Caffeine’s Effects on Sleep: The Good and the Bad
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Gerard Paul, Contributor
Do you drink coffee? I certainly do – and that's not an uncommon thing.
According to the Journal of Food and Chemical Toxicology, a full 85 percent of adults consume at least one caffeinated drink per day. And the old stalwart coffee leads the pack in terms of popularity.
Another shocking number for you? The American Sleep Apnea Association states that 70 percent of adults have some level of sleep disorder.
Between chronically insufficient sleep and the popularity of stimulant drink usage, you'd be entirely forgiven for thinking there's something there. Let's look at the links between sleep and caffeine – the good and the bad.
What is Caffeine?
To kick it off: what is caffeine?
Biologically speaking, caffeine is a stimulant that acts on the brain and central nervous system. In nature, it's a plant defense: caffeine is a natural pesticide that protects certain nuts, seeds, and berries from insect invasion.
You'll find it naturally in a variety of food items, including chocolate, tea, and coffee. Caffeine is also added to many beverages, including sodas and energy drinks.
Caffeine is a vasoconstrictor – it narrows your blood vessels. While it increases blood pressure and your heart rate, constricting your blood vessels also tend to help salve headaches and migraines. To that end, many migraine medicines combine a painkiller with caffeine.
Biological effects of caffeine
Caffeine most famously affects mental sharpness and energy. However, caffeine has complex effects, and the body is an even more complex machine.
Positive biological effects
Wondering what's really in your cup? These are some of the best known and well-publicized acute benefits of caffeine:
- Increased mental alertness
- Reduced drowsiness
- Increased mental focus
- Heightened mood
- Better short-term memory
- Boosted metabolism
- Decreased muscle fatigue
Negative biological effects
There's a flip side of the coin, however. For all of the positive effects, caffeine in excess (or caffeine in sensitive people) can cause these negative effects:
Agitation and anxiety
Restlessness
Heartburn and acid reflux
Diarrhea, nausea, and vomiting
Frequent urination
Importantly: insomnia and poor-quality sleep
Plus, caffeine has several well-documented adverse effects on pregnant and breastfeeding women.
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Sleep Effects of Caffeine
Caffeine is a naturally-occurring psychoactive drug. Don't be alarmed here. The word "psychoactive" merely means caffeine changes your mental state when you ingest it.
One way caffeine does this by blocking certain key receptor sites in the brain and central nervous system. Primarily, caffeine competes with adenosine, a neurotransmitter that induces fatigue.
By blocking adenosine, caffeine exerts its primary effects: namely, it keeps you awake, alert, and non-drowsy.
Alas, the same effects that are useful when getting work done can be a curse at bedtime. We'll get there – but first, let's talk about adenosine.
Why is adenosine important?
Adenosine is an essential part of ensuring the body receives sufficient quantities of sleep of adequate quality. Among many other things, adenosine also helps regulate the body's internal clock – that is, the body's natural sleep/wake cycle: its circadian rhythm.
Adenosine is one substance the body produces with somnogenic properties – especially during prolonged wakefulness. As the term suggests, somnogenic refers to inducing a state of sleep.
This is part of what signals the body about the onset of fatigue and the need to sleep. Adenosine also triggers a particular type of sleep called non-REM sleep (REM stands for "rapid eye movement").
Non-REM sleep is a phase of the sleep cycle where the brain is relatively quiet, which permits brain recovery and healing as needed.
Sleep Quality and Sleep Stages
The American Society for Clinical Pharmacology and Therapeutics found that the use of caffeine 30 minutes before sleep shifted the stages of sleep, with REM sleep taking place earlier than usual and deeper sleep taking place later than average.
As well, study participants had symptoms that mimicked insomnia after the use of caffeine before bedtime. It seems that caffeine's interactions with adenosine probably play some role in reducing sleep quality.
Caffeine and Sleep Latency
Sleep latency is the time it takes to fully transition from wakefulness to the earliest stage of REM sleep.
There is a known, research-confirmed link between caffeine and sleep latency. Just 200mg of caffeine an hour before bed – somewhere around the dosage in 1.5 - 2 cups of coffee – increased sleep latency by over 15 minutes on average.
What is the typical sleep latency for different ages?
In that same study, the typical sleep latency for participants aged 20-30 was 7.7 minutes, while participants aged 40-60 needed 9.4 minutes to fall asleep. Caffeine vastly increased the time necessary to fall asleep – upwards of tripling it in the younger participants.
Outside of caffeine's effects on the time it takes to fall asleep, sleep latency does increase as you get older.
And you know where I'm going with this: insomnia. One of the hallmarks of insomnia is increased sleep latency. For some people, insomnia might be a result of caffeine too close to bedtime.
Caffeine-induced sleep disorder
Let me also point out: caffeine can be physically addictive.
Further, the Diagnostic Standards Manual Version 5 (DSM-5) names four different psychiatric conditions linked to caffeine use:
caffeine intoxication
caffeine withdrawal
other caffeine-induced disorders (e.g., sleep, anxiety)
caffeine-related disorder not otherwise specified
It also lists caffeine as an addictive substance – but doesn't (yet?) pick a side on whether it is clinically significant. That's little comfort to you, though, if you're physically addicted – caffeine-linked disorders in sleep and anxiety can wreak havoc on a night of sleep.
Paradoxically, When Might Increase in Latency be Good?
I'd be remiss if I didn't mention that there are two sides to the coin when it comes to caffeine and sleep. Sometimes the reason you're drinking that coffee is to fight off the effects of sleepiness.
Take, for example, this study from the Annals of Internal Medicine: the use of caffeine before night driving supported better resistance to sleepiness behind the wheel. Extending the argument, shift workers, night shift workers, late-evening work hours, truck drivers, pilots, and other night workers may benefit from the use of caffeine when sleep would be dangerous – or fatal.
And, as you probably know – when you need to get some work done late at night, sometimes caffeine is a crutch you need.
Caffeine Affects Sleep Duration
Caffeine doesn't only affect sleep latency and quality – it also affects sleep duration. Sleep duration is what it sounds like: the total amount of time you spend asleep.
In the same sleep latency study, researches found 200mg of caffeine roughly an hour before bed also reduced total sleep duration by between 25 and 30 minutes.
What's the right amount of sleep?
The Sleep Health Journal published the results of a two-year research project to determine optimal sleep duration.
The amount of sleep they recommend decreases with age. Adults need between 7 and 9 hours, and older adults need between 7 and 8 hours.
And how are we doing? It's not great – the American Sleep Apnea Association reports that 70 percent of adults are chronically sleep-deprived at least once per week, and 11 percent get insufficient sleep every night.
Again, that's not great.
The Bottom of the Cup: Be Careful When You Drink
The bottom line: some of society's chronic sleep problems are undoubtedly linked to our collective addiction to caffeine. It's probably not the only cause – many of us sit down and stare at artificial lights for 8+ hours a day, too, for example (yes – guilty).
But with caffeine, there is a bit more you can do. According to the Journal of Clinical Sleep Medicine, it is best to avoid consuming any caffeine starting six hours before the desired bedtime to get the best and most restorative sleep.
For your best sleep, maybe start by turning that evening coffee into an evening water.
Gerard Paul writes about food & drink at ManyEats. He's often found with a cup of coffee too close to bedtime – and wrote this post after drinking quite a bit of caffeine.
New insight into how obesity, insulin resistance can impair cognition
Science Daily/April 22, 2019
Medical College of Georgia at Augusta University
Obesity can break down our protective blood brain barrier resulting in problems with learning and memory, scientists report.
They knew that chronic activation of the receptor Adora2a on the endothelial cells that line this important barrier in our brain can let factors from the blood enter the brain and affect the function of our neurons.
Now Medical College of Georgia scientists have shown that when they block Adora2a in a model of diet-induced obesity, this important barrier function is maintained.
"We know that obesity and insulin resistance break down the blood brain barrier in humans and animal models, but exactly how has remained a mystery," says Dr. Alexis M. Stranahan, neuroscientist in the MCG Department of Neuroscience and Regenerative Medicine at Augusta University. Stranahan is corresponding author of the study published in The Journal of Neuroscience that provides new insight.
In the brain, adenosine is a neurotransmitter that helps us sleep and helps regulate our blood pressure; in the body it's also a component of the cell fuel adenosine triphosphate, or ATP. Adenosine also activates receptors Adora1a and Adora2a on endothelial cells, which normally supports healthy relationships between brain activity and blood flow.
Problems arise with chronic activation, particularly in the brain, which is what happens with obesity, says Stranahan.
People who have obesity and diabetes have higher rates of cognitive impairment as they age and most of the related structural changes are in the hippocampus, a center of learning and memory and Stranahan's focus of study. Fat is a source of inflammation and there is evidence that reducing chronic inflammation in the brain helps prevent obesity-related memory loss.
In a model that mimics what happens to some of us, young mice fed a high-fat diet got fat within two weeks, and by 16 weeks they had increases in fasting glucose and insulin concentrations, all signs that diabetes is in their future.
In the minute vasculature of the hippocampus, the investigators saw that obesity first increased permeability of the blood brain barrier to tiny molecules like fluorophore sodium fluorescein, or NaFl. Diet-induced insulin resistance heightened that permeability so that a larger molecule, Evans Blue, which has a high affinity for serum albumin, the most abundant protein in blood, also could get through.
When they looked with electron microscopy, they saw a changed landscape. Resulting diabetes promoted shrinkage of the usually tight junctions between endothelial cells and actual holes in those cells. They also saw muscular cells called pericytes that wrap around the exterior of microscopic blood vessels in the brain to give them more strength and help move blood along, start to lose their grip, so blood vessels start to lose their tone and become dysfunctional and inflamed. Pericytes are known to express higher levels of Adora2a than endothelial cells, Stranahan notes. The high-fat diet also promoted swelling of protrusions on astrocytes called end-feet, which also are part of the blood brain barrier. Astrocytes are brain cells that normally nurture neurons, but the pathological state of obesity also altered their form and support.
Angiogenesis, the body's natural attempt to make more blood vessels -- albeit usually dysfunctional, leaky ones -- in response to impaired blood and oxygen flow was happening in the hippocampus by 12 weeks, and upon close inspection, blood vessels were inflamed.
When they gave a drug to temporarily block Adora2a, it also blocked problems with barrier permeability. Whether that could work in humans and long term as a way to avoid cognitive decline in obese humans, remains to be seen, Stranahan notes.
Next they developed a mouse in which they could selectively knock Adora2a out of endothelial cells.
In this transgenic mouse, they turned off Adora2a in the endothelial cells at 12 weeks, and at 16 weeks, when mice should have been exhibiting cognitive impairment and a leaky blood brain barrier, they instead had normal cognition and barrier function and no inflammation.
When they compared the transgenic mice that were on a high- or low-fat diet, they found evidence that the increased permeability of blood vessels in the brain initiates the cycle of inflammation and cognitive impairment.
While it's typically hard to jump from mice to men, the fact that this type of work actually started with human findings likely means that avoiding insulin resistance could potentially halt the increased permeability of the blood brain barrier and decrease in cognitive function, Stranahan says.
"If an individual has already progressed to insulin resistance, these studies underscore the importance of controlling blood sugar levels and avoiding progressing to insulin deficiency (diabetes), which opens the blood brain barrier even further."
The scientists report that the relative accessibility of blood vessels in the brain may also make them a good avenue for preventing obesity's effects on the brain.
It also points to the reality that a variety of drugs given to obese patients may impact their brains to a higher degree, which might be something for patients and their doctors to consider. Stranahan notes that for drugs intended to take action in the brain, such as those for Alzheimer's, that could be a good thing but still needs to be considered. Some commonly prescribed drugs like prednisone, on the other hand, already are really good at getting through and can potentially be bad for the brain, she says.
Next steps in her lab include figuring out where the signal arises that chronically activates Adora2 in fat mice. She suspects it's actually a cascade that includes endothelial cells getting stressed, which increases their metabolism, which means they use more ATP, which can activate Adora2a and set in motion a vicious cycle that eventually takes its toll on the blood brain barrier.
The concept that obesity could affect the blood brain barrier started with people a dozen years ago when Swedish researchers found obese individuals had higher levels of the major antibody immunoglobulin G in their cerebrospinal fluid, when it should have been in their blood. It was an important finding that suggested that obesity and diabetes could enable things to get from the blood to the brain that should not, Stranahan says. Animal studies confirmed it was happening but, again, few studies have looked at why, Stranahan says.
Blood vessels come up from the body and get exceedingly small and fragile as they dive into the brain. While blood vessels that supply areas like our arms and heart are meant to be more porous so they can share plenty of glucose, oxygen and immune cells and other things the body needs, the vasculature in the brain, is supposed to be much more restrictive, letting comparatively little through.
"It's more like a gate than a barrier," says Stranahan, and it's a dynamic barrier at that, based on what the brain is up to. "It's got transporters that can move things across and what is happening in the brain and in the blood can change the way it operates."
She notes that the brain is a huge consumer, sucking up 70 to 80 percent of our oxygen and glucose, but also more fragile than other tissues, super sensitive even to our own immune cells.
"It's like a kid who grows up playing outside in the dirt is going to have a more robust immune system than a kid who grows up staying inside and playing video games," Stranahan says.
Cognitive tests on mice in the study included object recognition and maneuvering a water maze. The scientists looked at other normal functions, like simple motor functions, to see if there were other effects and, at least at those early time points, did not identify others.
https://www.sciencedaily.com/releases/2019/04/190422082253.htm