The Zero-Minute Workout (Ep. 383) - Freakonomics about:reader?url=http://freakonomics.

com/podcast/exercise/

freakonomics.com

The Zero-Minute Workout (Ep. 383) -

Freakonomics
by Stephen J. Dubner Produced by Morgan Levey
32-40 minutos

Regular physical activity reduces “all cause mortality” by 40 to 50

percent. But fewer than 1 in 4 U.S. adults exercise enough. (Photo:
Flickr)

There is strong evidence that exercise is wildly beneficial. There is

even stronger evidence that most people hate to exercise. So if a
pill could mimic the effects of working out, why wouldn’t we want to
take it?

Listen and subscribe to our podcast at Apple Podcasts, Stitcher, or

elsewhere. Below is a transcript of the episode, edited for
readability. For more information on the people and ideas in the

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episode, see the links at the bottom of this post.

* * *

AUTOMATED VOICE: Pedal faster, Stephen.

Hey, this is Stephen Dubner. I’m at the gym.

AUTOMATED VOICE: Your current heart rate is 110 beats per

minute. Your target rate is 130 beats per minute.

We all know that exercise is good for us. We also know that most
people don’t get nearly enough. Thirty-four percent of U.S. adults
are “physically inactive”; another 20 percent are “insufficiently
active.” And, not surprisingly, almost 40 percent of U.S. adults are
classified as obese. To be reductive: many of us eat too much and
exercise too little. Now, why don’t we get more exercise? Let’s be
honest: it is hard work.

AUTOMATED VOICE: Stephen. I told you to pedal faster.

The cost of physical inactivity is massive — not just in illness and

death but in dollars too. Researchers from the Centers for Disease
Control and Emory University say the U.S. spends around $117
billion a year on healthcare due to inadequate physical activity. And
those are just the direct costs from treating cardiovascular disease,
diabetes, and so on. It doesn’t even include things like loss of
productivity.

AUTOMATED VOICE: There is a big hill coming up, Stephen. Are

you ready?

It’s strange, if you think about it. For thousands and thousands of
years, our ancestors worried about not getting enough food to eat,
and their daily life required physical activity. Today, food is
everywhere, and cheap, and super-fattening. And a lot of us have

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lives that require very little physical activity — which is why I’m
here, on this stupid bike.

AUTOMATED VOICE: I am not going to take that personally.

A lot of smart people have spent a lot of time and effort trying to get
people to exercise more. Mostly, they’ve failed. So what happens
next? Wouldn’t it be amazing if, instead of exercise, there was
something like an exercise pill?

AUTOMATED VOICE: I do not like that idea. I do not like that idea
one bit.

* * *

Okay — glad that’s over. So: obesity started out as a problem in

wealthier countries, but now it’s spread to middle- and low-income
countries. The contributing factors are not in dispute: we consume
too many calories, especially low-quality calories; and we don’t
burn off nearly enough calories with physical activity. Now, to be
fair, burning calories through exercise is a pretty inefficient process;
it takes a lot more exercise than you’d think to burn off one
cheeseburger. In that regard, it’d be better to just eat less. That
said, exercise is also considered a very valuable input for overall
health. That’s what we’ve been told at least. But let’s not take that
for granted; let’s see if we can find some real evidence for that
claim — and understand why exercise is supposed to be so good
for us. We’ll start with this man:

Michael JOYNER: My name is Michael Joyner, and I’m a physician

scientist at the Mayo Clinic.

A “physician scientist” meaning what?

JOYNER: I’m basically a physiologist who’s also a clinical

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anesthesiologist.

So that sounds pretty impressive: a physician scientist at the Mayo

Clinic. But just so you know, Michael Joyner was an unimpressive
student growing up in Arizona.

JOYNER: You’re correct, I was a sort of an indifferent student at

Rincon High School, and I started college in 1976 and went to
several schools in one year. I ended up, in 1977, at the University
of Arizona, where I promptly almost flunked out. And in December
of 1977, I’d actually signed up to take the test to become a Tucson
city fireman. And what happened was, I was out running a race, a
10K race.

Joyner was a pretty good athlete.

JOYNER: I ran track and field at the University of Arizona, where I

ran the 5,000 and the 10,000. I also ran a 2:25 marathon in the late
seventies.

If you’re not familiar with marathon times — 2 hours and 25

minutes, for more than 26 miles, that is a very fast time.

JOYNER: And then I continued to run until I was about 40.

He still exercises about an hour a day.

JOYNER: It varies between a relatively easy day of aerobic

exercise on the bike, or maybe some swimming, and then on the
opposite days, I do something relatively intense, which includes a
warm-up and then about 30 or 40 minutes of circuit training. And
because I’m 60 years old, is, I’ve done probably a little bit more
strength training the last five, ten years because, as you get older,
you really want to avoid frailty, muscle loss; you don’t want to slip
on the ice, that sort of thing.

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Back when Joyner was thinking about becoming a fireman, and he

was running that 10k race:

JOYNER: A man named Eddie Coyle, who’s a well-known exercise

physiologist, Eddie was a graduate student in the lab at Tucson at
the time, and he said, “Do you want to be a subject in a study on
lactic acid?” Said, “Sounds good to me.” So, I showed up and ran in
the lab, and I said, “Man, this is unbelievable. There’s actually
people who do this for a living.”

Joyner was told he could work in the lab as a student assistant if he

got his grades up.

JOYNER: I had a square-wave experience with my grades and

started basically getting straight A’s. And I saw that if you wanted to
do studies in humans where you put catheters in and do biopsies
and that sort of thing, it would be facilitated if you were a physician.
So, unlike a lot of physicians who get interested in research in
medical-school residency or fellowship, I actually went to medical
school with the express purpose of becoming a research-based
integrative physiologist.

It did take Joyner a while to get into medical school.

JOYNER: Because I had to do a little academic rehab to make up

for those first bad two years, and then I came to Mayo in 1987 and
I’ve been here ever since.

DUBNER: So, you’re a big deal in the field of physiology, exercise

physiology. Can you first, just for total laypeople, define physiology
for us?

JOYNER: If you think about anatomy, anatomy describes the parts

of the body. Physiology is really the engineering equivalent of that

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and says, “What do these different parts do alone and in

combination?” There are all sorts of regulatory mechanisms that
increase or decrease our breathing, increase or decrease our urine
output. What we do as physiologists is study these regulatory
systems and try to understand how all living forms adapt to
environmental challenges.

DUBNER: Okay, so, open ended-question: tell us what we know, in

a nutshell — we’ll get into details as we go — but tell us what we
know about the benefits of physical exercise.

JOYNER: What we know in a nutshell is that people who are

physically active, especially if they get somewhere between 150
and 300 minutes per week of moderately vigorous physical activity,
have a large reduction in their all-cause mortality — typically about
a 50 percent or maybe 40 percent reduction in their all-cause
mortality. And typically, they live somewhere, depending on the
study, between about four and seven years longer.

DUBNER: Wow, okay. Quickly, define for me “all-cause mortality.”

JOYNER: It just means you could die of anything. Could be cancer,

heart disease, infectious disease, and so forth. And that’s one of
the points people need to remember: we typically think of exercise
as being especially protective against death and disability and
diseases associated with the cardiovascular system. But it’s also
protective against a number of forms of cancer, and a number of
things like diabetes and other diseases.

Okay, so you may be saying to yourself: Michael Joyner sounds

credible, and he’s got great credentials. But we also know he’s a bit
of an exercise fanatic himself. So how can we be sure that it’s
exercise that’s actually causing better health outcomes? What sort

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of baseline physiological evidence is there for that claim?

JOYNER: Well, a couple of things. The best evidence comes from

various population cohorts, the most famous being the bus
driver/bus conductor data from after World War II in London, where
they showed the sedentary bus drivers had much higher rates of
coronary-artery disease and heart attack than the active conductors
who were walking around punching tickets, going up and down the
stairs all day. And they showed a similar thing when they compared
clerical workers to postmen. Again, all males, all members of the
British civil servants. And that’s where that 40, 50 percent reduction
in all-cause mortality and cardiovascular mortality came from.

Okay, that is a neat story, the bus drivers. But that was a long time
ago. Has the effect been shown more recently?

JOYNER It’s been shown over and over again in every sort of
cohort study. Then, you come to some other things. So if you start
looking at people with risk factors — people with hypertension, high
cholesterol, obesity, so forth and so on — people with high levels of
physical activity or cardiorespiratory fitness, their risk is markedly
blunted. So, I like to tell people that exercise and fitness really
absolve you of other sort of risk-factor sins.

Alright, fine — but a couple things here. Cohort studies, or

population studies — those are not the randomized, controlled trials
that scientists consider their gold standard. And how do we know
that people with high levels of physical activity, as Joyner’s
describing here, how do we know that there aren’t other reasons for
their good health? Maybe the people who are more likely to
exercise are the same people who are more likely to eat better, or
sleep better; maybe they’re the same people who don’t smoke, or

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who face less stress in their lives — stressors like poverty or

difficult work or home environments. How does Joyner know that
exercise is such a strong causal mechanism of good health?

JOYNER: You get into studies in individual humans, where you can
take people and do very brief periods of exercise training, improve
their glucose tolerance, improve the function of their blood vessels,
and improve a whole lot of biomarkers which are associated with
health. And then you go one step further to animal studies, and you
can really take a deep dive into the mechanisms behind those
positive changes.

Okay, what are those mechanisms? A lot of Joyner’s research is

about how physical activity increases blood flow to skeletal
muscles.

JOYNER: Your heart rate goes from 60 or 70 to around 200, so you

have about a threefold increase in heart rate. And then the amount
of blood pumped with each heartbeat also goes up. So, think about
that. At rest, a tiny amount of that blood flow — maybe 500 mls. —
is going to all the muscle in your body. During maximum exercise,
perhaps 16 or 17 liters is going to muscle.

DUBNER: Now, why is blood flow per se important or beneficial?

JOYNER: Well, the bottom line is, if you’re going to do prolonged

exercise, you’ve got to get oxygen from the lungs to the skeletal
muscles, so you have to have a big cardiac output. And you’ve then
got to get it to the muscles that are actually contracting. So, it’s just
a supply/demand situation.

DUBNER: Okay, so take me from there, though. So you do

vigorous exercise, it increases the blood flow a lot. What, then, are
the longer-term, I guess, physical and cognitive benefits of that

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increased blood flow?

JOYNER: One is that the blood vessels grow, they become larger
in diameter. The lining of the blood vessels, the vascular
endothelium, becomes more slippery and becomes more prone to
relax versus constrict, which makes your blood pressure lower. And
then the capillaries in small blood vessels around the skeletal
muscles also grow. So, because there’s this large increase in
cardiac output, all of the large blood vessels throughout the body
become larger, and the endothelial function increases; they
become more elastic, less stiff, which is also a good thing.

The other thing to remember is — and this is a really big finding in

the last 20 years — is that there are hormone-like substances
secreted by the skeletal muscle, which have remote effects. They
have effects on the liver to improve metabolism, they have effects
on blood vessels everywhere, and they also release something
called B.D.N.F.: brain-derived neurotrophic factor, which is good for
brain growth. And people think that’s at least one of the links
between physical activity and cognition, and preservation of
cognition as you age.

DUBNER: So it sounds like the benefits of exercise are massive

and widespread, and therefore we would all be idiots to not do a lot
of exercise, or at least enough exercise. So, Dr. Joyner, what share
of Americans do get what you’d consider to be enough exercise?

JOYNER: Oh, you see various numbers, depending on whether

they’re survey research or tracking research, but if it’s 20 percent,
that’s a generous number.

DUBNER: So, do you feel that you, personally, have been

preaching the gospel of exercise for a long time, and that people

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are not really buying?

JOYNER: I just try to point out the benefits and set a good example
and be as encouraging to people as I possibly can. People really
need to understand that they need to do something, do it regularly,
and it’s okay to take it in small bites. But until we have a wholesale
change in transportation and food policy and just the way things
are, I don’t see a whole lot changing. Most of the population’s
behavior aligns with various overt and covert incentives, and we
have a whole lot of incentives to be physically inactive and eat a lot.

I mean, there’s a terrific study from Toronto showing that the

walkability of whatever ZIP code equivalent you’re in in Toronto, the
walkability of that neighborhood predicted who gained how much
weight over 10 or 20 years. We have a built-environment problem.
We’ve got an incentive problem. As much as I’d like to tell
everybody to go exercise, we’ve also got a transportation-policy
problem. When you go to places like the Netherlands or Denmark,
where they are very biking-friendly, when whole cities are built to do
that, you see a lot of really fit people.

Ronald EVANS: The challenge is, we are endlessly pitted against

the technologic advances in civilization that tends to make us not
move.

That’s Ronald Evans.

EVANS: I am the director of the Gene Expression Laboratory at

the Salk Institute.

The Salk Institute for Biological Studies is one of the most important
biomedical research institutes in the world.

EVANS: And a lot of the work that we do studies the nature of

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genetic circuits that control metabolism.

Dr. Evans, like Dr. Joyner, is a big believer in the benefits of

exercise.

EVANS: Exercise is a beneficial factor that burns calories, but it

also activates many metabolic pathways that are pro-health.

But Evans is also a realist. And this, given the human propensity to
eat too much and exercise too little, has turned Evans into a
futurist. He wonders whether we should accept the fact that most
people are never going to exercise enough, and instead think of a
biomedical solution.

EVANS: Very big question, and it deserves a lot of thought.

What sort of solution is Evans working on?

EVANS: Exercise in a pill.

Details coming up, right after this.

* * *

Fact one: the typical modern human would do well to exercise more
than they do. Fact two: public-health advocates and others have
been urging us to exercise for many years. Fact three: their urging
doesn’t seem to work. Consider fact four: in the U.S., more than 80
percent of large companies offer programs that encourage, and
often incentivize, exercise and weight control. A randomized study
of one such company, BJ’s Wholesale Club, was recently published
in the Journal of the American Medical Association. It found that
employees in the wellness program did self-report that they were
more likely to exercise and manage their weight. But the data
revealed there were no significant differences in actual health
markers, including weight loss. And as we heard on last week’s live

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show, a world-class team of behavioral scientists recently did an

experiment over 28 days, with 53 different interventions, to try to
increase the exercise activity of people who were already members
of a gym.

Katy MILKMAN: So after our 28-day program, pretty much we saw

nothing in terms of behavior change.

That’s Katy Milkman, from the University of Pennsylvania:

MILKMAN: All 53 versions of the program, pretty much nothing

sticks. And that was the ultimate goal. So that was major failure.

With so much failure, you can understand why a lot of people look
for exercise shortcuts:

ANNOUNCER: The revolutionary new Ab Transform system is the

safe, effective, and affordable way to change the way you work out,
and look, forever.

But maybe there’s another kind of shortcut. Something a bit less

hucksterish. A bit more grounded in science. Which brings us back
to the biologist Ronald Evans from the Salk Institute. Evans is well
known in the field for having discovered a family of hormone
receptors that act as genetic switches.

EVANS: And if you think of genes as instruments in an orchestra,

you can have many different kinds of sounds, or many different
ways to have them work together. And the conductor that makes
the genes come on at the right time and orchestrate all that are
regulatory factors that are called transcription factors, that activate
the gene. So those are genetic switches. This is really the
underpinning of a lot of our body’s physiology is, while all cells have
the same number and same set of genes, individual cells activate

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different sets of genes and the receptors and the hormones control
gene networks. A lot of our physiology is about genetic control.

The discovery, and understanding of this mechanism of genetic

control has been incredibly important.

EVANS: Once you have a mechanism, then you can think of how to
actually develop therapies or drugs that can control that
mechanism. Everyone’s familiar with hormone replacement for
people. Sometimes we lose a thyroid gland for various reasons,
and you can replace that by finding the or making the hormone and
then giving it back to the person. The steroid hormones are
amongst the most widely prescribed drugs on the planet.

And, perhaps, the most famous steroid-hormone therapy: the birth-

control pill.

EVANS: And that’s all about using these receptors and in many
ways, the impact of this family of receptors, and pharmaceuticals
have changed society.

Ronald Evans may be on his way to creating a new pill, which once
again has the potential to change society.

EVANS: “Exercise in a pill.”

His lab is developing a pill that would mimic the effects of exercise
in the absence of actual exercise. Other labs around the world are
working on similar exercise mimetics, as they’re called, with various
mechanisms. Evans’s pill works by targeting one of two key
hormone receptors.

EVANS: There are two hormone receptors that we discovered that

are very, very close to each other but play exactly opposite roles,
and complementary roles, in body physiology as well as in disease.

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One of the hormone receptors is called PPAR-gamma. And it is the

master regulator of adipose tissue.

Adipose tissue is what most of us know as “fat.”

EVANS: You need this genetic regulator to activate the fat network.
It’s critical for survival. You need to store energy and fat to survive.
And then the partner for that, that’s called PPAR-delta, which we
discovered in 1995, that’s the receptor that burns fat. And most of
the problem with disease is too much storage and not enough
burning. So one of the ways that we have approached the problem
is looking at drugs that can be specifically built to target the fat-
burning receptor PPAR-delta. And that’s led to a number of
companies producing new kinds of molecules. And one of the
companies that I created a number of years ago developed a
screen technology that was licensed to Glaxo Wellcome, and they
built a drug called GW1516.

Glaxo Wellcome is now known as GlaxoSmithKline. GW1516

originally had a different purpose.

EVANS: It was made to change cholesterol levels and to try to

increase something called HDL. And this drug never made it into
F.D.A. approval. It had problems.

Problems like: causing tumors in the mice it was tested on. Evans
eventually began working with a less powerful version of the drug,
with the assumption it would be less toxic. Another difference: he
wasn’t looking at its effect on cholesterol.

EVANS: So, one of the surprising things that came out of studying
the GW1516 compound — and it was very dramatic result — is,
when we gave it to sedentary mice, or obese sedentary mice, either
one, for about 30 days, the GW drug progressively activated the

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genetic program that is normally activated by exercise.

I think we should hear that last bit again.

EVANS: The GW drug progressively activated the genetic program

that is normally activated by exercise.

In other words, their physiology seemed to indicate the mice had

been exercising.

EVANS: But these mice were not getting exercise. They were just
getting the pill.

As you can imagine, this was a pretty exciting research result. But
how well did the pill do in terms of giving the benefits of exercise in
a general sense?

EVANS: You have to be careful when you say, “Does the pill give
the benefits of exercise in the general sense?” because exercise is
a hundred things, but I should say, in general, exercise, no matter
how you do it, focuses on a few things. It increases energy
expenditure. It tends to increase burning of lipids and fats and
sugars. You get adult neurogenesis, and that enhances cognitive
performance. It also improves immune fitness, lowers inflammation
— so it has many benefits to the heart and other parts of the body.

Now, if we go to this, “What does PPAR-delta drug do,” in terms of

metabolic fitness in, let’s say, the brain, it does exactly the same
things. It gives you this increased energy expenditure, you burn
more lipids, you burn more sugar, and you correct your insulin.
Your adipose depot starts to shrink, so you lose weight. And the
drug, by itself, gives you adult neurogenesis.

The drug also seemed to boost endurance, at least in the mice.

After 30 days of giving them the drug, Evans and his team put the

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sedentary mice on a treadmill.

EVANS: It’s a mouse treadmill. It’s very cute. And we compared the
mice that got the drug with ones that did not get the drug. And the
difference was striking: the ones that got the drug could run
approximately one hour longer, continuous running, than the ones
that didn’t.

And what is the mechanism for this endurance effect?

EVANS: What the actual drug does, it increases fat burning by the
powerhouse of the muscle cell, which is called the mitochondria,
and the mitochondria can burn sugar or fat, but what the drug says
is, “We want the mitochondria to burn fat specifically and convert
fat into the chemical form of energy called ATP — but don’t burn
sugar.

That’s because the sugar — or glucose — is needed for brain

energy.

EVANS: The PPAR-delta drug powers the brain and powers the fat
by separating out the two energetic molecules in the body for
different purposes: one for the muscle and one for the brain. And
by doing that, you’re able to sustain your running time by an hour or
an hour and a half, if you’re a mouse.

So this sounds pretty much like a miracle drug, doesn’t it? Others
thought so too. Right before the 2008 Beijing Olympics, Evans
reached out to the World Anti-Doping Agency, or WADA, about the
potential for athlete abuse, and he eventually helped develop a test
for it. Soon after, WADA banned the drug. But in 2013, a bunch of
pro cyclists were caught using it. Fast-forward to today: Ronald
Evans and a pharmaceutical firm he co-founded, Mitobridge, are
working on a new form of the drug that’s meant to minimize side

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effects.

EVANS: So the Mitobridge drug has been in what’s called phase 1

studies and it’s now moving on to phase 2 studies. So, the most
critical is the phase 1, to me, because that’s the safety. They’re
now through that part. So, the next part is, does it work? And it
works very well in the mouse models, but we have to show that it
works well in people. We know it’s safe in people, but we now have
to show that it works. I would say, two or three years, that we will
have a pretty good idea if it’s working in human disease in a way
that could achieve F.D.A. approval.

To get the drug through FDA approval, Mitobridge is targeting

patients with Duchenne muscular dystrophy. That’s a genetic
disorder, typically striking young boys, who rarely survive into their
twenties.

EVANS: There is no real drug to treat it. But our approach is to

restore this balance of energy utilization in the muscle, and we can
stimulate that muscle to actually burn fat and become activated as
if it was being exercised.

But Evans clearly sees a much wider potential use for this drug.

EVANS: There is absolutely no way that the potential here is going

to be limited to one or two diseases. It will be very high, from
metabolic to neuro to vascular to aging. We can think of the
potential here in different ways, and maybe, to the wider question,
can it be used preventatively in some cases just to maintain health,
as opposed to just treating disease. And this is not an easy issue,
because taking healthy people and giving them a drug is not
common. Now, it does happen. A lot of people take adult aspirin for
their entire life because it’s thought to be helpful to reduce

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inflammation and reduce heart disease.

Tens of millions of Americans also take statins every day to forestall

heart disease; millions more take metformin to treat diabetes, or
even the onset of diabetes. We put fluoride in our water supply to
prevent tooth decay.

EVANS: Could you transition this to a society that is getting heavier

and running into the problem of obesity and diabetes and the
related complications? The answer is yes, but from a social and
ethical component, it raises a big question that should be
addressed. It’s not unusual for scientific advances to raise social
issues and questions. We have this all the time.

Indeed: just because a drug may soon exist that could mimic the
effects of exercise does not necessarily mean we should
immediately spike our water supply with it. So Evans’s drug, if it
does make it through F.D.A. approval, will surely have its
philosophical and ethical skeptics. But even now, it’s got its
physiological skeptics.

JOYNER: So, an exercise memetic.

That, again, is Michael Joyner from the Mayo Clinic.

JOYNER: If you think about it, the main ones have been designed
to try to increase the function of the mitochondria, the little
organelles in skeletal muscle, that burn carbohydrate and fat and
are critical to the metabolic benefits of exercise. And certainly, you
can stimulate those with drugs. But if you look at the broad class of
things that exercise does, it goes way beyond just affecting the
mitochondria. It affects, again, the blood vessels, the remote effects
of training, the effects on the brain, the effects on intermediate
metabolism, and all sorts of other things. You can find a mimetic for

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things that sort of look like exercise, but I don’t think you’re going to
find the big-picture drug or compound that can do the 10 or 15 main
things that exercise does for people.

DUBNER: What would you think of, let’s call it, the exercise
pharmaceutical, that works along the lines you’re describing there
on a mitochondrial level for those who can’t exercise due to, let’s
say, a physical handicap or some other condition. Do you like that
idea?

JOYNER: Absolutely. Absolutely. You start thinking about exercise

is good for your lipids, exercise is good for diabetes, exercise is
good for this and that, and there’s a terrific idea and very interesting
paper in the early 2000’s, I believe in the British Medical
Journal which said, why don’t we put everybody on low-dose
statins, low-dose antihypertensives — everybody over 50 — low
dose anti-diabetic drugs, and see what it would do to their life
expectancy and all-cause mortality. So, some people have argued
that really this is closer to an exercise mimetic than drugs that
target the mitochondria, for example.

But you can imagine that if a so-called “exercise pill” does come to
market, it might provide people the license to never exercise again.

MILKMAN: There’s been research showing that there can be

licensings effects with diet behaviors — you remind me that I’ve
been dieting well, then I maybe eat more.

Katy Milkman again, from the University of Pennsylvania.

MILKMAN: So if you give people a pill, and say, this has the effects
of exercise, will they feel licensed not to exercise? It’s a real risk.

EVANS: I do not actually like to think of it that way, because we are

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designed to move.

And that, again, is Ronald Evans, the man behind the exercise pill.

EVANS: The social issue is not just, should we give the drug to
everyone — it’s how do we manage the intrinsic advances that are
working against our health?

MILKMAN: He may not intend for it to replace fitness, but will

people take it and then feel that they’re licensed to skip workouts?
Whether that’s the intent of the medication doesn’t mean it won’t be
a nasty side effect.

Marcas Bamman, a physiologist at the University of Alabama,

Birmingham, is also not in favor of an exercise pill.

Marcas BAMMAN: Because there are thousands upon thousands

of molecular responses to exercise that cannot be recapitulated by
one pill.

Bamman has another idea, a sort of hybrid idea — which he feels

may be necessary, given the difficulty of turning an inactive person
into an active one.

BAMMAN: Going from true sedentary status to a regular exercise

training habit or behavior, there are a lot of steps required to make
that happen. And one of those that would be very tangible for
people is a prescription with good guidance.

A prescription meaning an individualized exercise regimen.

BAMMAN: It really doesn’t do the patient a lot of good for a

healthcare provider to just say, “Well, your blood pressure is high,
your glucose is high, and you need to lose some weight so you
should do more exercise.” They don’t know how frequent, what
intensity, what dose. Is it resistance, is it endurance, is it a

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combination?

Bamman and his research team at U.A.B. have been doing

research for 15 years on this idea. They started with older adults
and now work specifically on patients with Parkinson’s, multiple
sclerosis, and epilepsy. But their idea is that everybody could
benefit from an exercise prescription.

BAMMAN: Let’s just take the individual who comes to the clinic, 45
years old. They’ve got a body mass index of 32.

For the record, that is a pretty high B.M.I.— the equivalent of a five-
foot-ten person who weighs more than 220 pounds.

BAMMAN: They’ve got some level of insulin resistance going on,

they’ve got stage 1 hypertension, they’ve got some knee pain.

In a perfect world — or at least in Marcas Bamman’s world — a

physician would have a lot of good data on exactly what forms of
exercise, at what intensity and duration, would be most useful.

BAMMAN: If you can then point to that data and say to that person,
“The evidence is clear this works, and now I’m going to refer you to
somebody who knows how to implement this evidence-based
prescription,” that would have a major impact on whether or not
somebody adopts the change.

But the truth is, those data on ailment-specific exercise, are fairly
sparse.

BAMMAN: In terms of which type of exercise is best for a given

disease risk cluster, the research is really void in many areas.

That may be starting to change. The National Institutes of Health is

starting an exercise trial this summer as part of a program called
the Molecular Transducers of Physical Activity Consortium.

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BAMMAN: And that study is really comparing resistance training to

endurance training and trying to understand the molecular
mechanisms by which each of those modes of exercise training
induces potential health benefits.

You could also imagine that technology, especially smart

technology, has a larger role to play in helping us achieve our
fitness goals. Like making exercise equipment and apps that, rather
than beating us up:

AUTOMATED VOICE: Stephen. I told you to pedal faster.

Are a bit more encouraging.

AUTOMATED VOICE: Well, aren’t you the little champion? Five

whole minutes on the bike without a break. That’s your new
personal best.

* * *

Freakonomics Radio is produced by Stitcher and Dubner

Productions. This episode was produced by Morgan Levey, with
help from Daphne Chen. Our staff also includes Alison Craiglow,
Greg Rippin, Harry Huggins, Zack Lapinski, Matt Hickey, and
Corinne Wallace; we had help this week from Nellie Osbourne.
Our theme song is “Mr. Fortune,” by the Hitchhikers; all the other
music was composed by Luis Guerra. You can subscribe to
Freakonomics Radio on Apple Podcasts, Stitcher, or wherever you
get your podcasts.

Here’s where you can learn more about the people and ideas in this
episode:

SOURCES

Michael Joyner, physician scientist at the Mayo Clinic.

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Ronald Evans, director of the Gene Expression Laboratory at Salk

Institute.

Katherine Milkman, professor of operations, information, and

decisions at the University of Pennsylvania.

Marcas Bamman, physiologist at the University of Alabama,

Birmingham.

RESOURCES

“A Pill to Make Exercise Obsolete,” by Nicola Twilley (The New

Yorker, 2017).

“Warning to Beijing Olympics Over Pills That Mimic Exercise,” by

Jeremy Laurance (The Independent, 2008).

“The New EPO? — GW1516, AICAR and Their Use in Cycling,” by

Matt de Neef (CyclingTips, 2013).

“A Strategy to Reduce Cardiovascular Disease by More Than

80%,” by N.J. Wald (The British Medical Journal, 2003).

“London Transport Workers Study: Coronary Heart Disease and

Physical Activity of Work,” by Jeremy Morris (The Lancet, 1953).

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