Exploring psychotherapeutic issues and agents in clinical practice
We are entering the time of year when daylight hours become shorter and the “winter blues” set in for many of our patients. The term seasonal affective disorder (SAD) will be mentioned and questioned by our patients and their families, but how do we address this phenomenon?
SAD is not actually a stand-alone diagnosis, but rather a subtype of the affective disorders that describes distinct, seasonally occurring exacerbations of episodes of major depression or bipolar I and II (manic and hypomanic) disorders (Avery, 2017). The defining feature is that the onset and remission of SAD symptoms occur at characteristic times of year (American Psychiatric Association [APA], 2013). SAD can occur with the onset of the cooler months (fall and winter), characterized by hypersomnia, increased appetite, and depressed mood, or during the warmer (spring and summer) months where it is associated with insomnia, anorexia, weight loss, and irritability (Yildiz, Batmaz, Songur, & Oral, 2016). The seasonal mood fluctuations associated with SAD affect up to 10% of the overall population (Westrin & Lam, 2007) and up to 70% of individuals diagnosed with recurrent major depressive disorder (MDD) (APA, 2013). The mood and physical symptom exacerbations significantly impact an individual's psychosocial functioning and are extremely problematic as they may last up to 40% of the year (Yildiz et al., 2016). Adding to this impact, it is estimated that approximately 70% of individuals diagnosed with SAD will have a recurrence within the next year during the same season (Gartlehner et al., 2015).
Neuroscience Related to Seasonal Affective Disorder
Although the underlying etiology of SAD remains a mystery, various mechanisms have been proposed to describe this phenomenon. Alterations in the neurotransmitters serotonin, norepinephrine, dopamine, melatonin, and tryptophan; low levels of vitamin D; retinal sub-sensitivity to light; and circadian phase delay have all been suggested as contributors to SAD (Stewart, Roecklein, Tanner, & Kimlin, 2014). In addition, genetic variations have been found in those with SAD. Variations in the serotonin transporter (5-HTTLPR) and 5-HT2A gene as well as variations in the circadian clock genes, Period3 and NPAS2, have been associated with SAD (Levitan, 2007). To recommend the most effective treatment course for SAD, nurses must understand the various neurobiological changes that occur with this seasonally specific exacerbation of the affective disorders.
Circadian phase delays are thought to be one of the primary contributors to SAD (Rohan, Roecklein, & Haaga, 2009). Longer nights and shorter days lead to alterations in the release of melatonin from the pineal gland, with later release of melatonin and longer duration of secretion in the winter than the summer for those with winter-onset SAD (Wehr et al., 2001). Thus, regularly taking melatonin to induce sleep may be contraindicated for those with SAD. Similarly, vitamin D levels have been demonstrated to fluctuate seasonally due to changes in light exposure, with lower levels hypothetically playing a role in the onset of winter-onset SAD as well as a reduction in the synthesis of serotonin and dopamine (Frandsen, Pareek, Hansen, & Nielsen, 2014; Stewart et al., 2014).
The trimonoamines—serotonin, norepinephrine, and dopamine—are the neurochemicals most commonly associated with depression and mood fluctuations, and SAD is no exception. The serotonin transporter (SERT) is thought to remove too much serotonin from the synaptic cleft, leading to diminished serotonin levels, which contribute to the symptoms of SAD (Willeit et al., 2008). In fact, postmortem examinations of the general population during December and January have shown depleted serotonin (Gupta, Sharma, Garg, Singh, & Mondal, 2013). A decades old study implicates depletion of norepinephrine as a contributor to winter-onset SAD; this hypothesis was based on an increase in levels of norepinephrine following light therapy (Anderson et al., 1992). Levitan (2007) found that hypo-functionality of the dopamine 4 receptor gene led to lower levels of dopamine, which have been linked to the affective and appetite symptoms associated with SAD. Similarly, tryptophan, an amino-acid precursor to serotonin, depletion has been associated with the carbohydrate cravings and increased appetite observed in individuals with winter-onset SAD (Lam et al., 1996).
Treatments for Seasonal Affective Disorder
By definition, the symptoms of SAD will remit without treatment by the start of the next season—spring for fall/winter onset and fall for spring/summer onset. However, the symptoms may be so debilitating for individuals that other therapies may be required. Nurses encourage patients to adopt healthy lifestyle habits not only to improve their physical health but also their mental health. Patients experiencing the symptoms of SAD are no exception to these interventions, and the healthy lifestyle interventions listed in Table 1 should be encouraged and incorporated into individuals' daily routines.
Healthy Lifestyle Interventions for Seasonal Affective Disorder
As SAD is the seasonal exacerbation of an affective disorder, many patients will already be prescribed psychopharmacological agents to treat their diagnosis and symptoms. Maximizing the dosing of patients' prescribed antidepressant or anti-manic therapies may be the most beneficial course of treatment. The APA (2010) notes that SAD, also referred to as MDD, with seasonal pattern, can be treated with the entire range of treatments available for MDD. In addition, Michael (2016) notes that winter depression should not be the only target of SAD treatment if a patient is diagnosed with bipolar disorder; mania and hypomania may be exacerbated during the spring and summer months and also require treatment.
As SAD follows a somewhat predictable exacerbation of symptoms, once a patient has been diagnosed, planning pharmacological and other treatments to reduce the impact can be helpful. Using and maximizing the patient's current pharmacotherapies by adjusting the dosage or frequency, just as might be done for a prolonged situationally based exacerbation, would be the first step. If alternate medications are indicated, Wellbutrin XL® (bupropion XL) has the U.S. Food and Drug Administration's (FDA) approval for the indication of SAD. As bupropion is thought to be less likely to trigger a manic or hypomanic episode compared to other antidepressant agents (Fink, 2017), bupropion could be used to treat winter-onset and summer-onset SAD. In addition, bupropion is known to reduce the risk of sexual side effects as well as weight gain, which can accompany SAD. Although there is no true preventive medication for SAD, a case may be made for preventive or prophylactic treatment with bupropion XL. A review of multiple studies found a 44% risk reduction for the development of depressive symptoms when >1,000 patients diagnosed with winter-onset SAD were prescribed bupropion prior to the onset of symptoms (Modell et al., 2005), offering hope as a preventive measure for SAD. One point to note, regardless of the pharmaceutical agent used to treat SAD symptoms, is to reduce the risk of relapse, the therapy should continue until spontaneous remission of symptoms in the next season (Kurlansik & Ibay, 2012).
Bright Light/Light Box Therapy
No article on the topic of SAD would be complete without a discussion of bright light therapy (BLT), also known as light box therapy. BLT is not only specific to treatment of SAD, but also of depressive symptoms in general. BLT is based of retinal exposure to varied light intensities, brightness, or lux. Table 2 provides a comparison of light intensity based on the lux of various light sources. BLT is recommended as a stand-alone treatment for SAD as well as an adjunctive treatment to psychotherapies and pharmacotherapies. To date, the FDA has not approved BLT for the treatment of SAD or regulated the light box.
Comparison of Light Intensity
Although no prescription is required to order a light box for a patient, nurses can recommend this treatment provided they understand the various nuances needed for the therapy to be effective. First, it is important to understand the type of light that is beneficial to patients. BLT is most effective when full spectrum light, which emulates natural sunlight, is used. Table 3 provides light box treatment recommendations. According to the Mayo Clinic (2014), light box products should produce an even spectral distribution of 5,000 to 5,500 K, covering the electromagnetic spectrum from infrared to near-ultraviolet (UV) light, to be most efficacious; light boxes should also produce 10,000 lux of light. The typical treatment course consists of daily exposure of 20 to 30 minutes within the first waking hour of the morning. The light box should be positioned approximately 16 to 24 inches from the face, and individuals should have their eyes open, but not look directly at the light (Mayo Clinic, 2014). The light box should be specifically made for the treatment of SAD as it filters out most, if not all, UV light, unlike light boxes made to treat skin disorders, which emit UV light. Therapy should continue until the symptoms of SAD spontaneously remit with the onset of the next season or on the recommendation of the health care professional.
Light Box Recommendations for Seasonal Affective Disorder
If light boxes with lower lux are chosen for treatment, daily exposure time is greater. The higher the lux, the greater the retinal exposure in the least amount of time. Fluorescent bulbs emitting white light are the bulb of choice as incandescent light may damage the cornea and retina (Oren, Koziorowski, & Desam, 2013). Similar to antidepressant medication therapy, if symptoms have not improved within 2 to 4 weeks, the “dosage” of BLT should be increased by adding an evening “dose” to the regimen (Avery, 2017). Finally, as with medication therapies, adverse effects can also occur with light box therapy. Although typically mild, side effects of light therapy can include irritability/agitation, anxiety, visual disturbances/eye strain, headache, insomnia, fatigue, nausea, and the potential for mania/hypomania (Pail et al., 2011). Nurses must be familiar with patients' baseline symptoms to discern whether the light box therapy is exacerbating underlying pathology or creating adverse effects.
As the aforementioned treatments pertain primarily to winter-onset SAD, treatments for summer-onset SAD generally include the recommendation to limit exposure to natural sunlight to no more than 13 hours per day and to stay cool with air conditioning, especially at night (Avery, 2017). Although these recommendations may sound like common sense, or at least basic comfort measures, the idea is to reduce the exacerbation of irritability, weight loss, and insomnia, which may occur with summer-onset SAD.
SAD is an exacerbation of one of the affective disorders, which can have a profound impact on patients' lives for a good portion of the year. SAD does not only occur in the winter months, but also during the summer months with different symptomatology and treatments. The key to SAD is that the symptoms that appear at the onset of a season spontaneously remit without treatment at the onset of a new season. Nurses and clinicians can offer a variety of recommendations to aid in lessening the disruptions caused by seasonal mood fluctuations. Healthy lifestyle interventions, BLT, and even pharmacotherapy are options to reduce the negative impact of SAD on the quality of life of patients who experience these seasonal variations.
- American Psychiatric Association. (2010). Practice guideline for the treatment of patients with major depressive disorder (3rd ed.). Arlington, VA: Author.
- American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: Author.
- Anderson, J.L., Vasile, R.G., Mooney, J.J., Bloomingdale, K.L., Samson, J.A. & Schildkraut, J.J. (1992). Changes in norepinephrine output following light therapy for fall/winter seasonal depression. Biological Psychiatry, 32, 700–704. doi:10.1016/0006-3223(92)90299-F [CrossRef]
- Avery, D. (2017). Seasonal affective disorder: Treatment. Retrieved from http://www.uptodate.com/contents/seasonal-affective-disorder-treatment
- Fink, C. (2017). Bipolar disorder medication spotlight: Wellbutrin (bupropion). Retrieved from https://blogs.psychcentral.com/bipolar/2009/07/bipolar-disorder-medication-spotlight-wellbutrin-bupropion
- Frandsen, T.B., Pareek, M., Hansen, J.P. & Nielsen, C.T. (2014). Vitamin D supplementation for treatment of seasonal affective symptoms in healthcare professionals: A double-blind randomised placebo-controlled trial. BMC Research Notes, 7, 528. doi:10.1186/1756-0500-7-528 [CrossRef]
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- Gupta, A., Sharma, P.K., Garg, V.K., Singh, A.K. & Mondal, S.C. (2013). Role of serotonin in seasonal affective disorder. European Review for Medical and Pharmacological Sciences, 17, 49–55.
- Kurlansik, S.L. & Ibay, A.D. (2012). Seasonal affective disorder. American Family Physician, 86, 1037–1041.
- Lam, R.W., Zis, A.P., Grewal, A., Delgado, P.L., Charney, D.S. & Krystal, J.H. (1996). Effects of rapid tryptophan depletion in patients with seasonal affective disorder in remission after light therapy. Archives of General Psychiatry, 53, 41–44. doi:10.1001/archpsyc.1996.01830010043007 [CrossRef]
- Levitan, R.D. (2007). The chronobiology and neurobiology of winter seasonal affective disorder. Dialogues in Clinical Neuroscience, 9, 315–324.
- Mayo Clinic. (2014). Seasonal affective disorder (SAD). Retrieved from http://www.mayoclinic.org/diseases-conditions/seasonal-affective-disorder/basics/definition/con-20021047
- Michael, D.R. (2016). Seasonal affective disorder (SAD). Retrieved from http://emedicine.medscape.com/article/2500054-overview
- Modell, J.G., Rosenthal, N.E., Harriett, A.E., Krishen, A., Asgharian, A., Foster, V.J. & Wightman, D.S. (2005). Seasonal affective disorder and its prevention by anticipatory treatment with bupropion XL. Biological Psychiatry, 58, 658–667. doi:10.1016/j.biopsych.2005.07.021 [CrossRef]
- National Optical Astronomy Observatory. (n.d.). Recommended light levels. Retrieved from https://www.noao.edu/education/QLTkit/ACTIVITY_Documents/Safety/LightLevels_outdoor+indoor.pdf
- Oren, D.A., Koziorowski, M. & Desam, P.H. (2013). SAD and the not-so-single photoreceptors. American Journal of Psychiatry, 170, 1403–1412. doi:10.1176/appi.ajp.2013.13010111 [CrossRef]
- Pail, G., Huf, W., Pjrek, E., Winkler, D., Willeit, M., Praschak-Rieder, N. & Kasper, S. (2011). Bright-light therapy in the treatment of mood disorders. Neuropsychobiology, 64, 152–162. doi:10.1159/000328950 [CrossRef]
- Rohan, K.J., Roecklein, K.A. & Haaga, D. (2009). Biological and psychological mechanisms of seasonal affective disorder: A review and integration. Current Psychiatry Reviews, 5, 37–47. doi:10.2174/157340009787315299 [CrossRef]
- Stewart, A.E., Roecklein, K.A., Tanner, S. & Kimlin, M.G. (2014). Possible contributions of skin pigmentation and vitamin D in a polyfactorial model of seasonal affective disorder. Medical Hypotheses, 83, 517–525. doi:10.1016/j.mehy.2014.09.010 [CrossRef]
- Wehr, T.A., Duncan, W.C. Jr.. , Sher, L., Aeschbach, D., Schwartz, P.J., Turner, E.H. & Rosenthal, N.E. (2001). A circadian signal of change of season in patients with seasonal affective disorder. Archives of General Psychiatry, 58, 1108–1114. doi:10.1001/archpsyc.58.12.1108 [CrossRef]
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- Yildiz, M., Batmaz, S., Songur, E. & Oral, E.T. (2016). State of the art psychopharmacological treatment options in seasonal affective disorder. Psychiatria Danubina, 28, 25–29.
Healthy Lifestyle Interventions for Seasonal Affective Disorder
|Develop sleep hygiene habits:|
| • Adapt regular sleep and wake times|
| • Minimize blue light from television and electronic devices within 2 hours of sleep|
| • Maintain the bedroom at a comfortable temperature|
| • Avoid caffeine and alcohol, which disrupt restorative sleep|
| • Wake using a light to simulate dawn, as opposed to an alarm|
|Incorporate daily walks or outdoor activity, even on cloudy days|
|Incorporate aerobic exercise, approximately 30 minutes per day|
|Maintain a healthy diet without succumbing to increased carbohydrate cravings|
|Rearrange the indoor environment to maximize natural light from windows|
|Increase indoor lighting, especially full-spectrum light|
|Minimize stress through relaxation and meditation exercises|
|Make an effort to maintain social connections|
Comparison of Light Intensity
|Bright midday sun||50,000 to 100,000|
|General daylight||10,000 to 11,000|
|Bright light/light box therapy||10,000|
|Overcast skies||1,000 to 5,000|
|Indoor office/classroom lighting||500|
|Indoor home lighting||250|
Light Box Recommendations for Seasonal Affective Disorder
|Brightness of 10,000 lux|
|Full-spectrum light (5,000 to 5,500 K)|
|Little to no ultraviolet light exposure|
|Exposure of 20 to 30 minutes within the hour of waking|
|Position box 16 to 24 inches from the face|
|Sit with eyes open, but not looking directly into the light|
|Continue daily therapy until symptoms remit with the next season|