Seasonal Affective Disorder (SAD) caused by circadian phase shifts

 In the article "Circadian disruption and human health" by Anna B. Fishbein et al., circadian disruption is linked to psychiatric disease, such as schizophrenia and mood disorders. The article specifies the link between circadian disruption and the mood disorder, Seasonal Affective Disorder (SAD). SAD is distinguished as an inception or worsening of depression that occurs throughout the fall and winter months, when the duration of daylight decreases. It has been proven through research that SAD symptoms are the result of circadian misalignment due to seasonal shifts in temperate climates.

 

The article "Low circadian amplitude and delayed phase are linked to seasonal affective disorder (SAD)” by Luvna Dhawka et al., furthers research on the effects of circadian disruption on SAD by studying seasonal changes in circadian phase and amplitude as well as used computational modeling to simulate the SAD phenotypes reproduced by circadian clock gene variants across seasons. Their research is based on evidence that genetic polymorphisms of clock genes effect mood phenotypes and the hypothesis that circadian clock gene result in circadian misalignment due to phase shifts in circadian oscillations and lowered amplitudes. It is also based on the circadian phase-shift hypothesis that states that those with SAD experience depressive episodes during the winter months because of delayed circadian phases during those months.

 

The goal of their study was to establish a link between clock gene polymorphisms and circadian oscillations and amplitudes to understand the downstream effects of circadian disruption that result in SAD symptoms. Two different methods were used in the study; one to study in-vivo changes based on season in circadian clock genes taken from hair to test their hypothesis on circadian phase and amplitude, and another to study the effects of polymorphisms in CRY1 , CRY2, PER2, and PER3 genes (associated with SAD) on SAD phenotype conditions (circadian phase shift and lowered amplitude) to test the molecular mechanisms that direct SAD phenotype changes across seasons. They hypothesized that participants with SAD would have lower in-vivo amplitudes and a delayed circadian phase during the winter months compared to non-SAD participants. They also hypothesized that clock gene polymorphisms are associated with SAD phenotypes.

 

They adapted an already existing mathematical model created to explain how clock genes affect gene expression, changes in transcription period, and amplitude, to understand how gene polymorphisms effect molecular mechanisms involved in SAD phenotypes. They did this by including a seasonal light parameter and transcription parameters that relate to polymorphisms in CRY1, CRY2, PER2, and PER3 genes.

 

The result of their study provides evidence for the possible genetic and molecular mechanisms that drive SAD, such as delays circadian phase during winter months and low circadian amplitude. Their results provide a new framework to better understand how circadian rhythms connect to mood disorder pathways in general and lead the way for more efficient testing methods and diagnostic measures for individuals with SAD.

 

References:

 

Dhawka, L., Cha, Y., Ay, A., & Ingram, K. K. (2022, August 15). Low circadian amplitude and delayed phase are                    linked to seasonal affective disorder (SAD). Journal of Affective Disorders Reports. Retrieved March 3,                     2023, from https://www.sciencedirect.com/science/article/pii/S2666915322000877

 

Fishein, A. B., Knutson, K. L., & Zee, P. C. (n.d.). Circadian disruption and human health. The Journal of Clinical                 Investigation. Retrieved March 3, 2023, from https://loyolauniversitychicago-my.sharepoint.com/personal/rmorrison_luc_edu/_layouts/15/onedrive.aspx?ga=1&id=%2Fpersonal%2Frmorrison%5Fluc%5Fedu%2FDocuments%2FTeaching%20%2D%20Onedrive%2FNEUR%20300%20%2D%20Neuroscience%20Seminar%2FNEUR%20300%20%2D%20Spring%2023%2FNEUR%2F%2801%2E31%2E23%29%20%2D%20Phyllis%20Zee%2F148286%2E2%2D20211007151627%2Dcovered%2De0fd13ba177f913fd3156f593ead4cfd%2Epdf&parent=%2Fpersonal%2Frmorrison%5Fluc%5Fedu%2FDocuments%2FTeaching%20%2D%20Onedrive%2FNEUR%20300%20%2D%20Neuroscience%20Seminar%2FNEUR%20300%20%2D%20Spring%2023%2FNEUR%2F%2801%2E31%2E23%29%20%2D%20Phyllis%20Zee