the 1848–1850 American gold rush. Florence Nightingale reported entire shiploads of cabbage being tossed overboard during the Crimean War of 1853–1856 at the same time that soldiers were perishing from the disease. (The cabbage had been sent specifically to treat scurvy, but thanks to bureaucratic snafus, no one had ordered it to be distributed in the men’s rations.) Scurvy plagued prisoner-of-war camps in the twentieth century, and even emerged among the babies of wealthy and educated Americans and Europeans in the late 1800s and early 1900s, thanks to unfortified pasteurized cow’s milk (the heat destroyed the vitamin C). Nearly a century would pass after the British blockade before anyone truly understood why fresh fruit or cabbage was effective in preventing scurvy; till then, it continued to reappear wherever diets and circumstances allowed.

Though it might seem strange to us today, scurvy was in its time a very modern disease— an example, among many others in the story of nutrition, of how advancements in one area can lead to problems in another. True, scurvy existed in ancient times and was common in Northern Europe during the Middle Ages, when harvests were too small to provide adequate vitamin C through the long winter. But for seafarers, technology is what truly made it a concern: it only became prevalent after the development of long-?distance ships, navigational techniques that freed them from the shorelines for months at a time, and rations that, while often dangerously low in multiple vitamins, had enough calories to ensure that sailors wouldn’t starve.

In a way, scurvy was therefore an early example of a disease of civilization, a category of ailments caused by human-?driven changes in the environment. Just as public health experts now worry about what the rising rates of coronary heart disease and type 2 diabetes will do to our long-?term productivity, their predecessors had the same concerns about scurvy. Despite more than a century of separation, the underlying concerns are the same.

And even though we now know how to prevent them, vitamin deficiency diseases will never truly be relegated to the past. An estimated two billion people currently don’t have access to adequate vitamins. At least four outbreaks of scurvy have been reported worldwide since 1994. The bone-?softening vitamin D deficiency disease of rickets is prevalent in Indian slums and other areas in the developing world, and, while rare, cases have even been reported in British and American children whose diets and lifestyles don’t provide them with adequate amounts of vitamin D. Millions of people, particularly children, are deficient in vitamin A, and will go blind or die as a result. Folic acid deficiencies continue to cause devastating birth defects. General vitamin deficiencies can and do occur in refugee camps, prisons, and in any place—or in any population—without access to nutritionally adequate food.

The reason is simple, if strange to think about: despite the steady march of scientific advancement that separates us from our predecessors, there is nothing about our modern bodies that makes us invulnerable to scurvy or any other vitamin deficiency. Human beings have evolved to need vitamins; our bodies can’t function without a continuous supply. Unlike infectious diseases, which can be prevented and cured with vaccines and drugs, and sometimes wiped out entirely, there is no way the threat of vitamin deficiency diseases can ever be eradicated, or the diseases themselves permanently “beaten.” Instead, consistently good nutrition is their only prevention and their only cure. Today in America, scurvy might seem as distant as the Black Death. But take away our oranges, or our fortified foods, or our pills, and we’d be just as vulnerable as those sorry sailors.