PDF Discover Magazine October 2016 | Science of Aging PDF Download

PDF Discover Magazine October 2016 | Science of Aging PDF Download by Various (Author) Discover October 2016 Issue Science of Aging: does DNA hold the secrets to longevity? The power of one brain; drilling to doomsday; the science behind your credit score; to planet 9... and beyond; crowdsourcing cancer research

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Contents

OCTOBER 2016

VOL 37, NO 8

About 66 million years ago, an asteroid plummeted into the

Gulf of Mexico and changed life on Earth forever See page 42.

October 2016 DISCOVER 5

28 What It Takes to Reach 100

Live long and prosper, as the Vulcan salute goes Some people have managed

that first part much better than others, and the key could be in their DNA

BY LINDA MARSA

36 Your Attention, Please

MIT neuroscientist Earl Miller has made a name for himself with his research on

working memory, the brain’s scratchpad His next goal? To make us all smarter

BY ADAM PIORE

42 Drilling to Doomsday

Beneath the Gulf of Mexico lies evidence of one of Earth’s most cataclysmic

events Now, experts are getting their closest look yet BY ERIC BETZ

50 Weapons of Math Destruction

Sure, credit scores are important, but they hold more sway than you’d think

And in many cases, that can be a very bad thing.BY CATHY O’NEIL Cake photo: William Zuback/Discover; DNA candle: Jay Smith; background: Melis/Shutterstock

COLUMNS & DEPARTMENTS

6 EDITOR’S NOTE

Chasing Longevity

Living to 100 takes a stroke of genetic

luck and a dose of resilience

18 PROGNOSIS

A Mind in Time

Researchers are spending some quality

one-on-one time with patients’ brains

The results could steer the course for

future clinical treatment BY ADAM HADHAZY

22 MIND OVER MATTER

Think Outside the Brain

Feeling guilty? Take a page from

7 THE CRUX

How experts plan to give

the Ignorosphere some

love, an update on surgeon

Anthony Atala’s work on

3-D bioprinting, we add to

our blog family and more!

74 NOTES FROM EARTH

The Judas Fish

In Montana, the invasive lake trout is choking native fish populations With

a secret weapon, ecologists are finally turning the tide BY JANINE LATUS

78 HISTORY LESSONS

A Profile of Plague

The deadly pestilence of old is still around, and scientists are learning about its past and future BY HILLARY WATERMAN

82 20 THINGS YOU DIDN’T KNOW ABOUT … BATS

Forget your stereotypes, there’s more to these winged mammals of the dark than vampire lore BY GEMMA TARLACH

Lady Macbeth’s book and try washing your hands It works, and neuroscience backs it up BY MALLORY LOCKLEAR

24 BIG IDEA

Fighting Cancer With Data

Cracking the human genome means doctors can now personalize cancer treatments But not without teamwork and a whole lot of computing power

BY AIMEE SWARTZ

70 OUT THERE

To Planet 9 — and Beyond!

Past the celestial body formerly known

as a planet, i.e., Pluto, astronomers are continuing their hunt for the elusive Planet 9 BY COREY S POWELL

ON THE COVER

To Planet 9 and Beyond!p.70Crowdsourcing Cancer Researchp.24Science of Agingp.28The Power of One Brainp.18Drilling to Doomsdayp.42 Science Behind Your Credit Scorep.50

57 OUT THERE SPECIAL BONUS SECTION

Crucial tips for your 2017 eclipse planning, the amateur astronomer who beat NASA to the punch with his observations of Saturn, and how one legendary meteorite hunter has turned his eyes from the ground to the skies

Website access code: DSD1610

Enter this code at: www.DiscoverMagazine.com/code

to gain access to exclusive subscriber content.

Resilience For those who live

into their 90s and past 100, it’s a

crucial part of the equation, as

you’ll find out in our cover story

(see page 28) It’s grounded them

through wars, the Depression,

civil unrest and their individual

daily stressors

The notion of resilience has

been running through my head

lately, as I’ve watched footage

from the aftermath of police

shootings and terror attacks

What does it take to prevail

through that kind of pain, both

on an individual basis and across

society? I would argue that

resilience in the face of today’s

social upheaval is so grounded,

it’s in our bones, it’s in the very

structure of our cells.

It’s those cellular mechanics — the clockwork — that

appear to drive how we age The notion of a timekeeper is

at the heart of some researchers’ work to crack the code of

aging For most of us, the very process of aging eventually

dooms us to disease But for those of us who live beyond

100, it’s as if the cellular clocks have slowed down.

In addition, scientists have found that how these

centenarians live makes a difference A safety net of friends

and family Plenty of walking Real food Experiences

throughout their lives will shape how their genes function

In the quest for longevity, here’s to a big dose of resilience

and a way to slow down that cellular ticktock

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October 2016 DISCOVER 7

LIFE’S LIMITS

They might be tiny, but these microscopic plankton fossils, called planktonic foraminifera, are a nearly continuous 65 million-year record

of life on Earth University of Southampton evolutionary ecologist Thomas Ezard and his team compared the collection’s number of species with markers of ocean temperature and sediment composition during their life spans Data revealed a broader picture of how environmental variations affect biodiversity Cardiff University earth scientist Paul Pearson took this composite photo of Ezard’s subjects, each less than

a millimeter wide, with a scanning electron microscope  ERNIE MASTROIANNI; PHOTO BY PAUL PEARSON/CARDIFF UNIVERSITY

8 DISCOVERMAGAZINE.COM

Destination: Ignorosphere

Making Manned

Flights Possible

Extra Thrust Required

All aboard, scientists studying climate change.

Ever heard of the Ignorosphere? It’s what scientists have jokingly nicknamed the mesosphere, the third

atmospheric layer from Earth’s surface It’s always been tough for researchers to access and so has been

largely ignored But that’s about to change, thanks to work done by Project PoSSUM (Polar Suborbital

Science in the Upper Mesosphere)

While unmanned rockets, satellites and balloons — most notably NASA’s AIM satellite — have taken images of and collected data from the layer in the past, new suborbital vehicles will make it possible to send actual human scientists to the mesosphere to study noctilucent (NLC) clouds These ragged, spidery clouds began appearing

in the late 1800s, and their increasing frequency and geographic spread are believed to be a marker for climate change They’ve been difficult to study, however: They’re too high for detailed data collection via ground-based instruments, balloons or aircraft, and too low for orbital satellites The complex equipment that can measure fine-scale changes in the clouds’ composition needs a human operator

Project PoSSUM’s executive director, Jason Reimuller, says suborbital rocket planes are scheduled to launch from Alaska in 2018 They’ll head into the Ignorosphere

with scientific instruments like the ones pictured here  CAROLINE BARLOTT

Unlike commercial planes, which can use the lower atmosphere’s oxygen to give their fuel

systems a boost, suborbital rocket planes use liquid oxygen tanks to compensate for the

thin air and get the thrust they need.

PoSSUM plans to use XCOR

Aerospace’s suborbital rocket

plane Lynx; two people fit in

its flight pod.

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carbon dioxide and nitric oxide levels with

airglow — that sits just above

them The images will give

experts a better idea of the

mesosphere’s overall structure.

atures that will help determine how the clouds grow.

An aerosol sampler

will collect fine particles from the atmosphere, believed to be leftover meteor bits,

which may explain how the clouds form in the first place.

These rocket engines can be

used for thousands of flights,

potentially making scientific ventures more affordable.

The Lure of the Landfill

Birds give up on migrating and gorge on garbage instead

In 1822, a well-placed

arrow solved the mystery of why

some European birds would vanish

after summer and reappear in

spring A hunter in Mecklenburg,

Germany, killed a white stork that

already had an African projectile

lodged in its neck Nearly

two centuries later, European

researchers are trying to explain

a new phenomenon: Why have

many storks stopped migrating?

Roughly 14,000 of the

fair-weather fowl in Portugal have

given up flying south In a recent

study published in the journal

Movement Ecology, conservation

ecologists used GPS tags to track

17 of those white storks through their normal migration period

to figure out why.

Instead of heading to sub-Saharan Africa, the birds made regular

trips from their permanent nests to landfills dozens of miles away — something previously unheard of.

Aldina Franco and a team from the University of East Anglia followed the birds as they feasted behind dump trucks dropping off discarded meat at a landfill

Incredibly, the steady supply has allowed stork populations to increase tenfold since the 1980s.

“The landfill food enables the storks to raise a larger number of chicks per nest,” Franco says.

The storks are just one of many species shifting their migration patterns because of human behavior And these birds might soon reroute again: The European Union recently revised landfill rules so that food waste is handled under cover That could leave the storks looking elsewhere for their junk-food fix  ERIC BETZ

The easy access to food is just too enticing for white storks in Portugal The birds have stopped migrating in favor of feasting

at garbage sites like this one

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No, it’s not the little glob that clogs up your Elmer’s bottle A glueball is a particle comprising only other particles called gluons, which have no mass Gluons are the force particles that hold together quarks, which make up protons and neutrons That means a glueball

is made up entirely of force And scientists can’t even observe this unstable particle; they can only detect it by trying to calculate its decay But in 2015, researchers announced a promising new calculation technique that could help them finally pin down the elusive glueball

 LACY SCHLEY; ILLUSTRATION BY CHAD EDWARDS

TH AT WOR D YOU HEA R D

October 2016 DISCOVER 11

THE

ReDISCOV ER

The Discover blog network continues to grow

• In July, ace science writer Liz Kruesi launched her blog, Astrobeat, where

she’ll tune in to the rhythms of the universe and tell the stories of those who

are also listening For her first post, Liz dives into one of her favorite topics: the

perplexing black hole at the center of the Milky Way Check out more of her

unique takes on the cosmos at blogs.DiscoverMagazine.com/Astrobeat

• Senior Editor Gemma Tarlach is Discover’s authority on dinosaurs — she’s

obsessed over them since she was a little girl So in addition to writing about

Spinosaurus and serving up 20 things you didn’t know about any given topic,

she’s also launched a new blog, called Dead Things Gemma’s digging the dirt

on the latest finds, from dinosaur fossils to relics of lost civilizations Head over

New tech makes bioprinting more efficient.

In 2001, Anthony Atala became the first surgeon to build a human bladder and implant it, helping pioneer the field of bioprinting.

At the time, Atala was using a multistep process First, he would create a frame

from biodegradable, synthetic polymers, which are essentially plastics Then he’d paint cells grown from the patient’s bladder onto the frame with a custom 3-D printer — a

technique Discover detailed in a profile of Atala last year.

Now, Atala and a team from

the Wake Forest Institute for

Regenerative Medicine have

combined both processes with

a new tabletop device called an

integrated tissue organ printer.

A scanner traces the patient’s

body part, creating instructions

for the printer’s three ink nozzles

The “ink” is a clear gel mixture

of mature tissue cells, immature

stem cells and polymers designed

to mimic real tissues’ consistency

The ink looks syrupy at first, then

hardens to resemble the texture

of gelatin It’s printed in a layered

lattice, which leaves tiny channels

throughout the organ that act like

blood vessels and allow nutrients to be dispersed through the tissue.

Atala has now printed an ear, jawbone and muscle tissue with the integrated printer, all of which held their shape after being implanted into rodents Blood vessels grew

into the microchannels, and the rodents’ cells proliferated, making the implanted tissue more resilient over time.

Printed, personalized organs for human transplants are a long way off, but Atala’s studies show scientists are getting ever closer to finding a technological solution to one

of medicine’s greatest challenges  CLAIRE CAMERON

ON THE WEB

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Honeybees might be getting

their buzz from caffeine A study

published in Current Biology

found a boost in foraging

activity among bees that

frequented plants with naturally

occurring caffeine in their nectar.

— Jeff Lepler, Redford, Michigan

A Sorry, Jeff, but scientists still don’t really know why gravity works In a way, they’ve just barely figured out

how it works.

The Higgs boson discovery four years ago helped verify how objects acquired their mass, but that doesn’t shed much light on gravity itself

In the 17th century, Isaac Newton was the first to formally connect an apple falling toward Earth and Earth itself “falling” around the sun The force behind both was gravity, and Newton understood it as just an attraction that grew stronger between two objects the more massive and the closer they were

Albert Einstein came along a few centuries later and provided an interpretation: According to his general theory

of relativity, gravity is a property of space-time, the fabric of the universe The more massive an object, the more it warps space-time, causing nearby objects to “fall” toward each other

If an object is massive enough, it can actually create detectable gravitational waves, or ripples in space-time, which scientists saw for the first time earlier this year

But gravity is also one of the universe’s four fundamental forces (the others being electromagnetism, and the strong and weak nuclear forces) Because the other forces use “force carrier particles” to impart the force onto other particles, for gravity to fit the model, all matter must emit gravitons, which physically embody gravity Note, however, that gravitons are still theoretical

Trying to reconcile these different interpretations of gravity, and understand its true nature, are among the biggest unsolved problems of physics But, alas, what we do know does suggest antigravity is impossible  BILL ANDREWS

Visit DiscoverMagazine.com/Askfor more To submit a question, email us at Ask@DiscoverMagazine.com

INBOX

Thank You

“All in His Head,” from

the June 2016 issue,

peered into Einstein’s

experiments is brilliant! I haven’t

encountered a clearer description since I was a little

girl in the early ’50s, when my father would tell me

about scientific principles and curiosities as bedtime

stories I went to sleep with visions of Einstein’s

thought experiments, the redshift, photosynthesis,

infinite regressions and so on dancing in my head.

No, I didn’t go into science, but I have tried to

pass on to my children and grandchildren a sense

of wonder and curiosity about the natural world.

Thank you, Andy Berger.

Cia Gadd

Alberta, Canada

Some Killer Insight

In the June 2016 issue, “The Psychopath & The

Hare” looked at Robert Hare, who developed a

widely used test to identify psychopaths.

I have subscribed to Discover magazine almost

from the time it was established, and have always

enjoyed each issue.

However, your last issue with the article on

psychopathy has changed my life I immediately

got a copy of Kent Kiehl’s book The Psychopath

Listener I’ve read it twice The second reading

was to better understand how the work he has

done — amassing an unbelievable amount of data,

including fMRI records of psychopaths and

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By Julian Guthrie

Guthrie reveals the roots of the current space race among entrepreneurs in this fast-paced account of would-be rocket men chasing the $10 million XPRIZE, announced in

1996 but unclaimed until 2004.

UTOPIA IS CREEPY AND OTHER

PROVOCATIONS

By Nicholas Carr

It’s ironic that Carr, a Pulitzer Prize finalist, takes on modern life’s short attention spans and worship of the superficial in a series of essays, some barely a page and one merely a sentence But, as the title promises, these are rapid-fire volleys of ideas deceptively designed to engage at

a depth greater than 140 characters By turns wry and revelatory, and occasionally maddening, Carr succeeds in shaking the reader out of screen-zombie complacency.

SEEDS

ON ICE

Svalbard and the Global Seed Vault

By Cary Fowler

Deep in Arctic Norway sits a collection

of seeds from around the world,

a stockpile of genetic diversity that’s fast disappearing from cultivation Fowler,

a key player in the banklike facility’s creation, uses stunning images

of the site and its surrounding landscape as a springboard into bigger-picture issues, including the need for what some have called a “doomsday vault.” His tone is more hopeful than gloomy, however, in this fascinating look

at a place few of us would otherwise visit.

SUN MOON EARTH

The History of Solar Eclipses From Omens of Doom

to Einstein and Exoplanets

By Tyler Nordgren

When the moon clips our view of the sun or our own shadow blots out our satellite, we experience

it with the benefit of millennia

of knowledge We know years

in advance when an eclipse will happen, where on the planet it will be visible and, perhaps most importantly, that the world will not end

because of it

Our ancestors were not

so prepared

well-Astronomer and physicist Nordgren charts the path our species has taken from terror to scientific understanding, and he’s done it with wit and clarity

16 DISCOVERMAGAZINE.COM

GIANTS OF THE LOST WORLD

Dinosaurs and Other Extinct Monsters

to some of evolution’s greatest oddities

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of one person’s brain function

over many months could

unlock new therapies

BY ADAM HADHAZY

→Two mornings a week for the

better part of an 18-month

stretch, you could find Russell

Poldrack with his head inside a giant

metal doughnut — the business end

of a magnetic resonance imager As

Poldrack lay still for 10 noisy minutes,

the machine measured the activity

throughout his brain’s neural networks

Roughly once-a-week blood draws

followed, checking nutrient and gene

expression levels in his body

In total, Poldrack racked up 104

gratingly loud brain scans He got

stuck by needles, oh, four dozen times

On top of all that probing and poking,

he also kept frequent logs of diet, sleep

and stress

Poldrack took the axiom “know

thyself ” to obsessive new levels in

the service of his MyConnectome

project, the most intensive examination

undertaken of a single living person’s

brain MyConnectome aims to plug

gaps in the fundamental understanding

of how activity varies in the human

brain, across the 100 trillion

inter-connections of its 100 billion-odd

neurons

One of these knowledge gaps is

temporal Scientists have studied brain

changes on short terms of seconds and

minutes, such as when research subjects

complete a task, as well as on the long

term of years, documenting cognitive

decline during the aging process But

anything in between is unknown,

essentially mentis incognita.

“No one has ever looked at how the brain varies over the course of days, weeks and months,” says Poldrack,

a psychologist and neuroscientist at Stanford University

A second gap is personal Imaging studies — which for decades have revealed the brain regions behind our behaviors, appetites and mental disorders — have tended to lump together scans from a bunch of people, in the process overlooking individual cerebral variations

Studies have also largely assumed that measuring someone’s brain function at a point in time is generally representative of that person’s daily function at that point in life

That notion appears way off the mark, though, for people diagnosed with specific psychiatric disorders For

example, those with schizophrenia may end up in weeks-long active phases of disease, experiencing hallucinations, delusions, even full-blown psychosis Depression and bipolar disorder are other conditions that flare, then dissipate as the brain returns to an even keel

To open up new roads into treating these and other diseases, MyConnectome and studies like it are capturing a normal brain’s ebbs and flows The approach should help make personalized medicine possible, tailored to each patient’s unique neural wiring diagram, or connectome

“If we want to understand fluctuations in disease, the first thing

we need to do is to understand how

a healthy person’s brain function fluctuates,” says Poldrack

Prognosis

TAKING THE PLUNGE

Logistical roadblocks have long

stymied the collection of

brain-and-body fluctuations What healthy

person would want to report to a lab

for frequent MRIs and jabs? And who

would pay for the procedures?

Those objections became moot for

Poldrack several years ago, while at

the University of Texas at Austin A

friend involved in the Quantified Self,

a movement embracing technology for

self-tracking, finally convinced him

“My friend was goading me,” says

Poldrack “She said, ‘You’ve got

an MRI scanner in your basement

You’ve got to get in there!’ ”

(Poldrack’s lab still had to pay for

scans, but at an early-bird, pre-8 a.m

rate of $150 a go.)

In subjecting himself to

MyConnectome’s demands, Poldrack

drew inspiration from numerous

self-experimenting scientists One such

“human guinea pig,” Michael Snyder,

is now a colleague at Stanford

In 2012, Snyder and his research

team published a groundbreaking

study in which they analyzed the

levels of 40,000 molecules from 20 of

Snyder’s own blood samples, taken

over 14 months The effort yielded

the first “integrative personal-omics

profile,” or iPOP, documenting Snyder’s

unique set of active genes, metabolites,

proteins and other biomolecules

Snyder’s research goals were similar

to Poldrack’s MyConnectome in pointing the way toward a precision kind of medicine, focusing on patients’

particular biochemistries, as opposed

to today’s one-size-fits-most approach

“Snyder’s work made me think I can do interesting science with an

n of 1,” says Poldrack, using the scientific jargon for a sample size consisting of just a single individual

MyConnectome was born

SELF-EXAMINATION

Although analysis continues for the massive pile of data gathered from September 2012 to March 2014 for MyConnectome — or the “Russ-ome,” as Poldrack’s labmates call

it — some intriguing correlations have already emerged

Before his Tuesday MRI scans, Poldrack fasted and gave up his morning coffee On those days, the scan revealed stronger signals of coordination between regions for somatomotor (which senses touch and controls movement), attention and vision “These studies are a window into the brain-body connection,” says Poldrack Also, the metabolic markers and levels of gene activity in Poldrack’s blood varied considerably with diet and brain function, as well as the severity

of his psoriasis, an autoimmune disease that causes his scalp to flake.Another important finding was the fluctuating activity within certain regions in Poldrack’s brain, which stood out from the averaged point-in-time scans of multiple people used in conventional research Those

Data from Poldrack’s brain scans show changes in coordination between regions for movement control, attention and vision, as he shifted between states of being fasted and fed.

Neuroscientist Russell Poldrack undergoes one of 104 MRI scans at the University of

Texas Imaging Research Center At right, a slice of his brain is shown on a monitor.

blended scans usually find the greatest

difference in subjects’ prefrontal cortex,

the seat of individual personality

Poldrack’s data suggests researchers are

missing the even greater fluctuations in

an individual’s other brain regions over

time That means data on potentially

key differences within individuals

— and their relation to wellness and

illness — is getting lost in the wash,

Poldrack says

Future studies could flesh out the

significance of the “Russ-ome’s”

idiosyncrasies by comparing them

with the Human Connectome Project

(HCP), which Poldrack has served on

the advisory board of since it launched

six years ago This major international

effort is pooling the snapshot scans

of 1,200 individuals to create a

generic, but authoritatively thorough,

baseline brain map

“When we put the datasets side

to side, there will likely be some

interesting insights about how Russ’

brain and its structural organization

relate to the hundreds of individuals

we have charted,” says HCP

neuroscientist David Van Essen of

Washington University in St Louis

THE “ME” IN “MEDICINE”

Numerous researchers are currently

delving into Poldrack’s public datasets

and have expressed interest in pursuing their own MyConnectome-style studies, this time involving multiple individuals

Stanford’s Snyder is pleased about the growing push to understand human biological variation via personal connectome and other

“-ome” profiles, such as metabolomes (the total metabolites present at

a given time in our bodies) and proteomes (ditto for proteins) “My own view about this is you can’t have enough of these profiles,” Snyder says “The more we get, the more we learn, and we’re already learning that everyone’s baseline is different People are poised very differently to respond

to environmental cues.”

Poldrack and Snyder hope that the vastly expanded and frequent testing they’ve tried to pioneer on themselves will help personalize medicine, leading

to improved diagnoses and prognoses

“We’ll have a whole different world

where we’re measuring people in a lot more sensitive fashion,” says Snyder

His own experience is a telling one: During Snyder’s deep, inward look for the iPOP project, he witnessed himself

in real-time unexpectedly develop Type II diabetes He had none of the common risk factors and knew of no family history of diabetes Thanks to the frequent monitoring, and catching the disease early, Snyder was able to respond and slow its progression

Poldrack is likewise hoping for further insight into the foods, mental states and other factors that exacerbate his psoriasis As researchers tease out the daily goings-on of singular minds, perhaps millions of those with mental illness can hold out similar longings for relief as certain “triggers” of their conditions are identified

“Probably the best thing that can come out of [MyConnectome] is inspiring someone to go and do a really great job with a big population

of people studied over a long period

of time,” says Poldrack “We want to answer the question of what’s going wrong in the brain and the body.” D

Adam Hadhazy is a freelance science

writer based in New Jersey He writes for

New Scientist and BBC Future, among

other publications.

“The more we get, the more we learn, and we’re already learning that everyone’s baseline is different.”

Imaging studies that combine scans from many people, such as this diffusion

image (above) from the Human Connectome Project, don’t identify brain

variations in individuals In contrast, Poldrack’s individual scan (right) shows

an area in yellow, indicating an anomaly in his corpus callosum

Prognosis

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→It was December, and my

boyfriend and I were teasing

each other about the gifts we’d gotten

for one another

“Well, it’s a thing that I purchased

from a store,” I said, washing my face

as I got ready for bed

“It’s stuff in a box, but originally it

was in a bag,” he responded from the

other room

Fun, useless banter But at some

point, I got too specific I told him

one of his gifts was something

I ordered, but the particular things

would be a surprise to both of us

when he opened it As soon as I said

it, I knew I’d given too much away

— there were going to be follow-up

questions

And what I did next felt strange,

even as I was doing it I stopped

in the middle of my nightly ritual

of moisturizing my face and started

brushing my teeth instead

At the time, I thought maybe I

switched to the toothbrush because

lying to my boyfriend about his

gift would be less obvious if my

fibs were muffled and my face was

partially obscured

“Is it some sort of subscription

service?”

With brushing sounds: “Mmmm,

no.” (It was.)

“Is it some kind of food thing?”

I brushed harder, smothering

awkward laughter: “Nooo.” (It was

that, too.)

Somehow, I hid that he was getting

a monthly hot sauce subscription

I just attributed it to the oh-so-clever way I’d disguised my deception

But the motivation to suddenly brush my teeth may have been rooted in something much deeper:

the Macbeth effect, named after the scene in the Shakespeare play where Lady Macbeth’s complicity

in a murder leads her to imagine bloodstains on her hands Her guilt makes her feel physically unclean even though she actually isn’t

All of this has to do with something called embodied cognition, a relatively new idea asserting that as the mind influences the body, the body influences the mind “Embodiment is very interesting because it’s a new way to

do research on [sub]consciousness,”

says neuroscientist Michael Schaefer

at Medical School Berlin, “so we really can try to unravel things that we cannot see in a regular way.”

Going beyond ethics, scientists have found that physical experiences influence other aspects of cognition, too In 2014, researchers in Germany had people read an ambiguous

Think

Outside

the Brain

How our body can

influence our mind.

BY MALLORY LOCKLEAR

In Shakespeare’s famous play, Lady Macbeth’s guilt over her role in a murder is so great that she imagines bloodstains on her hands and compulsively washes them This phenomenon, called the Macbeth effect, ties into what scientists call embodied cognition.

Mind

Over

Matter

October 2016 DISCOVER 23

conversation while touching either

a rough or smooth surface When

they touched the rough surface,

participants were more likely to think

the conversation was adversarial and

harsh And a 2010 Science study

found that people tended to rate

a job candidate more highly if the

candidate’s résumé was attached to a

heavy, rather than a light, clipboard

So my urgent need to brush my teeth

as I steered my boyfriend away from

discovering his gift may not have been

a tool to mask my untruths Instead,

it might’ve been a personal need to

absolve myself of guilt as I cleaned

my lying mouth As Schaefer tells me,

“The Macbeth effect is very interesting

because it describes a link between

physical cleaning and moral purity

When you’ve done something bad to

a person, like lie, you have the need to

clean your body, and if you get to, you

feel better.”

This intrigued me, not only as a

guilty, serial gift-liar, but also as a

neuroscientist And it has intrigued

other neuroscientists and psychologists,

too, such as Schaefer

In a study published last December,

he and his team asked 35 participants

to read various scenarios and then

speak or write a prepared response

that was either truthful or a lie In

one scenario, the volunteers found an

important document that could hurt a

colleague if they didn’t return it Then

the subjects told the colleague they

did find it (the truth) or didn’t (a lie)

Afterward, researchers showed the

participants two products: a hand soap

and a toothpaste or mouthwash Then

they asked them to rank each product’s

desirability on a 4-point scale

Like previous studies, this one

found that if participants lied, whether

verbally or in a written note, they gave

the hygiene products better scores than

after telling the truth If they spoke

the lie instead of writing it, they rated

toothpaste and mouthwash higher than

hand soap (and vice versa.) So it seems

people find cleaning the “dirty” part of their body — the part that commits the lie — more desirable than cleaning the

A touch on the foot would register in a certain part of the cortex, and a touch

on the nose, another

Using fMRI, Schaefer and his team saw that when the study participants were rating hand-washing products, the part of their brains’ somatosensory cortex linked to the hand showed a flurry of activity Surprisingly, that activity was much stronger after writing a lie than writing the truth The same thing happened when they rated mouth-related products After speaking

a lie, the cortical area dedicated to their mouth was much more active

while people scored toothpaste and mouthwash products than it was after they told the truth

WARM FEELINGS

Now I’m faced with a problem If my boyfriend reads this, he might wise

up to my own Macbeth effect, giving

me away during future Christmas discussions Maybe there’s some other Shakespearean-inspired psychological phenomenon to help me deal with my lies? Or maybe I’ll exploit the findings

of another study

In a paper published in Social

Cognitive and Affective Neuroscience

in 2011, researchers at Yale described their discovery that people who touched a warm object were more likely to invest money with a stranger than people who touched something cold And, like Schaefer’s study, the team observed the temperature-influenced trust effect in the brain, in

an area known as the insula Along with regulating other functions, the insula becomes more active when someone faces risk

When a participant held something cold before deciding whether to trust

a stranger, the activity in the insula intensified But when the participant held something warm, the insula remained in a calmer state And a more relaxed insula is a more trusting insula.Turns out this warmth angle may actually be doubly useful for me

In a 2008 Science study, marketing

professor Lawrence Williams and social psychologist John Bargh found that people were more likely to pick out a treat for themselves if they had recently held something cold Yet when they’d held something hot, they were more apt to choose a gift for a friend

So maybe this December I’ll just manipulate my boyfriend’s insula and generosity with a warm cup of tea What could go wrong? D

Mallory Locklear is a science writer and has

a Ph.D in neuroscience.

In one study, people read a conversation while touching a smooth or rough surface The chat seemed more hostile while touching the latter.

Going beyond ethics, scientists have found that physical experiences influence other aspects of cognition, too

is now on a campaign to make this kind of tailored cancer care available

to more patients And, ironically, this individually focused approach likely hinges on the efforts of crowds

DATA-DRIVEN TREATMENTS

The approach is already routine for some cancer patients, such as women and men with breast cancer tumors that have high levels of a protein called HER2, or lung cancer tumors

→Eric Dishman, a former Intel

executive now at the National

Institutes of Health, was a

19-year-old college sophomore when he

was diagnosed with a rare form of

kidney cancer Over the course of

the next 23 years, he would receive

62 different kinds of chemotherapy,

immunotherapy and radiation Some

slowed the tumor’s growth, but never

for long The cancer spread from his

left kidney to right kidney

Just when it seemed Dishman

had run out of options, a chance

encounter in 2012 with a scientist

working for a now-defunct

genome-testing company presented an

opportunity he couldn’t refuse He

had his cancerous tissue sequenced,

a process that would compare his

cancer’s mutated DNA with a healthy

patient’s genome This would let

doctors look for genetic mutations

and other abnormalities that support

cancer growth, and to use that

information to devise a treatment

strategy For example, changes in

certain genes could indicate that his

cancer was more likely to respond to a

particular drug, while other mutations

might predict little benefit from a

specific therapy Once the doctors

sequenced his tumor, all he had to do

was wait And wait

Dishman says he was “literally at

death’s door,” when he got the call

from his doctor It had taken seven

months for a team of oncologists,

computer scientists and data crunchers

to analyze Dishman’s genetic data

and pinpoint a drug — for pancreatic

cancer — that would target the

unique features of his cancer This

Fighting Cancer With Data

Doctors can now tailor cancer treatments based on their patients’ genes, but expansion

will require new levels of data sharing and computing power

— from genetic sequences and imaging data to findings in personal health records.

Big

Idea

with mutations in the EGFR gene

These people can often benefit from

drugs that target specific

cancer-causing aberrations rather than

attacking the body as a whole

Most patients’ treatment trajectories

are not as straightforward In theory,

insights into the genetic underpinnings

of cancer, made possible through

genomic sequencing, will allow

people with even the

hardest-to-treat diagnoses to benefit from

individualized treatment approaches

Currently, only about 2 percent of

cancer patients have their genomes

sequenced These lucky few are most

often treated at elite cancer institutions

as part of a clinical trial However,

doctors are increasingly making use

of the new technology as it becomes

exponentially cheaper and faster

But devising treatment strategies

based on insights from sequencing

data, as was done for Dishman,

requires “monumental shifts in how

we share knowledge,” says Brian

Druker, director of Oregon Health &

Science University’s (OHSU) Knight

Cancer Institute

First, it requires data, and lots of

it That’s the only way to pinpoint the

mutations that cause cancers and fuel

their growth “Something that occurs

in 1 in 5,000 people seems like a fluke

You really need a dataset of 500,000

or a million people to start seeing

patterns,” Druker says

And second, it requires enormous computing power Sequencing a single genome yields a terabyte or more of data; Dishman’s kidney tumor yielded

5 terabytes

STRENGTH IN NUMBERS

Druker and a growing number of scientists believe that amassing and deciphering this torrent of data requires the same open-source ethos that computer programmers have embraced to revolutionize software development This approach makes the source code of a computer program openly available, and any improvements or modifications to the code are publicly shared

It could work with cancer, too

“Open source means that, rather than sharing code, scientists and clinicians share data and build upon each other’s knowledge,” says John Wilbanks

of Sage Bionetworks, a non-profit biomedical research organization

in Seattle that supports open science projects While few can dispute the benefits of accessibility — after all, scientists depend on the past research

of others — Wilbanks says there’s a

“prevailing data-hoarding culture.”Many scientists remain protective

of career-advancing findings or intellectual property that could be commercialized Others cite patient privacy concerns, particularly given the recent spate of data breaches within health care organizations And data detached from names can still sometimes be used to identify supposedly anonymous patients.Even among those inclined to share, some practical challenges exist Moving data from one institution

to another can be expensive, and it can take weeks to ship hard drives

or download the data Few cancer centers have the resources to invest

in powerful enough computers or robust enough networks to support the mammoth datasets The result, says Dishman, is a “computational bottleneck that stymies progress.”It’s a bitter pill to swallow for an estimated 1.7 million people in the U.S who will be diagnosed with cancer this year alone, especially for those with rare cancers But they may soon have a new option

QUICK CANCER QUERIES

Intel and OHSU have teamed up through a new, open-source platform called the Collaborative Cancer Cloud (CCC) The initiative enables cancer centers to access and analyze vast amounts of anonymous patient information — from genetic sequences and imaging data to findings in personal health records

Unlike other open-source initiatives, which ask centers to transfer or retrieve data from one centralized location, the CCC allows researchers

to keep their data local Users access

a virtual registry of all this data via

Former Intel executive and cancer

survivor Eric Dishman (above), now at

NIH, wants to put vast cancer genome

databases in the hands of doctors The

Knight Cancer Institute’s Brian Druker

(right) leads one such high-profile effort.

This colored scanning electron micrograph shows a pancreatic cancer cell

“The idea is, you can blast a virtual query to sites around the world, who together have insight from a million other patients’ data, and ask, ‘Are there any patients that look like the patient in front of me on a genetic level?’ ” says Druker “ ‘And what treatments worked for them?’ ” Theoretically, the system would automatically return de-identified information about similar patients.

Today, when Druker wants to gain insight from patient data beyond his own institution, he must do so manually, by phone or email It’s a painstaking process that can take weeks or months Though the CCC has just launched, its goal is to make this happen in less than a day by

2020 as more cancer centers join and share data

“You get sequenced in the morning,” says Druker “Your data is then compared against millions of other patients By the end of the day, your doctor can say, ‘Yes, we have found the treatment for you and the data to support that choice.’

“You can’t tell a patient to be patient They need treatments today,”

he added D

Aimee Swartz is a freelance writer based

in Washington, D.C She frequently covers health, with a focus on rare diseases and precision medicine

the cloud — that is,

a network of remote

servers hosted on the

internet, like the one

where your email and

selfies are stored

In addition, the CCC provides users

with cloud-based access to a collection

of tools commonly used for genomic

analyses, which means centers don’t

have to shell out for costly in-house

hardware and analytics stacks

“Rather than ask people to move

the data out, we bring the computer

power in,” says Dishman

A GROWING MOVEMENT

The CCC isn’t the only cloud-based

data commons The National

Cancer Institute is developing a

platform to house data from the

Cancer Genome Atlas — a massive

catalog of genomic data from over

11,000 cancer patients And several

institutions have their own clouds

where cancer data is kept

“The problem is these clouds aren’t

connected to other clouds We want

to connect them all because, really,

we’ll not be able to find the root cause

of cancers and the best treatments

for those cancers without studying,

literally, data from millions of

patients,” says Dishman

So far, in addition to OHSU, the

Dana-Farber Cancer Institute in

Boston and the Ontario Institute for

Cancer Research in Toronto have joined the CCC, and Dishman says “dozens of others” have expressed interest

Most cancer centers already have the necessary computing capabilities

“If they don’t, it’s as simple as downloading the CCC tools,” says Dishman And while he expects many will run CCC on Intel servers, it’s not

a requirement “You don’t have to buy our products to be part of CCC,” says Dishman “Because it’s open source, it can just as easily run on other computer architectures.”

Druker says doctors can tap the

“The idea is, you can blast a virtual query to sites around the world, who together have insight from a million other patients’ data, and ask, ‘Are there any patients that look like the patient in front of

me on a genetic level?’ ”

Killer T cells (green) surround a cancer cell (blue), where they will deliver the death blow via chemicals stored

in vesicles (red)

Big

Idea

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for Curious Minds

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THE YEAR IN SCIENCE

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28 DISCOVERMAGAZINE.COM

“There are just two of us left now,” Jemima Westcott says wistfully Only she and her kid brother, a sprig at age 94, remain of a once-thriving family Westcott’s older sisters died

at age 105 and 107, and she marked her own 105th birthday in January at a dinner party

in her cozy condo in Brandon, Manitoba, surrounded by her children and grandchildren

Widowed for 50 years, she still lives alone, cooking and cleaning for herself — her only concession to old age is using a walker

Westcott has lived through iconic events

of the 20th century She has vivid memories

of the celebrations when soldiers returned home from World War I; of big picnics on her family’s farm on the windswept prairies;

of gas rationing during the second world war, when she was a young mother with five kids; and of traveling across Europe, North Africa and the U.S., and even diving in the Great Barrier Reef during a yearlong stint in Australia after she retired

“I’ve had an adventurous life,” says the former schoolteacher, an admitted night owl who stays up into the wee hours and

likes to sleep in Her secret to a long life?

“Resilience.”

Westcott may be on to something She’s a participant in the New England Centenarian Study, a long-term research project at the Boston Medical Center that studies why people like her enjoy such exceptional longevity What they’ve found, thus far, is that healthy habits and positive attitudes will only get you so far: Centenarians are winners

of the genetic lottery and, like Westcott, have

a clustering of long-lived relatives They are remarkably intact mentally, and up to 90 percent of them can function independently into their ninth decade Surviving past age

100 means they’ve largely evaded the scourges that kill their peers before they reach their 90s (what’s called compressed morbidity),

or sidestepped the worst aspects of these life-threatening diseases — even if they strike sooner — because they have combinations

of protective genes, what researchers call

“greater functional reserves.”

“Even though they have these illnesses, they handle them better than other people and

The secrets to staying young may lie

in the DNA of the oldest among us.

BY LINDA MARSA

What it Takes

to Reach What it Takes

to Reach

30 DISCOVERMAGAZINE.COM

have better protective mechanisms,”

says Thomas Perls, a geriatrician at

Boston University and director of the

New England Centenarian Study “In

other words, the older you get, the

healthier you have been.”

Now scientists like Perls are

sifting through millions of DNA

markers to spot the constellation

of longevity genes that’s carried

in every cell of these centenarians’

bodies Perls and his colleagues

have uncovered 281 genetic markers

that seem to perform a protective

function, slowing aging and making

this group less vulnerable to disease

Other researchers, in sequencing the

genome of centenarians, have found

they possess fewer of the genes that

contribute to major diseases “They

live longer, in part, because they don’t

get sick,” says Stuart Kim, one of the

study co-authors and a geneticist at

Stanford University

How does this happen? Scientists

suspect there may be some kind of

intrinsic biological clock that runs

slower in some people and quicker in

others, which would accelerate aging

and wear down the body’s protective

processes Those with faster clocks are

then more vulnerable to the onset of

fatal diseases and die sooner Research

into the genetics of long-livers, and

into other biological systems that may

influence aging, offers some tantalizing

clues into the underlying mechanics of

these clocks Deciphering precisely how

they work could enable us to tinker with these internal timepieces and genuinely slow down the aging process

REAL AGE

Timing seems to be a key piece of the puzzle Biological age doesn’t always match what’s on a person’s birth certificate After all, we’re not surprised to see a 70-something debilitated by illness, or a 74-year-old who barnstorms around the country, running for president Some people simply age faster than others, and scientists are beginning to understand why New research using data from a landmark longitudinal study has been particularly eye opening Known as the Dunedin study, it followed more than 1,000 people from their births in the early 1970s in the same hospital in southern New Zealand

Most research looks at aging in older people, but the seeds of age-related diseases are planted decades earlier — that’s why these researchers

believe it’s crucial to study aging in the young They aim to shed light on why

we become vulnerable to the assaults

of time and the chronic diseases linked

to aging, such as cancer, heart disease, diabetes, and loss of mental acuity

Scientists in the U.S., U.K., Israel and New Zealand looking at the Dunedin data used it to track 18 biological measures, including liver and kidney function, blood sugar and cholesterol levels, balance, cognitive ability, cardiovascular fitness and even gum recession in 954 study participants

As expected, most people’s biological age clustered around their early 40s, within a few years

of their actual ages, according to results released last year But there were wide variations: A handful were up to a decade younger, while many had a biological age in their 50s; one participant had a biological age of 61 Even before midlife, some participants were aging much faster They were already having trouble with

Scientists suspect

there may be some

kind of intrinsic

biological clock

that runs slower in

some people and

climbing stairs and difficulties solving

unfamiliar mental tasks, their balance

was worse, their livers were starting

to fail, and they were in poorer

overall health

“When we assembled all the data,

we were quite struck about the

coordinated changes we did see in all

the systems of the body,” says Daniel

Belsky, the study’s lead author and

a gerontologist at Duke University’s

Center for Aging “Clearly, there are

basic molecular mechanisms of aging

that cause the various diseases that

disable and ultimately kill us.”

THE CELLULAR COUNTER

More than 50 years ago, a researcher

uncovered the first clues that an

internal biological clock might

regulate age — and that it’s not just

the daily assaults from the external

wear and tear of life that cause us to

wither and eventually die That’s when

Leonard Hayflick discovered what

would become known as the Hayflick

limit In the late 1950s, as a young

microbiologist at the Wistar Institute

in Philadelphia, Hayflick studied

viruses that might cause cancer While

there, he worked with cell cultures

derived from human fetal tissue

One day, the cell division in one of the

flasks seemed to be slowing down, and after about the 40th doubling, the cells stopped reproducing

At that time, scientists believed all cells were immortal — marinate them in the proper nutrients, and they would divide forever Hayflick thought

he had made a technical mistake or that the cells were contaminated

But then he observed the same halt

in cell division in other cultures with different fetal tissues He went back through his records, looking for clues

to the anomaly, and discovered that

of the many cultures he had made, it was always the oldest ones that had stopped replicating

While cancer cells are immortal — their hallmark is wildly reproducing out of control — Hayflick discovered that normal cells have a limited life span Even when cells are frozen for months, subsequent research demonstrated, when they thaw out, they pick up their cell division where they left off until they hit between 40 and 60 doublings

“When I discovered that normal cells had a memory, I nearly fell

of my chair No one ever thought normal cells had a memory,” Hayflick recalls “There had to be some sort

of intracellular counting mechanism

or meter that tells the cells how many divisions it has gone through But where?”

In 1975, Hayflick and graduate student Woodring Wright proved the counting device was in the cell nucleus, but they didn’t have the technological tools to unlock the precise mechanism Even though Hayflick’s discoveries went against accepted scientific dogma

— “I was the first one to show that aging had its origins inside the cell,”

he now says — they ultimately sparked

an explosion in the study of aging But another decade would pass before

a candidate emerged for Hayflick’s

“replicometer.”

DNA FRAGMENTS

Despite all the accolades heaped upon her for groundbreaking research, Elizabeth Blackburn retains the homespun warmth, sharp wit and

plucky spirit of her native Australia Early this year, the Nobel Prize-winning biochemist left her lab at the University of California, San Francisco, to head up the Salk Institute, the scientific incubator founded by polio vaccine pioneer Jonas Salk The center is housed in a cluster of modern concrete and glass buildings perched on the coast in La Jolla, Calif We sit at a conference table in her airy office, with floor-to-ceiling windows looking out

In the 1970s she landed at Yale

At the time, scientists believed all cells were

immortal — marinate them

in the proper nutrients, and they would divide forever.

Leonard Hayflick

University, where she sequenced the

tips of chromosomes of a single-celled

organism, Tetrahymena — “pond

scum,” she cheerfully offers These tiny

strips of DNA, called telomeres, cap

the end of chromosomes Scientists

long suspected they stabilized the

structure of the chromosome,

preventing the tips from fraying, much

like the plastic sheaths at the ends

of shoelaces to prevent them from

unraveling But how?

Each time a cell divides, the telomere

gets shorter, but its function had long

been unclear “We had the seeds of an

idea [that] there could be a clocklike

thing, because every time the DNA

replicated, the end of the chromosome

wasn’t replicated,” Blackburn recalls

It wasn’t until the late 1980s that a

strong connection was made between

telomeres and cellular aging, in a

breakthrough that resulted from a bit

of scientific serendipity Blackburn’s

former graduate student, Carol Greider,

was dating a biologist who shared lab

space with Calvin Harley, a biochemist

studying aging at McMaster University

in Ontario Casual conversations in the

lab grew into a full-scale collaboration

that melded Harley and Greider’s

areas of expertise — cell senescence and telomeres

The result was two landmark papers published in 1990 and 1992 that made

a convincing case that telomeres might

be the cellular timing device behind the Hayflick limit With each cell division, telomeres dwindle until they are just tiny nubs, which prompt cells

to malfunction, stop replication and finally die off This research provided

“some good clues that we were going

in the right direction,” says Blackburn,

“but it took years and years of observations by lots of scientists before the puzzle pieces were put together to form a real picture of what happens.”

STUNTED TELOMERES

Telomere shortening is now considered

a biomarker of cellular aging, and more evidence suggests that these tiny fragments of DNA may be one of the culprits behind age-related decline

Subsequent studies have shown that shortened telomeres are linked to many age-related diseases, including heart disease, diabetes, Alzheimer’s, stroke and obstructive lung disease “These are the major killers of the elderly,”

says Blackburn “We’re starting to go

beyond just correlations and seeing a real element of causality here.”

Even chronic stress can wear away our telomeres, according to research done in the early 2000s that looked

at mothers caring for children with chronic diseases Blackburn and UCSF psychologist Elissa Epel’s work found that the most stressed-out women had shorter telomeres that translated into an extra decade or so of aging compared with their matched controls

— showing that external stressors can throw a monkey wrench into the cell’s molecular mechanics

More recent research, presented at

a scientific meeting in 2012, analyzed saliva samples from more than 100,000 people who belonged to Kaiser Permanente, an HMO in Northern California The major take-home message: People with stunted telomeres die at younger ages What was equally intriguing is that even though women outlive men, as young adults their telomeres are about the same length While everyone’s telomeres dwindle

as they grow older, a big split occurs after age 50, when telomere shortening among men accelerates The gender division continues to widen until about

TELOMERES AND AGING

Elizabeth Blackburn talks about the link.

Telomeres are tiny fragments

of DNA at the end of each

chromosome Nobel laureate

Elizabeth Blackburn has spent

her career studying their

function Here, she talks about

the role they play in aging

DISCOVER:Are telomeres the

clock behind aging?

BLACKBURN: As a loose

approximation, aging is

clocklike because there’s a

progressiveness to it But

we’ve got to be smarter about

what that word aging really

means Is human aging your

risk of getting the diseases

of aging? Well, in that case,

centenarians never age And yet, they clearly do age: They get wrinkled and frail and smaller — they’re doing well but they’re not young people

Aging has multiple aspects, and we tend to oversimplify

it A lot of different kinds

of things come into play

in different stages If we avoid all the major diseases, there’ll still be an aging process, which is not identical

Telomere shortening seems

to underlie the risks for the diseases that kill you

DISCOVER:In what way?

BLACKBURN: Every sign,

including genetics, says there’s some causality [between telomeres] and the nasty things that happen

with aging, the really nasty diseases that kill us — heart disease, diabetes, cancer, even Alzheimer’s We know

Elizabeth Blackburn

32 DISCOVERMAGAZINE.COM

age 75, when those with the blunted telomeres die from disease.

These results demonstrate at

a molecular level what scientists tracking centenarians had observed:

Longer-lived people have a biological advantage that enables them to escape

or better withstand what Blackburn calls “the hail of bullets” that kill the majority of us “Most mortality in the population happens around age

75, and anybody who lives longer has been somehow biologically selected,”

says Blackburn “We know telomere shortening drives cells into senescence

So it is reasonable to say that this is driving pathologies in humans.”

But telomeres aren’t the whole story

THE EPIGENETIC CLOCK

“There’s a knot in here that’s going

to give you trouble,” Jose Valencia warns me, speaking in Spanish through

an interpreter while he massages the fleshy pad of skin between my left thumb and index finger, then flashes

a mischievous, toothy grin, as if to tell me I’d better be careful Barely

5 feet tall and clad in crisp khakis and

a short-sleeve striped shirt, Valencia sits placidly on a bench in front of

the cinderblock house he shares with his granddaughter, Keren Gonzales Valencia, in El Torito, Costa Rica, a tiny village honeycombed by dirt roads where the rainforest meets the beach

It is a sultry November day with temperatures hovering in the low 90s It’s the end of the rainy season on the Nicoya Peninsula in the northwest corner of Costa Rica, and the jungle

is lush from months of torrential downpours A healer of local renown, Valencia taught himself anatomy by dissecting chickens — three of which lazily strut across the yard while we talk He massages strained muscles and fixes dislocated joints when doctors are too busy, he says Even the local expat surfers and retirees come see him when their backs hurt

A farmer all his life, Valencia retired

at age 80 when he was diagnosed with leukemia, but it barely slowed him down He’ll be celebrating his 97th birthday in a few days, he tells me, and shares bittersweet recollections of being a lovesick teenager eight decades earlier: There were no roads, and the only way he could visit his sweetheart

in the next town was to walk along the beach He attributes his long life

telomeres shorten, and

eventually cell division stops.

DNA

telomere shortening drives

cells into senescence [aging]

If you look at people with

wrinkled skin versus not

wrinkled skin, the people

with sagging, UV-damaged

skin have shorter telomeres

than people with smooth,

unwrinkled skin If you’re in

the bottom third of telomere

length, your cardiovascular

disease risk goes up 40

percent, which is not a trivial

number Pessimism correlates

with shorter telomeres So

you can put all this together

and say it’s reasonable that

some of this is really driving

pathologies in humans

DISCOVER: So the shorter the

telomeres, the more likely it is

you’ll be stricken with diseases and that you’ll age faster?

BLACKBURN: If you inherit very short telomeres, you get this terrible disease now being called the “telomere syndrome.” It’s extremely rare because these poor children don’t survive into adulthood

But because there are billions

of us on the planet, it’s happened often enough that there are now hundreds of individuals and many afflicted families around the world A child will come into the clinic with a skin disorder, but that’s not the real problem: They have terrible gut disorders and their whole body is fraught with problems,

and they have this whole spectrum of very nasty, very early onset diseases, which are the ones that often appear with age

About 10 percent of them die of some rare cancer, and a lot of them die of infections, and their guts don’t work properly and they’re really sickly But then you look at the parents and the grandparents because this gene has to come from somewhere And you find the grandparent with the gene had pulmonary fibrosis So the molecular cause is exactly the same base pair change

in a telomerase gene But

it played out in the body

differently The grandparent’s telomeres were shorter than their peers’ and the parent’s telomeres were even shorter, and the child’s were really short

So what if people inherited somewhat shorter telomeres and never completely recovered or do things that

we know externally promote shortening of telomeres, like smoking or living in stressful situations? They might do just fine, but if there’s something else going on combined with the shorter telomeres, that might be enough to kill them Telomeres are not the end of the story, but they play a role

34 DISCOVERMAGAZINE.COM

to hard work, good food and family

— his wife died less than a year ago

and his extended family of children,

grandkids and great-grandkids

all live nearby

But his longevity is not unusual

for the Nicoya Peninsula, an 85-mile

sliver of pristine beaches, cow pastures,

farms and wooded hills, where

residents often reach ages of 90, 100 or

even 110 Despite their poverty, locals

live far longer than their wealthier

counterparts elsewhere The peninsula

is one of the world’s five Blue Zones,

where more people live past 100 than

in other parts of the world The other

four longevity hot spots are Okinawa,

Japan; Loma Linda, Calif.; Sardinia,

Italy; and Ikaria, Greece

In 2005, Costa Rican demographer

Luis Rosero-Bixby found that

Costa Ricans who survive to age

60 end up having the longest life

expectancy of anyone in the world

Subsequent research in 2012 found

that older residents of Nicoya lived

even longer, up to three years more

than other Costa Ricans In research

published in 2013, Stanford University

epidemiologist David Rehkopf and

his colleagues wanted to find out why

They took DNA samples from Nicoya

residents who were older than 60 to

measure the length of their telomeres

They turned out to be longer than

those of other Costa Ricans, with an

average difference of about 81 base

pairs, equivalent to the benefits of

quitting smoking or getting regular physical activity

Why do those on the Nicoya Peninsula live so long? The key seems to be in the nation’s familiar catchphrase: pura vida, or “pure life.” Costa Rica, a centuries-old democracy with universal health care,

no standing army and the highest literacy rate in Central America, has been relatively insulated from the corruption, narco-terrorism and civil wars that have plagued neighbors like Panama, Nicaragua and Guatemala

Researchers believe Nicoyans’ leisurely pace of life, plant-based diet, network

of family and friends, regular exercise and purposeful lives seem to be their recipe for longevity

While outside forces — stress,

poverty, environmental toxins — can accelerate aging, the reverse seems

to be true, too Our life experiences exert a profound influence on how

we age and can even alter the ways genes function without changing the underlying DNA sequence; these genetic changes are called epigenetic traits A research team at UCLA led

by biostatistician Steven Horvath has uncovered an epigenetic biological clock that may provide a key puzzle piece in deciphering how this happens

— and help explain why Nicoyans live

so long “For those people who age more slowly, somehow their epigenetic clock ticks more slowly,” Horvath says

“There’s an intrinsic process that drives aging, and that may be what’s captured

by this epigenetic clock.”

Our life experiences

exert a profound

influence on how

we age and can

alter the ways

THE MECHANICS OF AGING

For the German-born Horvath,

a boyish 48-year-old with broad

features and a puckish sense of

humor, the discovery is the fruition of

a lifelong dream, dating back to high

school, when he decided to devote his

career to prolonging the human life

span But it wasn’t until 2006 that the

advent of big data allowed him to sift

through millions of data points to

ferret out biomarkers that correlated

with age

His team focused on a naturally

occurring process that’s part of

the body’s internal housekeeping

system, called methylation, which

makes chemical modifications

to our genome that are strongly

influenced by environmental factors

Horvath was able to obtain over 50

datasets — from researchers in Spain,

Germany, Italy, the U.S., U.K and

Australia — that contained the genetic

profiles of thousands of subjects in

studies looking at methylations in

healthy tissue

Over the course of three years,

Horvath and his team analyzed

nearly 8,000 tissue samples from

these datasets, which included blood,

saliva and cells from organs like the

brain and the colon The UCLA

team identified 353 DNA markers

from 51 types of cells and tissues

and examined how age affects their

DNA methylation levels throughout

a lifetime They then used the data

to devise an algorithm that can

accurately determine the age of

diverse organs, tissues and cell types

When they compared a tissue’s biological age and its chronological age, the clock proved to be remarkably accurate in predicting age Stem cells plucked from embryos were deemed extremely young by the clock, while neural cells from centenarians were estimated to be about 100 And even cells that were young, such as white blood cells that may be just a few days

or weeks old, still carried the distinct genetic imprint of their 50-year-old donor “The 353 markers on the DNA provide a weighted average that gives you a very accurate measure of the age of the tissue,” says Horvath

Since then, he has used the epigenetic clock as a tool to begin

to understand the mechanics of aging Subsequent research on Italian centenarians revealed that the offspring of these centenarians

were substantially younger, up to about five years, according to their epigenetic clocks, than the progeny of non-centenarians

But perhaps Horvath’s most significant finding had its genesis in

2013, when researchers from the Los Angeles Gerontology Research Group, which studies supercentenarians (those who live to 110 and older), supplied him with tissue samples from three centenarians and three supercentenarians, one of whom recently died at age 112 What Horvath uncovered was astonishing

— and may eventually lead the way to extending our life

The research team analyzed the epigenetic age of up to 30 anatomic sites from the 112-year-old woman They discovered that the cerebellum is the youngest part of the body and didn’t age nearly as fast as other areas The neuron-packed brain region — it’s tucked underneath the cerebral hemispheres and plays a role in motor control and cognitive functions, such as attention and language — seemed to stop aging at the 80-year benchmark, which meant it remained fully functional but somehow impervious to deterioration of time for decades

Earlier this year, Horvath and his colleagues took a step toward answering this question Their analysis uncovered small variations in two genes related to the accelerated aging

of the cerebellum What was especially

“exciting” about this finding, he says,

is that these variations were near a neural highway that previous studies have shown helps regulate life span

in worms and flies, and that stopping chemical signals from this brain pathway extends the life span of mice While this discovery is still not a

“smoking gun,” says Horvath, “if we can understand why the cerebellum ages more slowly, we can figure out how to slow down all the other parts and uncover interventions that might

be able to reverse this process.” D

Linda Marsa is a Discover contributing editor

and author of Fevered: How a Hotter Planet

Will Hurt Our Health and How We Can Save

Ourselves

Loma Linda,

California

Nicoya, Costa Rica

Sardinia, Italy

Ikaria,

Blue

Zones

Longevity hot spots

across the globe

Steven Horvath

36 DISCOVERMAGAZINE.COM

the prefrontal cortex

— home to working memory — as a switch operator working the brain’s railroad tracks.

ATTENTION,

PLEASE

MIT neuroscientist

Earl Miller has

changed the way

38 DISCOVERMAGAZINE.COM

The jarring contrast between the two Earl Millers

is a fitting way to begin a discussion of the ing neuroscientist’s work

pioneer-After all, some of Miller’s biggest contributions

to the field over the past 20 years have explored exactly how contrasts like these are possible; how

it is, in other words, that human beings — or any other animal with a brain — are able to seamlessly adapt behavior to changing rules and environ-ments How is it that distinct populations of brain cells, or neurons, are able to work together to quickly summon an appropriate response? How

do we know when it’s fitting to play a Patti Smith bass line, and when it’s time to explain the complex workings of brain waves?

This mental flexibility is so fundamental that it’s easy to take it for granted But there are few functions the brain must perform that are more

complex or crucial to survival than recognizing when something has changed and then calling

up all the disparate information needed to adapt appropriately

“Think about what we’re doing here,” Miller says “Right now We’re sitting on chairs We’re taking turns talking This is based on rules We’ve learned how to behave in this context we’re in right now.”

To pull off tasks like these, the brain uses something called working memory Cognitive psychologists coined the term in 1960 as they tried

to explain the fundamental structure of the human thought process

You can think of working memory as the brain’s conscious mental scratchpad — the chalkboard for attention and decision-making Try to hold that last sentence in your mind, or memorize a phone number you’re about to dial, and you’ll have

engaged this critical brain system

Miller has spent the past two decades trying

to understand the mechanisms behind working memory, and he believes the key lies in the brain’s prefrontal cortex Insights into this thin layer of neurons at the front of the brain could answer questions that have flummoxed scientists for gen-erations It might have practical use, too

Experts have long known that we have a virtually unlimited capacity to store new long-term memo-ries Yet there’s a limit on how much information

we can cram into our working memory

In studying the prefrontal cortex’s functions, Miller and others are coming closer to finally explaining this contradiction And by solving this riddle, we may find ways to get beyond those limits.Someday, Miller believes, he’ll be able to make

us all smarter

I n the rehearsal space of the Boston band

What She Said, Earl Miller lays into his

bass guitar, plucking out a funky groove He

sticks out his tongue Mick Jagger style, as

the band’s drummer hammers away behind

him, clowning it up for photos splashed

onto social media In a black band tee, faded

cargo pants and signature newsboy cap, Miller

looks like a seasoned musician you’d see in any

corner dive bar.

But at his nearby office at MIT, Miller is

noth-ing if not professorial How could that rocker in

the cap be the same bookish academic now gazing

solemnly at me across his paper-strewn desk at the

Picower Institute for Learning and Memory?

A STUDY IN

CONTRASTS,

Earl Miller plays

bass at the Tavern

at the End of the

World in Boston’s

Charleston

neighborhood

BUILDING THE PICTURE

Much of what we know about how neurons allow

animals to make sense of their surroundings began

with experiments performed on the visual cortex

of animals by David Hubel and Torsten Wiesel As

postdoctoral students at Baltimore’s Johns Hopkins

University in the 1960s, they set out to solve a

long-standing mystery: What happens in the brain when

we see objects and shapes?

Every one of us has about 100 billion neurons,

separated by gaps called synapses Neurons talk to

each other by passing signals across these spaces

When one neuron’s signal is strong

enough, it causes the neuron on the

other side of the synapse to fire an

electrical spike When that second

neu-ron fires, it passes messages to all the

other neurons it’s connected to, which

can cause those neurons to fire This

sequential firing of neurons allows us to think, to

move — and to see

Hubel and Wiesel inserted tiny, pin-shaped

micro-electrodes directly into a cat’s visual cortex to

mea-sure the activity there By projecting angled lines

onto the surface of the animal’s retina, they

demon-strated that each neuron in this thin sheet at the

back of the head has a distinct function

Some fired with the greatest intensity in response

to lines at specific angles, while others fired at angled

lines moving in a specific direction It is the

consecu-tive firing of these individual, specialized neurons,

each responsible for a specific detail in a picture or

pattern, they argued, that helps us build complex

images in our mind’s eye

Their work was so impressive within the field that

it earned them the Nobel Prize in Physiology or

Medicine in 1981

As it happened, Miller entered college at Kent

State University the same year — though back then,

Miller dreamed of becoming a doctor

That quickly changed when he started working in

a neuroscience lab

“The moment I first dropped an electrode into

a slice of brain and heard all these neurons

firing away like a thunderstorm, I was hooked,”

Miller recalls

As a Princeton University graduate student,

Miller studied the inferior temporal cortex, a patch

of neurons slightly forward of the visual cortex

Scientists had demonstrated this was the region that

knits together a unified image from all the complex

individual components Hubel and Wiesel

identi-fied Then it starts the “higher level” processing of

the outside world

By the time Miller earned his Ph.D in 1990, he

was asking the questions that would later define

his career: What happens in the inferior temporal

cortex after a unified picture emerges? How do our brains tell us what it means?

Miller tried to answer those questions while ing in the lab of National Institute of Mental Health neuroscientist Bob Desimone Miller was looking for neurons that fired only when an animal spotted

work-an item it was storing in short-term memory Miller and Desimone trained animals to hold a single image in mind — such as an apple — and release a lever when that picture reappeared on a screen

If the animal remembered the first picture it saw and released the lever, a drop of delicious juice

would roll down a tube and into its cage

The pair noticed that certain parts of the animal brain were inherently sensitive to repetition — regardless of whether it translated into a valued juice reward Some neurons fired when animals saw

a second banana or second image of trees It was

as if the brain was on automatic pilot, primed to notice repetition without any active effort to do so, even when that repetition had no meaning

But the pair also discovered a second type of firing pattern When the animal spotted a picture it

was actively holding in his memory — hoping for a

juice reward — not only did different neurons fire, those neurons fired far more intensely

“Something was switching the volume to make these neurons fire, more or less, depending on the nature of the memory,” Miller says “That got me wondering Who’s turning up or down the volume?”

Experts have long known that we have a virtually unlimited capacity to store new long- term memories Yet there’s a limit on how much information we can cram into our working memory.

THE PREFRONTAL CORTEX, high- lighted here

in an MRI scan, plays a crucial role in working memory — the brain’s chalkboard for attention and decision-making.