A Surprising Effect of Sugar On The Immune System - The Atlantic

3/27/2019 A Surprising Effect of Sugar on the Immune System - The Atlantic
SCIENCE
Feed a Cold, Don’t Starve It

Sometimes sugar causes inflammation. Sometimes it does the opposite.
JAMES HAMBLIN SEP 8, 2016
REGIS DUVIGNAU / REUTERS
Do you feed a fever and starve a cold? Or is it the opposite? I can never
remember. I never cared to. I thought it was just something people said when
https://www.theatlantic.com/science/archive/2016/09/glucose-inflammation/498965/ 1/12
they didn’t know what else to say.
Ruslan Medzhitov cares. He’s a distinguished professor of immunobiology at

Yale. And in the journal Cell today, his team showed some dramatic benefits to
starving a bacterial illness—but feeding a viral illness.
This is contrary to the standard advice of doctors, which is reflected on the

bastion of solace, WebMD:
Do you starve a cold and feed a fever when you're feeling under the weather?
… Good news—starving is never the correct answer. When you eat a
nutritional, well-balanced diet, many other factors fall in place that keep your
body functioning optimally.
It’s true that the fever distinction is useless. Both bacteria and viruses can give
us fevers. And the holistic benefits of a well-balanced diet are tough to
overstate. But in cases of infectious disease, the rule that Medzhitov has
discovered seems to have merit. As he first put it, “Starve a bacterial infection
and stuff a viral infection.”
To be more precise, we do not feed or starve the bacteria or viruses themselves,

but we may be able to modulate the different types of inflammation that these
infections cause. “I want to be cautious here not to oversimplify and
generalize,” Medzhitov warned. The most accurate and compelling way to put
it, then, really: “Fasting has opposite consequences in different types of
inflammation.”
And by opposite, he means opposite, life and death. In that way, his new
findings could change not just the way we eat when we come down with a
common cold, but how doctors treat the end stages of infections—when they
spread throughout the blood and becomes known as sepsis, a condition that
kills thousands of people every year.
***
It all starts with the idea that losing your appetite is a symptom of a lot of
illnesses. Why? Wouldn’t it be best to fortify ourselves with all the nutrients we
can?
A temporary loss of appetite is known to doctors as anorexia (not to be

confused with anorexia nervosa). Medzhitov counts anorexia alongside other
common but rather mysterious “sickness behaviors” including altered sleep
patterns, depression, and social withdrawal. He has been fascinated with how
these things might contribute to our survival. Should they be embraced—listen
to what your body is telling you—or fought?
A popular idea behind temporary anorexia is that it seems to happen for a

reason: it protects us against certain infections. We alter our metabolisms to
deprive our invasive species of fuel. As nutrients and minerals become scarce,
the infectious organism will starve before our bodies do. It’s a race to the
bottom.
Consider the classic food-poisoning bacterium Listeria monocytogenes.

Medzhitov’s team infected a bunch of mice with Listeria, and, predictably, the
mice stopped eating. They eventually recovered. But when the researchers fed
the mice the same food—force-feeding them, as they had no appetites—they
died.
Why, exactly, would that happen? Was some specific element in the food
keeping the infection alive?
To figure that out, the Yale team broke down the food by macronutrients (fats,
lipids, and carbohydrates). And, indeed, it seemed that the mice could survive
the illness when they were forcibly fed proteins or fats. What they couldn’t take
was the sugar glucose.
(Glucose comes to us not just by way of what we traditionally think of as sugar,

but from any starchy food like bagels or crackers where carbohydrate chains
break down into glucose in our mouths and stomachs.)
To double-check that these negative effects of sugar were real, the researchers
fed glucose to some mice and then administered a rescue drug (2-deoxy-D-
glucose) that blocks the body’s ability to metabolize that glucose—and they
survived. In the case of this infection, it could seem, the bacteria need to be
starved of sugar.
This is the sort of misguided thinking that leads people to go on cleanses, to

deprive themselves of food unnecessarily, and to risk making things even
worse. The story is much bigger than avoiding sugar. In other diseases, glucose
seems to be beneficial. Critical even.
When Medzhitov infected the mice with the influenza (flu) virus, the mice were
more likely to survive if they were force fed. Denying them food—especially
glucose, either by withholding it or administering the antagonist 2-deoxy-D-
glucose—caused the mice to die. As the researchers write in the journal, in
influenza infection, “inhibition of glucose utilization is lethal.” Whereas
glucose was “required for survival in models of viral inflammation, it was lethal
in models of bacterial inflammation.”
How could that be?
The mechanism doesn’t seem to have anything to do with starving the

infectious agent. Rather, it has to do with modulating our own responses to the
infections. Here we are dealing with two very different types of inflammation.
In one case, glucose exacerbates inflammation. In the other, it is critical to
survival.
***
When you stop eating, the body starts using fat reserves for calories. Keep
fasting, and you start to convert some of that fat into ketones. That switch from
burning glucose to burning fat and generating ketones (ketogenesis) is
commonly referred to as moving to a “fasting metabolism.”
This switch seems to be important—necessary, even—in the body’s response to

bacterial sepsis. Ketogenesis limits the body's formation of substances known
as reactive oxygen species, which can damage cells. When you introduce
glucose (as in, if you eat sugar, or any carbohydrate that breaks down into
sugar), that switch to a fasting metabolism is undone. The sugar triggers the
release of the hormone insulin, which tells the body that we don't need to use
our fat reserves, bringing ketogenesis to a grinding halt. So when the mice were
given glucose, the inflammatory process caused damage to neurons in the
brain, causing the mice to convulse and die.
Meanwhile the virus triggered a different type of sepsis, in which removing

glucose was uniformly lethal. In that case, glucose seemed to be necessary for
adapting to the stress of viral inflammation, by preventing stress-mediated
apoptosis (cell death). Without that, an area in the brainstem was destroyed by
inflammation, and the mice would stop breathing.
Together, these mechanisms reframe the typical approach to treating

infectious disease. Medzhitov’s manipulations weren't focused on killing the
pathogen, per se, or starving it, but on using nutrition to modulate the host’s
responses.
But would the same thing work in people? Could we eat to acutely modify our
immune responses? Could we take 2-deoxy-D-glucose to temporarily block
metabolism of glucose?
Medzhitov thinks the idea “very exciting,” especially because sepsis is an

intractable condition. The only known treatment is antibiotics and mechanistic
measures to keeping a person’s heart beating until the process abates. It’s
unpredictable. So the Yale team plan to move expeditiously to testing this in
human clinical trials.
Reducing caloric intake has been tested in people with sepsis before, but the
results have been mixed. As a consequence, the recommendation in critical-
care medicine is to keep people on a balanced diet. (As one Stanford School of
Medicine guide directs physicians, “Nutrition, whether enteral or parenteral
[via the gut or into the veins], should not be neglected given the high metabolic
demands of the septic patient.”)
But Medzhitov thinks the reason the clinical results of fasting during sepsis
have been mixed is that patients weren’t separated based on whether their
inflammation was the result of a bacterium or virus: “Hopefully if we divide
patients based on the cause of sepsis,” he said, “that could provide a way to
manage this terrible condition.”
In principle, one day a doctor could give a diagnosis along with a specific
dietary recommendation. That could speed recovery and limit the global crisis
of antibiotic overuse. It might even be—I hesitate to say in the middle of a
diabetes epidemic—an excuse to eat sugar.
This emphasizes the critical point that carbohydrates, like the other
macronutrients, are not simply good or bad. Despite whatever diet fad comes
about next week, or the week after. As the Yale researchers conclude, their
work “implicates a differential need for metabolic fuels as a function of
infection.” That is, as more research accumulates in this area, it adds to the
understanding that we do well to count food as medicine.
In the immediate term, Medzhitov’s takeaway is to follow our cravings when

we’re sick, because they may reflect evolutionary mechanisms that evolved to
be protective: “So, for example, when you have the flu, you kind of feel like
having some tea and honey. That may be the body’s way of telling us that we
need some glucose. I suspect we have these mechanisms that tell us what we
prefer to eat (or not to eat) when we’re sick. Those are the mechanisms we
should probably listen to.”
We want to hear what you think about this article. Submit a letter to the editor or
write to letters@theatlantic.com.

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3/27/2019 A Surprising Effect of Sugar on the Immune System - The Atlantic

Feed a Cold, Don’t Starve It

JAMES HAMBLIN SEP 8, 2016

REGIS DUVIGNAU / REUTERS

they didn’t know what else to say.

Ruslan Medzhitov cares. He’s a distinguished professor of immunobiology at

This is contrary to the standard advice of doctors, which is reﬂected on the

To be more precise, we do not feed or starve the bacteria or viruses themselves,

A temporary loss of appetite is known to doctors as anorexia (not to be

A popular idea behind temporary anorexia is that it seems to happen for a

Consider the classic food-poisoning bacterium Listeria monocytogenes.

(Glucose comes to us not just by way of what we traditionally think of as sugar,

This is the sort of misguided thinking that leads people to go on cleanses, to

How could that be?

The mechanism doesn’t seem to have anything to do with starving the

This switch seems to be important—necessary, even—in the body’s response to

Meanwhile the virus triggered a diﬀerent type of sepsis, in which removing

Together, these mechanisms reframe the typical approach to treating

Medzhitov thinks the idea “very exciting,” especially because sepsis is an

In the immediate term, Medzhitov’s takeaway is to follow our cravings when

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