Seasonal Affective Disorder (SAD)

Introduction

What Should I Know About Seasonal Affective Disorder?

Everyone gets the blues during the dark days of winter. For those living in colder climates and even those in the Southern hemisphere, it seems as though winter will never end. For some, the feelings of depression that come during the winter seem overwhelming. In these individuals, the depression they experience is valid and can become severe. (1)

Seasonal Affective Disorder (SAD) was first defined in 1984 when NA Rosenthal published a paper in the Archives of General Psychiatry (2) in which he described the disorder and some basic findings of his experience with light therapy. Rosenthal described SAD as being characterized “by recurrent depressions that occur annually at the same time each year.” (3) Since this syndrome was first identified, researchers have published hundreds of studies aimed at unraveling its pathology. Thus far, it has been determined that SAD occurs more often in women with initial episodes in early adulthood. (4)

Theoretical causes of SAD have included elevated melatonin levels, (5) alterations in circadian rhythm, (6) genetic differences in photoreceptors, and glucose metabolism (7) . The primary focus of research over the years has been on the body’s reaction to light and the lack of light during the winter months. Studies have indicated that there may be a relationship between eye color and light sensitivity whereas those with darker colored eyes tend to consistently react differently than those with light colored eyes. (8) To date, controversies over the role of light continue, as do the controversies over the role of melatonin and serotonin; however light therapy remains consistent as a form of treatment for the disorder.

Because Seasonal Affective Disorder is a seasonal depression, treatment and diagnosis often duplicate those that are provided in a person suffering mild to moderate depression.

Statistic

National Mental Health Association, 2001

  • Young people and women are at the highest risk for the disorder, but it can affect anyone.
  • An estimated 25 percent of the population suffers from mild winter SAD, and about 5 percent suffer from a more severe form of the disorder.

Signs and Symptoms

The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.

Those diagnosed with SAD experience symptoms of depression that occur regularly during the fall or winter months and seem to subside in spring and summer. (In some rare cases, the seasons of the year are reversed.) These symptoms must occur for two consecutive years. Those who experience these symptoms report feeling anxious, persistently sad, empty, and tired. Interestingly, these symptoms vary greatly in degree and according to gender and race. (9) Studies indicate that men exhibit more obsessive/compulsive traits and may be more suicidal while women tend to gain more weight and experience insomnia.

Treatment Options

Conventional

In treating patients with SAD, most physicians will address the condition as an uncomplicated depression. Since theories of cause indicate a role of serotonin regulation, SSRI’s (selective serotonin reuptake inhibitors) are often prescribed.
These drugs block the re-uptake of serotonin by itself, without touching other neurotransmitters. (10) Other drug therapies in the investigative state include alprozalam (Xanax) (11) and methergoline, a hormone regulator. (12)

Conventional therapy also includes the use of full spectrum light therapy. The efficacy of this treatment remains controversial because in some patients it is effective and in others it is not. Some researchers believe that the reason that it may not be effective in some patients is that compliance with the requirements of this therapy may not be consistent.

Nutritional Suplementation

Vitamin D
Vitamin D has been studied as a therapeutic treatment for SAD with preliminary findings indicating a positive role for this vitamin. In a study conducted in Finland, researchers looked at the relationship between Vitamin D and serotonin and melatonin synthesis. They concluded that, “Calcitriol might inhibit the binding of melatonin to the nuclear retinoid Z receptors, which would result in the increased serotonin levels.” (13) Another small study conducted in Australia found that patients taking up to 800iu of Vitamin D reported improved symptoms. (14) Because these studies are preliminary, the dosage range reported to improve depressive symptoms vary greatly. One study that compared the effectiveness of phototherapy (light therapy) to Vitamin D therapy, found better results with the Vitamin D therapy, however the dosage was at 100,000 iu (15) which is far above the dosages used and considered safe. A study using only 400iu of Vitamin D, did not see any positive results. (16)

S-Adenosylmethionine (SAMe)
S-adenosylmethionine (SAMe), widely available as a dietary supplement, is one of the most studied non-drug antidepressants. SAMe is a naturally occurring substance manufactured in the body from the amino acid methionine. It is critical for production of neurotransmitters.

A recent meta-analysis (a research method that pools the data from many small studies to draw a conclusion based on large numbers of subjects) concluded, “The efficacy of SAMe in treating depressive syndromes and disorders is superior with that of placebo and comparable to that of standard tricyclic antidepressants. Since SAMe is a naturally occurring compound with relatively few side effects, it is a potentially important treatment for depression.” (17) Several studies report that SAMe is more effective than tricyclics. (18) , (19)

In another meta-analysis, the benefits of SAMe as an antidepressant were again confirmed. SAMe was found to provide better antidepressant benefits than a placebo (“dummy pill”) and it worked as well as the standard tricyclic antidepressant medications, with relatively few side effects. The results of this meta-analysis prompted the authors to state that SAMe is, “a potentially
important treatment for depression.” (20)

Clinical trials show SAMe is fast acting, adding to its value as a natural antidepressant. (21)

Phenylalanine
Phenylalanine and tyrosine are additional amino acids the body needs to produce neurotransmitters. These nutrients are used to manufacture dopamine, norepinephrine, and epinephrine, three neurotransmitters that influence and regulate mental and emotional states.

Antidepressant activity has been reported in studies using D-phenylalanine or with a mixture of D-phenylalanine and its twin amino acid, L-phenylalanine (DLPA). Several studies have reported results equal to or better than tricyclic antidepressants, without side effects. (22) , (23) People usually respond within two to four weeks, and in one study, severely depressed patients responded well. (24)

Individuals with high blood pressure should only take phenylalanine under close supervision of their primary care provider. It should not be used by people with phenylketonuria (PKU), melanoma, or those taking MAO inhibiting antidepressants.

5-Hydroxytryptophan (5-HTP)
5-hydroxytryptophan has been studied as an alternative to drug therapy for depression and while the role of serotonin synthesis in
SAD is not fully determined, 5-HTP may be beneficial in some cases. The results for patients experiencing depression linked to reduced serotonin levels appear promising. (25) Studies showed a reduction in depressive episodes for test subjects and fewer side effects compared with those associated with some pharmaceutical antidepressants. (26)

5-HTP may also help sleep disorder sufferers get some rest. In one study, patients suffering from mild insomnia experienced significant improvement taking 5-HTP before bedtime. (27)

People taking anti-anxiety drugs or other antidepressants should not take tryptophan or 5-HTP without the close supervision of a qualified health care professional because it can increase both the effect and the toxicity of antidepressant drugs.

Herbal Suplementation

St. John’s Wort
So far, the studies have shown St. John’s wort to work effectively in mild to moderate depression; whether it works as well in severe depression has not yet been tested. (28) , (29) , (30)

Since this herb has been studied and used successfully in treating mild to moderate depression, it has been reviewed as well for treatment of the depressive symptoms of SAD. (31) , (32) , (33) Studies with St. John’s wort have used an extract of the herb standardized to contain 0.3% hypericin, which is one of the herb’s main ingredients. The established effective dose is 300 mg of this St. John’s wort extract, taken three times a day. It is viewed as safe and effective by the German Commission E, which is a recognized authority on herbal medicine.

One possible drawback in the use of St. John’s wort has surfaced. St. John’s wort seems to stimulate liver enzymes, which eliminate drugs from the body. This means that taking the herb along with certain drugs might prevent the drugs from working as they should. Interactions along this line between St. John’s wort and anticoagulants, indinavir, cyclosporin, digoxin, ethinyl estradiol/desogestrel, and theophylline have occurred. (34) Also, several reports have suggested that taking of St. John’s wort and SSRI’s together could raise serotonin levels too much. “Serotonin syndrome” could result with symptoms that include sweating, tremor, confusion, flushing, and agitation. (35) , (36) Use St. John’s wort with caution if individuals are on these medications

Rhodiola
For the treatment of depression, active ingredients of rhodiola, namely rosavin and salidroside, in animal studies seem to enhance the transport of tryptophan and 5-HTP, the serotonin “precursors” discussed earlier into the brain, and decrease the action of COMT (catechol-O-methyltransferase), an enzyme that breaks down serotonin. (37) Russian scientists have used Rhodiola alone or in combination with antidepressants to enhance mental state and decrease the symptoms of SAD or Seasonal Affective Disorder common to Northern European countries. Additional studies need to be performed to verify its effectiveness for this particular function.

References

  1. Sher L. Suicidal behavior and seasonality. Nord J Psychiatry. 2002;56(1):67.
  2. Rosenthal NE, Sack DA, Gillin JC, Lewy AJ, Goodwin FK, Davenport Y, Mueller PS, Newsome DA, Wehr TA: Seasonal Affective Disorder: A Description of the Syndrome and Preliminary Findings with Light Therapy. Arch Gen Psychiatry. 1984; 41:72–80.
  3. Rosenthal NE, Sack DA, Gillin JC, Lewy AJ, Goodwin FK, Davenport Y, Mueller PS, Newsome DA, Wehr TA: Seasonal Affective Disorder: A Description of the Syndrome and Preliminary Findings with Light Therapy. Arch Gen Psychiatry. 1984; 41:72–80.
  4. View Abstract: Attar-Levy D. [Seasonal depression]. Rev Prat. Nov 1997 1;47(17):1899-903.
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