By Ruth Hobson, ND | January 28, 2025

As healthcare professionals, it’s essential to understand the physiological and neurological foundation of Seasonal Affective Disorder (SAD) to better support patients during seasonal transitions. This article provides a focused overview of SAD and the critical role neurotransmitters, melatonin, and cortisol play in its manifestation, enabling clinicians to offer targeted, evidence-based interventions. 

Understanding Seasonal Affective Disorder (SAD) SAD is a subtype of major depressive disorder characterized by its seasonal recurrence, typically presenting during fall and winter when daylight exposure decreases. Common clinical features include: 

• Persistent depressive mood or affect 
• Anhedonia (loss of interest in previously enjoyable activities) 
• Profound fatigue and reduced energy levels 
• Cognitive impairments, including difficulty concentrating 
• Hypersomnia or altered sleep patterns 
• Cravings for high-carbohydrate foods and associated weight gain 

SAD prevalence is higher in regions with prolonged winters and limited sunlight exposure, with females and younger adults being disproportionately affected. 

Neurotransmitter Dysregulation in SAD A growing body of research highlights the significant role of neurotransmitters in the pathophysiology of SAD. Key neurotransmitters include: 

1. Serotonin: Reduced serotonin activity, likely influenced by diminished sunlight exposure, is a hallmark of SAD. Decreased serotonin levels correlate with depressive symptoms, altered emotional regulation, and carbohydrate cravings that can lead to weight gain.  
2. Melatonin: Prolonged darkness during winter months leads to increased melatonin secretion during the day which can disrupt circadian rhythms and contribute to hypersomnia and lethargy. 
3. Dopamine: Impaired dopamine function may explain the reduced motivation and reward-seeking behavior observed in SAD patients. 

Diurnal Cortisol and Seasonal Affective Disorder Diurnal cortisol patterns are often disrupted in patients with SAD. Research indicates that individuals with SAD may exhibit flattened diurnal cortisol curves with reduced morning peaks and elevated evening levels. These blunting effects have been shown to exacerbate depressive symptoms, impair energy regulation, and contribute to sleep disturbances.  

Cortisol Awakening Response (CAR) and SAD The cortisol awakening response (CAR) is a distinct feature of diurnal cortisol rhythms, characterized by a sharp increase in cortisol levels within the first 30-45 minutes after waking. In individuals with SAD, CAR may be blunted or delayed, reflecting impaired HPA axis reactivity. This dysregulation can contribute to symptoms such as fatigue, reduced stress resilience, and mood disturbances.  

Clinical Support Strategies Familiarity with the neurochemical patterns of SAD equips clinicians to recommend effective therapeutic interventions. Evidence-based strategies include: 

• Bright Light Therapy (BLT): Administered at 10,000 lux for 20-30 minutes preferably in the morning. BLT is considered a first-line treatment for SAD. It mitigates symptoms by suppressing melatonin production and enhancing serotonin activity. 
• 5-HTP: A natural amino acid and precursor to serotonin, maybe effective in restoring serotonin levels and alleviating depressive symptoms 
• Vitamin D Supplementation: Low vitamin D levels are common in SAD patients. Supplementation may support the serotonin and dopamine pathways and improve overall mood. 
• Cognitive Behavioral Therapy (CBT): CBT tailored for SAD (CBT-SAD) reframes maladaptive thoughts and behaviors associated with the condition. 
• Lifestyle Interventions: Encourage patients to "move their bodies, spend time outdoors for grounding and exposure to natural light, and optimize sleep hygiene." A great one for this is walking as it's been shown to improve one's mood afterwards even when one doesn't want to walk! 
• Botanical Interventions: St. John’s Wort (Hypericum perforatum), has been shown to have antidepressant properties, potentially improving mood and reducing symptoms of depression. Saffron (Crocus sativus) has also gained attention for its mood-boosting effects, with studies indicating it may be as effective as conventional antidepressants for mild to moderate depression. 
• Supplements to consider: Omega-3 fatty acids (from fish oil or flaxseed oil) have anti-inflammatory effects that may help alleviate depression, while Vitamin B12 is essential for maintaining serotonin levels, with deficiencies often linked to depressive symptoms. 

Testing for Neurotransmitter and HPA Axis Imbalances: For healthcare providers looking to deliver individualized care, urine neurotransmitter and salivary diurnal cortisol and melatonin testing can offer valuable windows into your patient's neuroendocrinological picture by highlighting the biochemical imbalances that could be driving a patient’s symptoms. By identifying specific deficits or dysfunctions, you can tailor interventions with greater accuracy and effectiveness. Integrating lab testing into your diagnostic toolkit not only enhances patient outcomes but also sets your practice apart as a leader in personalized medicine. 

References 

Bhagwagar Z, Hafizi S, Cowen PJ. Increased salivary cortisol after waking in depression. Psychopharmacology (Berl). 2005;182(1):54-57. 

Finkelstein, J., et al. (2010). "Vitamin B12 deficiency in patients with depression: A systematic review." The Journal of Clinical Psychiatry, 71(4), 469-474. 

Freeman, M. P., et al. (2006). "Omega-3 fatty acids and depression: scientific evidence and clinical implications." Journal of Clinical Psychiatry, 67(12), 1956-1963. 

Fries E, Dettenborn L, Kirschbaum C. The cortisol awakening response (CAR): facts and future directions. Int J Psychophysiol. 2009;72(1):67-73. 

Gold PW, Chrousos GP. The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences. Proc Assoc Am Physicians. 1999;111(1):22-34. 

 Golden RN, Gaynes BN, Ekstrom RD, et al. The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence. Am J Psychiatry. 2005;162(4):656-662. 

Hausenblas, H. A., Schoulda, J. A., & Smoliga, J. M. (2015). "Saffron (Crocus sativus L.) and its effects on mood and depressive symptoms: A systematic review and meta-analysis." Phytotherapy Research, 29(5), 724-733. 

Lam RW, Levitt AJ, Levitan RD, et al. Efficacy of fluoxetine in the treatment of seasonal affective disorder: a randomized controlled trial. Am J Psychiatry. 2006;163(5):805-812. 

Lansdowne AT, Provost SC. Vitamin D3 enhances mood in healthy subjects during winter. Psychopharmacology (Berl). 1998;135(4):319-323. 

 Linde, K., et al. (2008). "St. John's Wort for depression: A systematic review and meta-analysis of randomized controlled trials." BMC Complementary and Alternative Medicine, 8(1), 6. 

Partonen T, Lönnqvist J. Bright light improves vitality and alleviates distress in healthy people. J Affect Disord. 2000;57(1-3):55-61. 

Rohan KJ, Roecklein KA, Haaga DA. Cognitive-behavioral therapy for seasonal affective disorder: a review and meta-analysis. Clin Psychol Rev. 2009;29(5):447-459. 

Terman, M., et al. (2006). "Light therapy for seasonal and nonseasonal depression: Efficacy, protocol, and side effects." The American Journal of Psychiatry, 163(5), 862-869. 

Thorn, L., Evans, P., Cannon, A., Hucklebridge, F., Evans, P., & Clow, A. (2011). "Seasonal differences in the diurnal pattern of cortisol secretion in healthy participants and those with self-assessed seasonal affective disorder." Psychoneuroendocrinology, 36(6), 816-823. 

Neurotransmitter Testing & Treatment: A Clinician's Guide

Presented by Lylen Ferris, ND | February 5, 2025 at 12 PM Pacific

Learning Objectives:

• Review general treatment concepts for optimizing neurotransmitter (NT) levels
• Discuss typical clinical presentations of individual neurotransmitter deficiencies and elevations
• Understand the physiology of neurotransmitter NT secretion and metabolism in order to support these processes to balance NT levels without the use of prescription medications
• Become familiar with genetic and lifestyle factors that influence NT levels
• Learn to incorporate NT evaluation and treatment in your practice utilizing either the Neurobasic profile or the Comprehensive Neurotransmitter Profile
• See how testing NT precursors and metabolites along with the NTs can help your interpretation and fine tune your treatment strategy

Laboratory, Endocrine, & Neurotransmitter Symposium

February 28 - March 2, 2025 in Austin, TX or Online

Earn up to 18.0 AMA PRA Category 1 Credit(s)™

The Laboratory, Endocrine and Neurotransmitter Symposium (LENS) combines curriculum driven by research and real-world clinical scenarios, taught by engaging and seasoned practitioners and educators. Attendees return year after year to LENS to dive deep into neuroendocrine topics, leaving the weekend with a full toolkit of clinical tips, protocols, and practical applications that can be implemented right away in their practice.

Sign up by January 31st, 2025 to save with our early bird prices!

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