What Causes SAD?
The 24-hour sleep-wake cycle, known as the circadian rhythm, is governed in part by the regular rise and fall of hormones, especially melatonin. Melatonin, the master sleep hormone, is produced in the pineal gland. Researchers have identified a regular ebb and flow to human physiology and behavior throughout a normal 24-hour cycle (Hirota 2004). Our overall pattern of sleep-wake depends on the proper functioning of an internal circadian clock, which lies deep in the brain. This circadian clock works with photosensors in the eyes to sense darkness. When darkness falls, the body begins to secrete melatonin, which is one of the factors that cause sleep. Melatonin continues to be secreted throughout the night, although levels alter, and toward dawn, melatonin secretion gradually diminishes, allowing for wakefulness in the morning.
When there is a problem with this system, sleep disorders and other psychological problems can occur. Recent research has identified a number of possible abnormalities that may help explain and offer therapeutic targets for SAD.
The Melatonin Theory. Early research focused on the shorter photoperiod in winter, hypothesizing that shorter days led directly to SAD. Researchers initially attempted, with some success, to lengthen the photoperiod by exposing individuals to bright light in the morning and evening (Rosenthal 1984; Winton 1989). Next, researchers focused on the secretion of melatonin, which controls the sleep-wake cycle.
Although the 24-hour rhythm of melatonin secretion is generally the same in SAD patients and controls during winter months, researchers hypothesized that people with SAD had increased duration of melatonin secretion in the early morning hours (Checkley 1993; Partonen 1996). This would explain why people with SAD have difficulty waking up and do not feel alert in the morning. Experiments with drugs to block melatonin secretion in the morning, thus decreasing the duration of its secretion, found the symptoms of SAD were relieved (Schlager 1994).
The Phase-Shift Theory. According to the phase-shift theory, developed in the late 1980s, people with SAD suffered from circadian rhythms that had fallen out of sync with the normal circadian cycle, which is not quite 24 hours long. Some people may be “phase-advanced” (ie, their bodies release melatonin too early in the evening) while others may be “phase-delayed” (ie, they continue to release melatonin for too long into the day). According to the phase-shift theory, this abnormality occurs because the seasonal changes in light exposure somehow disrupt normal functioning of the circadian clock.
Retinal hypersensitivity. One study found that the retinas of people with SAD are significantly less sensitive to light than those of controls, possibly because of neurotransmitter dysfunction (Hebert 2004). However, other studies found that people with SAD are hypersensitive to light (Terman 1999).
Neuroimmune dysfunction. Significant wintertime elevations of interleukin-6, a pro-inflammatory cytokine, have been noted in patients with SAD (Leu 2001). Pro-inflammatory cytokines like interleukin-6 cause greater production of enzymes that deplete tryptophan from the blood. The result is serotonin deficiency in the brain (and the onset of depression).
Other studies have noted elevated neopterin (a marker of immune function) in response to reduced tryptophan in SAD patients (Stastny 2003). These findings suggest that decreased tryptophan levels might lead to an overactive immune system (Hoekstra 2003).
Low levels of neurotransmitters. Research suggests that people with SAD, like those with most other depressive disorders, may have low or abnormal levels of important neurotransmitters, including serotonin (a precursor to melatonin), acetylcholine, and dopamine (Jepson 1999; Schwartz 1997; Depue 1989, 1990).
Among people with SAD, serotonin levels vary from season to season, with some of the lowest levels observed during December and January (Carlsson 1980). This may explain why patients with SAD crave carbohydrates during the winter season: serotonin is involved in regulating feeding and satiety (Lam 2000a). Studies have also shown the rate of production of serotonin in the brain is dependent on the length of exposure to bright sunlight and turnover of serotonin in the brain is much lower during the winter season (Lambert 2002). Administration of m-chlorophenylpiperazine (a serotonin-like drug) produced increased activation and euphoria in depressed patients with SAD, but not in controls or in SAD patients during summer (Schwartz 1997). Some research suggests the change in serotonin levels may result from reduced levels of vitamin D3, which are often observed in cases of SAD. Administration of 400 or 800 International Units (IU) of vitamin D3 to people with SAD during late winter appeared to improve mood (Lansdowne 1998).
Untreated patients with SAD also have lower concentrations of norepinephrine compared to their normal counterparts (Schwartz 1997). Research suggests that reduced norepinephrine activity is linked to hypersomnia (ie, increased need for sleep), which is common among people with SAD (Lam 2000b). Finally, low dopamine activity has been observed in SAD patients (Depue 1989, 1990).