Seasonal Affective Disorder
Targeted Nutritional Interventions for SAD
Melatonin. Melatonin, a hormone produced in the pineal gland, is responsible for regulating sleep and core body temperature at night (Arendt 2005). The role of melatonin in SAD is complicated and the subject of some controversy. Under normal circumstances, melatonin levels increase in the evening, prior to bedtime, peak in the middle of the night, and decrease gradually as morning approaches (Macchi 2004). Among people with SAD, excessive duration of melatonin secretion has been implicated, but researchers are far from settled on this theory as the main cause of SAD. Nevertheless, low-dose melatonin taken at night has been shown to be effective in improving mood in patients with SAD (Lewy 1998a; Rohr 2002).
Additional Support for SAD
Nutrient therapy for SAD operates along principles similar to those of pharmacological therapy: increased serotonin levels may relieve symptoms. To understand how these nutrients work, it is necessary to understand how serotonin is synthesized. In the body, tryptophan is converted to 5-hydroxytryptophan (5-HTP) by the enzyme tryptophan hydroxylase; this conversion can be inhibited by a deficiency in vitamin B6 or insufficient magnesium (Birdsall 1998). In turn, 5-HTP is converted to serotonin, which is subsequently converted to melatonin, with S-adenosyl-l-methionine (SAMe) serving as the methylating agent (Macchi 2004; McKee 1999). Thus, any nutrients that support healthy levels of tryptophan or promote healthy methylation would theoretically help improve levels of serotonin and relieve the symptoms of SAD.
Tryptophan. Light therapy is usually considered the first-line treatment for SAD, but about 40% of patients treated with light therapy do not respond (Ghadirian 1998). This may be due in part to a deficiency of tryptophan (Lam 1996), which is necessary for the synthesis of serotonin and sometimes recommended as a natural antidepressant. Some data suggest that light stimulates the conversion of tryptophan to serotonin (Lam 1996). Some studies indicate that tryptophan may be used to enhance light therapy (Lam 1997), while others show that tryptophan can produce benefits equal to those of light therapy in patients with SAD and may lengthen the time to relapse (Ghadirian 1998). One study in patients with SAD who had been treated with light therapy noted rapid depletion of tryptophan resulted in a reversal of the therapeutic effects of bright light treatment (Lam 1996).
Tryptophan depletion in an experimental setting in patients with SAD has also been associated with an increase in plasma neopterin (Stastny 2003). Neopterin is a marker of immune function; high levels are associated with increased immune system activity. This suggests low levels of tryptophan may cause elevated neopterin levels, which, in conjunction with reduced serotonin, may worsen depression associated with SAD (Stastny 2003). These findings have important implications in patients with autoimmune disorders (eg, rheumatoid arthritis, multiple sclerosis, and Alzheimer’s disease), in which levels of immune system cytokines (such as interleukin-6) may already be elevated (Maini 2000; McGeer 1995; Thornton 1997).
Tryptophan was a popular dietary supplement until 1989, when an epidemic outbreak of eosinophilia-myalgia syndrome (EMS) was associated with the use of tryptophan in the United States. About 95% of cases were traced to a single overseas supplier, although many people who took tryptophan from this supplier did not develop EMS. In 1989 the FDA issued a nationwide recall for all products containing tryptophan, and subsequently banned importation of tryptophan from overseas sources (Das 2004).
5-hydroxytryptophan (5-HTP). 5-HTP is the immediate precursor in the biosynthesis of serotonin from tryptophan. Oral 5-HTP crosses the blood-brain barrier easily and can be as effective as tryptophan in increasing levels of serotonin (Birdsall 1998). Administration of 200 to 600 mg 5-HTP has been shown to be effective in treating insomnia and improving quality of sleep (Guilleminault 1973; Soulairac 1977; Wyatt 1971). 5-HTP has been found safe in treating SAD when used alone but has been shown to increase cortisol levels (Jacobsen 1987). It is important to note that concomitant use of 5-HTP and SSRIs or monoamine oxidase inhibitors (MAOIs) can result in serotonin syndrome, a condition characterized by agitation, confusion, delirium, tachycardia, diaphoresis, and fluctuations in blood pressure (Martin 1996). However, no definitive cases of toxicity have emerged worldwide in the past 20 years in patients using 5-HTP alone as a dietary supplement (Das 2004).
Vitamin B6 and S-adenosyl-l-methionine (SAMe). The conversion of tryptophan to 5-HTP can be inhibited by a deficiency of vitamin B6 or insufficient magnesium (Birdsall 1998). Also, the conversion of 5-HTP to serotonin, and serotonin’s subsequent conversion into melatonin, rely on SAMe as a methylating agent (Macchi 2004; McKee 1999). Vitamin B6 is an important cofactor involved in the production of serotonin. Vitamin B6 deficiency should be considered in SAD; particularly in the elderly, who may suffer from vitamin deficiencies (Hvas 2004).
Magnesium. Studies indicate that a healthy circadian rhythm is associated with normally fluctuating magnesium levels, which peak in the evening, with fluctuations noted in the morning (Touitou 1978; Ising 1995). Insufficient magnesium levels can inhibit the conversion of tryptophan to 5-HTP, which can affect the production of serotonin and melatonin (Birdsall 1998). Research suggests that magnesium depletion may be associated with dysregulation of the biological clock, resulting from either an increase or decrease in melatonin, as is evident in SAD (Durlach 2002).
St. John’s wort. St. John’s wort has been shown to be effective against severe depression and depressive symptoms of SAD (Vorbach 1997; Kasper 1997). In one study, 900 mg of hypericum, an extract of St. John’s wort, was found to be as effective as light therapy in SAD (Kasper 1997). Another study found that 900 mg of hypericum in combination with bright light (3000 lux) or dim light (< 300 lux) therapy reduced depressive symptoms in patients with SAD (Martinez 1994). Its exact mechanism of action has not been clearly established; however, researchers propose that St. John’s wort affects the uptake and reuptake of MAOIs like serotonin and norepinephrine (Nangia 2000).
Omega-3 fatty acids. Omega-3 fatty acids have a role in the synthesis of serotonin, and there is encouraging data about their use in depressive disorders. Also, because the incidence of SAD is associated with higher latitudes, it seems logical that people who live in the Arctic would suffer from very high rates of a winter depressive disorder. Researchers, however, have found that SAD is very rare among Icelandic peoples, who eat a lot of omega-3 fatty acids in cold water fish. When fish consumption goes down, the incidence of SAD begins to increase (McGrath-Hanna 2003; Cott 2001; Magnusson 2000).
As mentioned previously, pro-inflammatory cytokines cause greater production of enzymes that deplete tryptophan in the blood, which can result in serotonin deficiency in the brain. These new findings about cytokine-induced degradation of tryptophan explain why nutrients like fish oil (which suppress inflammatory cytokines) alleviate depression.
Although studies have not been conducted examining the role of omega-3 fatty acid supplementation in SAD, these essential oils have multiple health benefits, and considering the suggestive data in Arctic people who consume a lot of fish oil, it is probably prudent to add omega-3 fatty acids to a supplementation program.
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