Factors that cause bad sleep hygiene and lower sleep quality include smoking, drinking alcohol, and ingesting caffeine before bedtime

f02a.jpg (13763 bytes)Sleep quality is impacted by one’s lifestyle and presleep behaviors. When lifestyle and presleep habits (sleep hygiene) interfere with the quality of sleep, a person is left struggling with insomnia, sleeping at unintentional times, or excessive sleepiness. Bad sleep hygiene results from the following common habits: smoking, drinking alcohol, taking sleep medications, and ingesting caffeine soon before bedtime. Leading a stressful lifestyle or having an irregular sleep/wake schedule can also contribute to bad sleep hygiene. These factors lower sleep quality in the following ways:

Smoking Before Bedtime
Although many smokers claim, “I smoke to calm down,” many studies show that nicotine increases the production of the neurotransmitter acetylcholine, which regulates wakefulness. Increased levels of acetylcholine increase wakefulness.

Nicotine also has a stimulatory effect on serotoninergic neurons in the dorsal raphe nucleus (DRN) in the brain, which plays a role in initiating the onset of sleep. Normally, these fibers fire rapidly during wake, decrease firing in slow wave sleep, then become nearly quiet during rapid eye movement (REM) sleep. Nicotine, however, causes the serotoninergic fibers to continue firing at a higher-than-normal rate during sleep. Wakefulness is increased and the amounts of REM sleep and slow wave sleep are reduced. Because these two stages play a role in mental and physical restoration, reduced amounts cause a person to feel unrefreshed on awakening.

Alcohol Before Bedtime
Alcohol is a central nervous system depressant. This depressive action affects the respiratory system by lowering the tone of the muscles that would normally keep the upper airway open. Apnea results and a person repeatedly awakens during sleep in order to breathe. The repeated arousals fragment sleep and cause sleepiness the following day. Alcohol also increases the incidence of myoclonus. These brief limb contractions can cause frequent arousals and fragment sleep.

Studies on alcoholics who have become abstinent show that the effects of alcohol on sleep architecture—decreased amounts of slow wave sleep and REM sleep—can persist from several months to many years after abstinence. Even in nonalcoholics, drinking moderately 6 hours before bedtime can affect sleep architecture by lowering the amounts of stage 1 and REM sleep.1

Scientists are not sure how alcohol brings about these changes on sleep architecture. One hypothesis is that interactions between alcohol and neurotransmitters such as serotonin, gamma-aminobutyric acid (GABA), or the nucleoside adenosine bring about these changes.2 Another possibility is that the neuronal receptor sites for these neurotransmitters may be altered by alcohol and its metabolites. This alteration inhibits the neurotransmitters from binding to their receptor sites and exerting their effect on sleep, thus affecting sleep quality.

Sleep Medications Before Bedtime
Sleep medications in the benzodiazepine family of drugs alter sleep architecture by reducing the amounts of slow wave sleep and REM sleep while increasing the amount of stage 2 sleep. Benzodiazepines increase the amount of 10-15 Hz brain activity while suppressing brain activity that is less than 10 Hz (delta waves and theta waves). Hence, wake-like activity intrudes into all sleep stages. In slow wave sleep, this activity can superimpose on the delta wave activity creating alpha-delta sleep, which subjectively feels very nonrestorative.

The effects of nonbenzodiazepine medications (zolpidem and zopiclone) on sleep architecture are conflicting. Some studies show that they have benzodiazepine-like effects on sleep architecture while others show that they have no effect on sleep architecture.

Another effect of sleep medications is that they can depress the tone of the respiratory muscles and bring about apneas. Frequent arousals from the resultant apneas fragment sleep.

Caffeine Before Bedtime
Caffeine antagonizes the actions of adenosine, which promotes sleep. Normally, adenosine would inhibit the release of excitatory neurotransmitters (choline), which play a role in maintaining wakefulness. Sleep ensues and various metabolites of adenosine then seem to govern each stage of sleep. Adenosine is most present during stage 1; 5′-nucleotidase, stage 2; inosine and adenoside monophosphate (AMP), stages 3 and 4; and 5′-nucleotidase and lactate, REM sleep.3 With the normal actions of adenosine inhibited by caffeine, sleep is delayed.

The stimulatory effects of caffeine remain active for several hours. Caffeine soon before bedtime may keep a person from falling asleep at a desired time.

Irregular Sleep/wake Schedule
The circadian rhythm depends on a consistent sleep/wake schedule. Some research also suggests that it is light rather than sleep and wake that more strongly controls a person’s circadian rhythm and that light at the wrong time can unintentionally reset it.

Third shift workers demonstrate the strong effect that light has on the circadian rhythm. Many struggle with sleepiness even when adhering to a consistent sleep/wake schedule. Studies have shown that subjects struggle less with sleepiness when exposure to periods of light and dark is very strictly controlled.4

Frequently shifting one’s work schedule or flying across the time zones offsets not only one’s sleep/wake schedule but also the light/dark schedule. This makes it hard for the circadian rhythm to remain set. The result of a constantly shifting circadian rhythm is insomnia or sleepiness at inopportune times.

A study by Spathe-Schwalbe et al5 shows that sleep with frequent arousals (such as would occur with apnea) or sleep deprivation (such as would occur with an irregular sleep/wake schedule) can cause levels of cortisol—a stress hormone—to remain high. When subjects were abruptly awakened for either the sleep deprivation protocol or for the frequent arousal protocol, the abrupt arousal caused an immediate rise in the level of cortisol. This level remained elevated throughout the night. As explained in the following section on stress and anxiety, elevated levels of cortisol can increase wakefulness.

Stress and anxiety
During times of stress, the hypothalamus floods the bloodstream with corticotropin-releasing hormone (CRH). This stimulates the pituitary to release adrenocorticotropic hormone (ACTH). ACTH then induces the adrenal glands to release cortisol and other stress hormones.

Cortisol and ACTH help to lessen the impact of stress on the body. Cortisol, a glucocorticoid, raises the blood levels of glucose during times of trauma, fright, infection, bleeding, and disease. ACTH, a mineralocorticoid, regulates blood pressure during such times.

Blood levels of these hormones normally rise and fall rhythmically throughout the day with the highest levels occurring in the evening and the first half of the night. During times of stress, cortisol and ACTH continue their rhythmic rising and falling but do so at higher-than-normal levels.

The presence of high levels of cortisol and ACTH increases wakefulness. Once a person is asleep, high levels of these hormones inhibit slow wave sleep. Insomnia and reduced amounts of slow wave sleep during stressful times leave a person feeling unrefreshed on awakening.

A good quality of sleep can be restored by correcting bad sleep hygiene. Some corrections are simply a matter of reversing prebedtime behavior while some require more encompassing lifestyle changes. For people suffering from bad sleep quality, following these tips can correct bad sleep hygiene and once again give a restorative quality to sleep.

Lifestyle Changes
• Maintain a consistent sleep/wake schedule. Do not take naps. Napping throws off the circadian rhythm. If a regular nap is taken, it should not be longer than an hour and should be scheduled in the early part of the day (morning or early afternoon).

• Use a full-spectrum light box regularly during the night shift to ward off sleepiness or to maintain a consistent light/dark schedule when traveling across time zones.

In 1980, it was learned that bright light with an intensity of 2,500 lux (which is five times greater than normal room light) could suppress melatonin production.6 This fact has been a lifesaver for many third shift workers and people who have to travel across time zones frequently. Since melatonin promotes the onset of sleep, the ability to control melatonin production allows a worker to control sleepiness.

Despite this effect on melatonin production, bright light’s effect on body temperature controls sleepiness more effectively. A period of bright light exposure (called a pulse) lasting 3 or more hours immediately before the body’s lowest temperature (TMIN) causes the body’s temperature rhythm to shift so that TMIN will occur about 2 hours later on the following day. Conversely, a pulse immediately after TMIN causes the body’s temperature rhythm to shift so that TMIN occurs about 2 hours earlier the following day. Pulses immediately before or after TMAX have neither of these effects.

A person is sleepiest at TMIN and most alert at TMAX. The strategic use of bright light can be used to shift TMIN to daytime hours. An ideal schedule to accomplish this goal begins with a pulse immediately before TMIN to induce it to shift to a later time the following day. The following day, a pulse of light immediately before the new TMIN time is used to again shift TMIN. Successively doing this will ultimately shift TMIN (the sleepiest time) to a desired time of day. Once TMIN is at a desired time, bright light must then be used at the same time each night to stop any more shifting.

Light boxes now come in various intensities. Most boxes for home and work use come in intensities of less than 2,500 lux since this intensity is bothersome to the eyes or makes it difficult to see a computer screen.

• Adhere strictly to a “dark” schedule. Night shift workers or workers frequently traveling across time zones need to minimize exposure to light after a shift is over to create an artificial night.

Exposure to as little as 10% of the intensity of light provided by sunlight can hinder the onset of melatonin production. Sunglasses can be used on the drive home to reduce this effect of sunlight. Sunglasses with side shields can filter out 93% of sunlight while most sunglasses without side shields will filter out 90% of light. Also, if a person has used bright light therapy during a night shift, sunlight—being brighter—can cancel the beneficial effects of the therapy.

In the home environment, incoming light can be limited by covering windows with black paper, light-reducing shades, or dark curtains.

Regina Patrick, RPSGT, is a contributing writer for Sleep Review.

References
1. Landolt HP, Roth C, Dijk DJ, Borbely AA. Late-afternoon ethanol intake affects nocturnal sleep and the sleep EEG in middle-aged men. J Clin Psychopharmacol. 1996;16:428-446.
2. Landholt HP, Gillin JC. Sleep abnormalities during abstinence in alcohol-dependent patients. Aetiology and management. CNS Drugs. 2001;15:413-425.
3. Diaz-Munoz M, Hernandez-Munoz R, Suarez J, et al. Correlation between blood adenosine metabolism and sleep in humans. Sleep Research Online. 1999;2:33-41.
4. Eastman CI, Martin SK. How to use light and dark to produce circadian adaptation to night shift work. Ann Med. 1999;31:87-98.
5. Spathe-Schwalbe E, Gofferje M, Kern W, et al. Sleep disruption alters nocturnal ACTH and cortisol secretory patterns. Biol Psychiatry. 1991;29:575-854.
6. Lewy AJ, Wehr TA, Goodwin FK, Newsome DA, Markey SP. Light suppresses melatonin secretion in humans. Science. 1980;210:1267-1269.

Additional Reading
Feige B, Voderholzer U, Riemann D, et al. Independent sleep EEG slow-wave and spindle band dynamics associated with 4 weeks of continuous application of short half-life hypnotics in healthy subjects. Clin Neurophysiol. 1999;110:1965-1974.
Myeck MJ, RA Harvey, PC Champe. Anxiolytic and hypnotic drugs. Harvey RA, Champe PC, eds. LippincottĀ¹s Illustrated Reviews: Pharmacology. 2nd ed. Philadelphia: Lippincott-Raven Publishers; 1997:89-98.