Since the dawn of time, human beings have
known that they need to eat food to be able to survive, because it’s by eating food
that we gain our strength. In other words, food is our source of energy. Just like a
car needs gas, we need to eat food to fuel our body. But energy is not enough.
In the first years of the 19th century, French scientist Francois Magendie observed that
when he fed a group of dogs only sugar or only oil, they would all die within a month.
Sugar and oil both provided energy, but they did not provide the stuff that we need to
build and maintain the structures in our body: proteins. Proteins are our only source of
nitrogen, and without them, life is not possible. At the beginning of the twentieth century,
most scientists believed that eating was just a matter of getting two things: enough proteins,
to build and maintain our body, and enough energy to fuel it, from carbohydrates and
fats. But there was already a lot of evidence suggesting
that nutrition is much more complicated than that. It had been known for decades that food
can convey some particular ‘factors’ whose deficiency can cause disease and death. Since ancient times, for example, many suspected
that diet had something to do with scurvy, a disease that causes a progressive deterioration
of the body eventually resulting in death. Scurvy especially plagued sailors who embarked
on months-long journeys, with limited access to fresh food. And whenever for one reason
or the other, may be a famine, a war, or a siege, a population had limited access to
fresh food, the incidence of scurvy would skyrocket.
In the second half of the 18th century, Scottish physician James Lind was conducting the first
clinical trial ever recorded in the history of science, and it’s not without a little
pride that nutritionists like to tell this story, because the first clinical trial ever
was a dietary intervention. Dr Lind thought that scurvy could be treated by eating acidic
foods, and so he recruited twelve sailors affected by scurvy, and divided them in six
groups of two. They were all eating the same diet, but on top of that, each group received
a different acidic food. Most of those acidic food, like vinegar, didn’t do anything at
all. Only two groups were substantially improving: the group eating two oranges and one lemon
every day, and the group drinking a quart of fruit cider every day. In 1753, Dr Lind
reported his findings in a book, A treatise of the scurvy, which unfortunately went virtually
unnoticed. A few years later, British explorer James
Cook and his crew set sails for a very long journey of over three years. But interestingly
enough, during this whole time, he didn’t have one single case of scurvy. Of course
he couldn’t bring oranges or lemons with him, because they are all perishable: what
saved him and his crew was consumption of a rather unusual food: sauerkraut, fermented
cabbage, that contrary to fresh fruit and vegetables can be easily preserved in big
wooden barrels where its fermentation takes place.
It was clear at that point that there had to be something, in oranges, lemons, cider
and sauerkraut, that is able to prevent and cure scurvy. But it was not acidity by itself,
like Dr Lind believed. It is one specific molecule that our body needs to synthesize
collagen, and that was finally identified in 1937 by Albert Szent-Gyorgyi, who won a
nobel prize for it. This molecule is ascorbic acid, better known as vitamin C. About a century after Captain Cook’s expeditions,
a dutch scientist named Christian Eijkman was sent by his government on a mission to
Indonesia to study beriberi, a serious neurologic disease that was killing tens of thousands
of people in that region. His task was trying to identify the germ that was causing it.
Dr Eijkman came across very interesting observations. He noticed that beri beri was especially common
among those populations whose staple was white rice, and even more so among prison inmates,
whose tough diet was basically rice and little else. In some Indonesian prisons, to make
their lives even more miserable, inmates were not even given good rice, but rice mixed with
husks, the byproduct that’s left after rice milling and polishing to make white rice from
brown rice, and that was normally given to the pigs. But low and behold, among these
prisoners subjected to this very humiliating treatment, the incidence of beri-beri was
dramatically lower. Indeed, he observed time and again that when
polished white rice in a patient’s diet was replaced with whole grain brown rice,
the disease would disappear. With this information, Eijkman set up a very elegant experiment.
He took a group of chickens, and fed half of them white, polished rice, and the other
half brown, unpolished rice. The chicken fed refined rice all developed beriberi and died
very soon, while none of the chickens fed whole rice contracted the disease. At that
point, he got a group of diseased chickens and fed them just the discarded outer husks
that are left after polishing rice. The chickens all quickly recovered.
At this point, Dr Eijkman had all the pieces of information he needed to put the puzzle
together, but he was so stubbornly misled by what he had already decided, that he just
couldn’t see it. “There must be something in the outer husk of rice”, he wrote, “that
confers resistance to the beriberi germ”. We know today that there’s no beriberi germ,
beri beri is just another disease of nutrition deficiency, and specifically it is caused
by the lack of a nutrient that was finally identified in 1926. This essential nutrient
is thiamin, or vitamin B1, that is present in the external layers of rice, but is removed
when brown rice is polished to make white rice. A few decades after Dr Eijkman research, Dr
Joseph Goldberger was dealing with another disease that was plaguing several hundred
thousand people in the south of the united states, and killing about 1 in 10. It was
called pellagra, from the latin “rough skin”, characterized indeed by severe skin rashes,
and mental impairment. Most scientist again believed it was caused
by a germ, but Dr Goldberger was not convinced. If it was an infectious disease, he wondered,
then why would it be so common among prison inmates, but not their well-fed guards? This
was a disease hitting above all poor people, people whose diet was mainly made up of corn.
Dr Goldberger hypothesized that pellagra was a deficiency disease, caused by a poor diet,
and not by a germ. Among general skepticism, he went on to conduct experiments on prison
inmates affected by pellagra, and made them follow a more varied diet, including meat.
In just a few weeks, they fully recovered. To further prove his theory, he then recruited
eleven healthy prison inmates, and they accepted to go on an unbalanced, corn-based diet. In
a few months, more than half of them developed pellagra. It was obvious to Dr Goldberger
that there had to be some essential nutrient, which was absent in corn, and whose deficiency
caused pellagra. But this was not as obvious to most of his colleagues, who still believed
there had to be a germ causing pellagra, and that a poor diet was just a predisposing factor.
So to prove his point, Dr Goldberger collected pellagra patients’ skin fragments, nasal
secretions and other bodily fluids, and injected himself with them. Since indeed there was
no pellagra germ, he remained perfectly healthy. What was causing the disease was again the
lack of an essential nutrient, which was later identified as niacin, or vitamin B3, also
referred to as pellagra-preventive vitamin, PP. There was only one thing that Dr Goldberger
couldn’t figure out: he knew that the diet of many rural Mexican populations was also
based on corn, which they used to make tortillas, and yet they didn’t develop pellagra. How
was that possible? The trick is, there actually IS niacin in corn, but it is bound to proteins
in a form that is not available for absorption into our body. However, when corn is soaked
and cooked in an alkaline solution, as the Mexican did by cooking corn in limewater to
make tortillas, free niacin is released from the proteins and it becomes bioavailable.
This is why the Mexicans were not developing the disease. You are probably wondering if
the corn you eat undergoes such treatment, and the answer is yes, the canned yellow corn
kernels that you find on the shelves of your grocery store have been pre-cooked in alkaline
water to make niacin bioavailable. We could go on an on telling little stories
like these, for rickets and vitamin D, iodine and goiter, iron and anemia, and so on for
about 40 essential elements. We will tell some of these stories later in
this course when we study the vitamins and minerals, but for now, I think I have made
the point to help us understand the first goal of nutrition: we need to eat to prevent
deficiencies. Not only deficiencies of energy and proteins,
but also deficiencies of many other essential nutrients that we need in much smaller amounts,
but that are absolutely necessary to sustain life, and without which we face disease and
death. The major risks related to an unbalanced diet
today are much different than what they were in the past. In our rich, post-industrialized
countries, we don’t die of protein-energy malnutrition, scurvy, beri-beri or pellagra
anymore. But this is not to say that we shouldn’t worry about nutrient deficiencies. Even without
getting to the point of overt, clinical deficiencies that result in disease, suboptimal intakes
of many nutrients are still extremely common even in our rich countries, and they result
in suboptimal health.