Why We Sleep

part of this experiment, otherwise known as daylight savings time.
In  the  Northern  Hemisphere,  the  switch  to  daylight  savings  time  in  March
results  in  most  people  losing  an  hour  of  sleep  opportunity.  Should  you  tabulate
millions of daily hospital records, as researchers have done, you discover that this
seemingly trivial sleep reduction comes with a frightening spike in heart attacks
the  following  day.  Impressively,  it  works  both  ways.  In  the  autumn  within  the
Northern  Hemisphere,  when  the  clocks  move  forward  and  we  gain  an  hour  of
sleep  opportunity  time,  rates  of  heart  attacks  plummet  the  day  after.  A  similar
rise-and-fall relationship can be seen with the number of traffic accidents, proving
that the brain, by way of attention lapses and microsleeps, is just as sensitive as
the heart to very small perturbations of sleep. Most people think nothing of losing
an hour of sleep for a single night, believing it to be trivial and inconsequential. It
is anything but.
SLEEP LOSS AND METABOLISM: DIABETES AND WEIGHT GAIN
The less you sleep, the more you are likely to eat. In addition, your body becomes
unable to manage those calories effectively, especially the concentrations of sugar
in your blood. In these two ways, sleeping less than seven or eight hours a night
will increase your probability of gaining weight, being overweight, or being obese,
and significantly increases your likelihood of developing type 2 diabetes.
The global health cost of diabetes is $375 billion a year. That of obesity is more
than $2 trillion. Yet for the under-slept individual, the cost to health, quality of life,
and a hastened arrival of death are more meaningful. Precisely how a lack of sleep

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sets you on a path toward diabetes and leads to obesity is now well understood
and incontrovertible.
DIABETES
Sugar is a dangerous thing. In your diet, yes, but here I’m referring to that which is
currently circulating in your bloodstream. Excessively high levels of blood sugar,
or glucose, over weeks or years inflicts a surprising harm to the tissues and organs
of your body, worsens your health, and shortens your life span. Eye disease that
can end in blindness, nerve disease that commonly results in amputations, and
kidney  failure  necessitating  dialysis  or  transplant  are  all  consequences  of
prolonged  high  blood  sugar,  as  are  hypertension  and  heart  disease.  But  it  is  the
condition of type 2 diabetes that is most commonly and immediately related to
unregulated blood sugar.
In a healthy individual, the hormone insulin will trigger the cells of your body
to  swiftly  absorb  glucose  from  the  bloodstream  should  it  increase,  as  happens
after eating a meal. Instructed by insulin, the cells of your body will open special
channels on their surface that operate like wonderfully efficient roadside drains at
the  height  of  a  downpour.  They  have  no  problem  dealing  with  the  deluge  of
glucose  coursing  down  the  transit  arteries,  averting  what  could  otherwise  be  a
dangerous flood of sugar in the bloodstream.
If  the  cells  of  your  body  stop  responding  to  insulin,  however,  they  cannot
efficiently absorb glucose from the blood. Similar to roadside drains that become
blocked  or  erroneously  closed  shut,  the  rising  swell  of  blood  sugar  cannot  be
brought back down to safe levels. At this point, the body has transitioned into a
hyperglycemic  state.  Should  this  condition  persist,  and  the  cells  of  your  body
remain  intolerant  to  dealing  with  the  high  levels  of  glucose,  you  will  transition
into a pre-diabetic state and, ultimately, develop full-blown type 2 diabetes.
Early-warning  signs  of  a  link  between  sleep  loss  and  abnormal  blood  sugar
emerged in a series of large epidemiological studies spanning several continents.
Independent of one another, the research groups found far higher rates of type 2
diabetes  among  individuals  that  reported  sleeping  less  than  six  hours  a  night
routinely.  The  association  remained  significant  even  when  adjusting  for  other
contributing factors, such as body weight, alcohol, smoking, age, gender, race, and
caffeine  use.  Powerful  as  these  studies  are,  though,  they  do  not  inform  the
direction of causality. Does the state of diabetes impair your sleep, or does short
sleep impair your body’s ability to regulate blood sugar, thereby causing diabetes?
To  answer  this  question,  scientists  had  to  conduct  carefully  controlled
experiments with healthy adults who had no existing signs of diabetes or issues

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with blood sugar. In the first of these studies, participants were limited to sleeping
four  hours  a  night  for  just  six  nights.  By  the  end  of  that  week,  these  (formerly
healthy) participants were 40 percent less effective at absorbing a standard dose
of glucose, compared to when they were fully rested.
To give you a sense of what that means, if the researchers showed those blood
sugar readings to an unwitting family doctor, the GP would immediately classify
that  individual  as  being  pre-diabetic.  They  would  start  a  rapid  intervention
program  to  prevent  the  development  of  irreversible  type  2  diabetes.  Numerous
scientific  laboratories  around  the  world  have  replicated  this  alarming  effect  of
short sleep, some with even less aggressive reductions in sleep amount.
How does a lack of sleep hijack the body’s effective control of blood sugar? Was
it  a  blockade  of  insulin  release,  removing  the  essential  instruction  for  cells  to
absorb  glucose?  Or  had  the  cells  themselves  become  unresponsive  to  an
otherwise normal and present message of insulin?
As  we  have  discovered,  both  are  true,  though  the  most  compelling  evidence
indicates the latter. By taking small tissue samples, or biopsies, from participants
at the end of the above experiments, we can examine how the cells of the body are
operating. After participants had been restricted to four to five hours of sleep for a
week, the cells of these tired individuals had become far less receptive to insulin.
In this sleep-deprived state, the cells were stubbornly resisting the message from
insulin  and  refusing  to  open  up  their  surface  channels.  The  cells  were  repelling
rather than absorbing the dangerously high levels of glucose. The roadside drains
were  effectively  closed  shut,  leading  to  a  rising  tide  of  blood  sugar  and  a  pre-
diabetic state of hyperglycemia.
While many in the general public understand that diabetes is serious, they may
not appreciate the true burden. Beyond the average treatment cost of more than
$85,000  per  patient  (which  contributes  to  higher  medical  insurance  premiums),
diabetes  lops  ten  years  off  an  individual’s  life  expectancy.  Chronic  sleep
deprivation is now recognized as one of the major contributors to the escalation
of  type  2  diabetes  throughout  first-world  countries.  It’s  a  preventable
contribution.
WEIGHT GAIN AND OBESITY
When your sleep becomes short, you will gain weight. Multiple forces conspire to
expand  your  waistline.  The  first  concerns  two  hormones  controlling  appetite:
leptin and ghrelin.
II
Leptin signals a sense of feeling full. When circulating levels of
leptin are high, your appetite is blunted and you don’t feel like eating. Ghrelin, in
contrast, triggers a strong sensation of hunger. When ghrelin levels increase, so,

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too, does your desire to eat. An imbalance of either one of these hormones can
trigger  increased  eating  and  thus  body  weight.  Perturb  both  in  the  wrong
direction, and weight gain is more than probable.
Over the past thirty years, my colleague Dr. Eve Van Cauter at the University of
Chicago has tirelessly conducted research on the link between sleep and appetite
that  is  as  brilliant  as  it  is  impactful.  Rather  than  depriving  individuals  of  a  full
night  of  sleep,  Van  Cauter  has  taken  a  more  relevant  approach.  She  recognized
that more than a third of individuals in industrialized societies sleep less than five
to six hours a night during the week. So in a first series of studies of healthy young
adults of perfectly normal weight, she began to investigate whether one week of
this societally typical short sleep was enough to disrupt levels of either leptin or
ghrelin or both.
If you are a participant in one of Van Cauter’s studies, it feels rather more like a
one-week  stay  at  a  hotel.  You  will  get  your  own  room,  bed,  clean  sheets,  a
television, Internet access, etc.—everything except free tea and coffee, since no
caffeine is allowed. In one arm of the experiment, you will be given an eight-and-a-
half-hour  sleep  opportunity  each  night  for  five  nights,  recorded  with  electrodes
placed on your head. In the other arm of the study, you are only allowed four to
five hours of sleep for five nights, also measured with electrode recordings. In both
study arms, you will receive exactly the same amount and type of food, and your
degree of physical activity is also held constant. Each day, your sense of hunger
and food intake are monitored, as are your circulating levels of leptin and ghrelin.
Using  precisely  this  experimental  design  in  a  group  of  healthy,  lean
participants,  Van  Cauter  discovered  that  individuals  were  far  more  ravenous
when  sleeping  four  to  five  hours  a  night.  This  despite  being  given  the  same
amount of food and being similarly active, which kept the hunger levels of these
same individuals under calm control when they were getting eight or more hours
of  sleep.  The  strong  rise  of  hunger  pangs  and  increased  reported  appetite
occurred rapidly, by just the second day of short sleeping.
At  fault  were  the  two  characters,  leptin  and  ghrelin.  Inadequate  sleep
decreased concentrations of the satiety-signaling hormone leptin and increased
levels  of  the  hunger-instigating  hormone  ghrelin.  It  was  a  classic  case  of
physiological  double  jeopardy:  participants  were  being  punished  twice  for  the
same offense of short sleeping: once by having the “I’m full” signal removed from
their system, and once by gaining the “I’m still hungry” feeling being amplified. As
a  result,  participants  just  didn’t  feel  satisfied  by  food  when  they  were  short
sleeping.

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From a metabolic perspective, the sleep-restricted participants had lost their
hunger control. By limiting these individuals to what some in our society would
think  of  as  a  “sufficient”  amount  of  sleep  (five  hours  a  night),  Van  Cauter  had
caused a profound imbalance in the scales of hormonal food desire. By muting the
chemical  message  that  says  “stop  eating”  (leptin),  yet  increasing  the  hormonal
voice that shouts “please, keep eating” (ghrelin), your appetite remains unsatisfied
when your sleep is anything less than plentiful, even after a kingly meal. As Van
Cauter has elegantly described to me, a sleep-deprived body will cry famine in the
midst of plenty.
But  feeling  hungry  and  actually  eating  more  are  not  the  same  thing.  Do  you
actually  eat  more  when  sleeping  less?  Does  your  waistline  really  swell  as  a
consequence of that rise in appetite?
With  another  landmark  study,  Van  Cauter  proved  this  to  be  the  case.