summarize: It would be nice if science could locate some sort of “sleep switch,” some
brain pathway that could be triggered, or inhibited, to make us fall asleep
instantly and cycle smoothly in and out of deep sleep and REM sleep all
night, until we wake up feeling refreshed. But that hasn’t happened yet.
It’s not for lack of effort on the part of big pharma. Sleep is such a
problem for so many people that there are about a dozen FDA-approved sleep
medications on the market. The first real blockbuster sleeping medication,
Ambien (zolpidem), generated $4 billion in revenues within the first two
years after it was approved in the 1990s. The demand was huge, but the
phenomenon goes back much further than that. The drug morphine, first
isolated from the opium poppy in 1806, was named for Morpheus, the god of
dreams, because it put people to sleep quite effectively. This was fitting, in
that sleeping and dreaming can be a refuge from both physical and emotional
pain. But morphine, being addictive, is obviously not ideal as a sleep drug.
Currently, the US sleep medication market is estimated to be worth about
$28 billion a year. But the number of prescriptions has actually been
declining recently, perhaps because consumers are catching on to the fact
that, by and large, these medicines do not actually work very well. They can
be good at inducing unconsciousness, but then again, so was Muhammad
Ali’s right cross. Sleep medications such as Ambien and Lunesta do not
promote healthy, long-lasting sleep so much as they tend to promote a sleeplike state of unconsciousness that does not really accomplish much if any of
the brain-healing work of either REM or deep sleep. One study found that
Ambien actually decreased slow-wave sleep (deep sleep) without increasing
REM, meaning people who take it are basically trading high-quality sleep for
low-quality sleep. Meanwhile, Ambien has the well-publicized side effect that
some users have been known to walk around and do things while “sleeping,”
leading to all sorts of problems.
The pharmaceutical industry then came up with a new class of sleep drugs
that purportedly solved the sleepwalking problem by blocking a wakepromoting brain chemical called orexin. Interestingly, orexin was initially
thought to be more relevant to appetite, which it also regulates (by increasing
hunger). But so-called orexin antagonist inhibitors such as Dayvigo
(lemborexant) and Quviviq (daridorexant) have been approved for treating
insomnia, and they appear to be promising—not least because users have
better ability to respond to auditory stimuli at night (e.g., a parent who wants
to sleep but still be able to respond if a child is crying). They are, however,
quite expensive.
Then there are the older benzodiazepine drugs, such as Valium
(diazepam) and Xanax (alprazolam), which remain very popular—almost
ubiquitous in our society—and are also sometimes used to treat insomnia.
These typically induce unconsciousness without improving sleep quality.
Somewhat worryingly, their use has also been associated with cognitive
decline, and they are generally not recommended for older adults beyond very
short-term time horizons (nor is Ambien, by the way).
When new patients come into our practice, it is not uncommon for them
to be relying on one of these sleep aids. If they are using Ambien or Xanax
once a month, or only with travel, or to help them sleep during a time of
emotional distress, it’s not alarming. But if they are using such drugs
regularly, it becomes our highest priority to get them off these sleep aids and
have them begin to learn to sleep correctly without them.
One drug that we do find helpful for assisting with sleep is trazodone, a
fairly old anti-depressant (approved in 1981) that never really took off. At the
doses used to treat depression, two hundred to three hundred milligrams per
day, it had the unwanted side effect of causing users to fall asleep. But one
man’s trash is another man’s treasure. That side effect is what we want in a
sleep medication, especially if it also improves sleep architecture, which is
exactly what trazodone does—and most other sleep meds do not.
[*4] We
typically use it at much lower doses, from one hundred milligrams down to
fifty milligrams or even less; the optimal dosing depends on the individual,
but the goal is to find the amount that improves their sleep quality without
next-day grogginess. (We have also had good results with the supplement
ashwagandha.)
—
There is still no pharmacological magic bullet for sleep, but there are some
fairly effective things you can do to improve your ability to fall asleep and
stay asleep—and, hopefully, sleep well enough to avoid all the scary stuff that
we’ve been talking about in this chapter. Keep in mind, however, that these
tips and strategies are not going to be effective if you have a true sleep
disorder, such as insomnia or sleep apnea (see below for questionnaire
assessments that you can take to your doctor for discussion).
The first step in this process echoes the first step in a recovery program:
we must renounce our “addiction” to chronic sleep deprivation and admit that
we need more sleep, in sufficient quality and quantity. We are giving
ourselves permission to sleep. This was actually rather difficult for me at first,
as I had spent decades practicing just the opposite. I hope by now I’ve
convinced you of the importance of sleep, across multiple dimensions of
health.
The next step is to assess your own sleep habits. There are numerous sleep
trackers out there that can give you a pretty good idea about how well you are
actually sleeping. They work by measuring variables such as heart rate, heart
rate variability (HRV), movement, breathing rate, and more. These inputs are
used to estimate sleep duration and stage and do so with reasonable (but not
perfect) accuracy. While I’ve found these to be quite helpful in optimizing my
own sleep, some people get worked up over poor sleep scores—which can
further impair their sleep. In these situations I insist that my patients take a
tracker holiday for a few months. It’s also worth reiterating that long sleep is
also often a sign not only of poor sleep quality, but other potential health
problems.
In parallel, you should make a longer-term assessment of your sleep
quality over the last month. Probably the best-validated sleep questionnaire is
the Pittsburgh Sleep Quality Index, a four-page document that asks questions
about your sleep patterns over the last month: for example, how often you
have had trouble falling asleep within thirty minutes, have woken up during
the night, have had difficulty breathing (i.e., snoring), have had trouble staying
awake during the day (such as while driving), or have “felt a lack of
enthusiasm for getting things done.”
It’s easy to find the questionnaire and scoring key online,
[*5] and I often
find that it helps persuade my patients that it’s time to take sleep seriously and
make it a priority in their lives. There’s another, even simpler quiz called the
Epworth Sleepiness Scale, which asks users to rate how likely they are to fall
asleep in certain situations, on a scale of 0 (not likely) to 3 (very likely):
Sitting and reading
Watching TV
Sitting in a meeting or other public place
As a passenger in a car for an hour
Lying down to rest in the afternoon
Sitting and talking to someone
Sitting after lunch (without alcohol)
In a car, stopped for a few minutes in traffic
A total score of 10 or more indicates excessive sleepiness and likely points to
an issue with sleep quality.
[*6]
Yet another helpful screening tool is the Insomnia Severity Index, which
provides an opportunity to reflect on and report your experience of sleep
problems and their impact on your functioning and well-being.
[*7]
One important but often-ignored factor in sleep assessment is that
different people may have widely differing “chronotypes,” which is a fancy
way of saying that someone is a “morning person” or “not a morning person.”
We all have different relationships to the circadian cycle, and much of that
relationship is genetic: a morning person and a night owl will have different
circadian genes.
[*8] Studies have found that some individuals are genetically
predisposed to leap out of bed first thing in the morning, while others
naturally tend to wake up later (and go to sleep later), not really hitting their
stride until sometime in the afternoon. The latter are not “lazy,” as was long
assumed; they may simply have a different chronotype.
Like so much else in biology, this has a possible basis in evolution: if all
members of a clan or a tribe adhered to the exact same sleep schedule, the
entire group would be vulnerable to predators and enemies for several hours
every night. Obviously not ideal. But if their sleep schedules were staggered,
with some individuals going to bed early while others were more inclined to
stay up late and tend the fire, the group as a whole would be much less
vulnerable. This may also explain why teenagers want to go to bed late and
then sleep in: Our chronotype appears to undergo a temporary shift in
adolescence toward late sleeping and later rising. School start times,
unfortunately for both teens and for those of us who are parents, remain
stubbornly fixed at very early hours—but there is a growing nationwide
movement to push school times later, to better suit adolescent sleep schedules.
Last, it is important to rule out—or rule in—the possibility of obstructive
sleep apnea, which is surprisingly prevalent yet underdiagnosed. It is possible
to get a formal test for this, in a sleep lab or at home, but there is yet another
questionnaire, called STOP-BANG, that correlates pretty strongly with the
formal apnea test.
[*9] If you snore, have high blood pressure, feel tired most
days, or if your partner has observed that you stop breathing occasionally
during the night, even for a moment, you are a candidate for further sleep
apnea testing by a medical professional. (Other risk factors include having a
BMI greater than thirty and being male.) Sleep apnea is a serious medical
problem that can have implications for cardiovascular health and dementia
risk.