Blue Monday and Seasonal Affective Disorder

Blue Monday is considered by many to be the saddest or most depressing day of the year. This day is set on the calendar on the third Monday in January, when many people suffer from seasonal affective disorder (SAD) or simply Winter depression. According to color psychology, the day is associated with blue, a color that denotes passivity, sadness, pessimism or apathy (1) and hence the name assigned to this day.

But where does this expression come from and what is true about it? 

The origin of this expression dates back to 2005, and was first used by motivation expert Cliff Arnall, who also proposed a mathematical formula to show why the third Monday of the year was the saddest day. This formula was modified years later to read as follows:

• W refers to the weather, 

• D to debts, 

• d to the monthly salary, 

• T to the time elapsed since the end of Christmas, 

• Q to the time since an unsuccessful attempt was made to carry out some purpose, 

• M to the level of motivation, and 

• Na to the need to do something. 

In no case was it specified how to measure these variables, not even the more concrete ones, such as time since Christmas, salary or debts, much less the more abstract ones, such as the level of motivation or the need to do something. 

Although the fact that a mathematical formula has been developed to measure which day is the saddest of the year seems to give it credibility, nothing could be further from the truth, as many experts argue the lack of methodological principles. Therefore, the term Blue Monday is a pseudoscientific term and, despite using real factors affecting mood for its calculation, the approach of its equation is totally arbitrary (2). 

An example of the real factors that are considered to declare Blue Monday the saddest day of the year, and that clearly affects mood is the weather. During the winter some people experience increased sadness for no apparent cause, especially in areas with fewer hours of daylight during these months. This is known as a seasonal affective disorder, and although it is most experienced during the winter months, some people experience it in the spring or summer. 

What is seasonal affective disorder?

Seasonal affective disorder (SAD) is a state of seasonal mood swings characterized by recurrent depression usually in the fall or winter that spontaneously subsides in the spring or summer. Tiredness, overeating, carbohydrate craving and depressed mood are the most common symptoms. In some people, SAD develops into depression that severely affects their daily life (3). 

Winter depression is a multifactorial disorder involving chronobiological mechanisms related to circadian rhythms, melatonin, serotonin turnover and photoperiodism, i.e., the length of hours of darkness relative to hours of light in a 24-hour period (4). 

This disease has a high risk of recurrence and persistence. Approximately two-thirds of people diagnosed with SAD will suffer symptoms again the winter following their diagnosis. In the 5 to 11 years following the initial diagnosis, 22-42% of patients continue to suffer from SAD, and 33-44% develop a non-seasonal pattern in subsequent episodes. In fact, the disorder resolves completely in only 14-18% of patients (3, 5). 

How is this disorder diagnosed?

The diagnostic criteria are as follows:

• A temporal relationship is observed between the occurrence of depressive episodes and a particular time of the year. 

• Complete remissions also occur at a characteristic time of the year. 

• Within the past 2 years, two major depressive episodes that demonstrate the temporal relationships defined in the previous two criteria have occurred, and no non-seasonal major depressive episodes have occurred during that same period.

• Seasonal major depressive episodes (as described above) outnumber non-seasonal major depressive episodes that may have occurred throughout the individual’s lifetime (5).

Is there a treatment for SAD?

The seasonal aspect of SAD offers a promising opportunity for prevention. Because of the importance of decreased light exposure in this disorder, many studies have focused on the efficacy of phototherapy, being used in most cases as the first line of treatment. Phototherapy, also known as “light therapy,” is a technique that uses electromagnetic radiation and, in the case of treatment for SAD, full-spectrum visible light (6). The exact mode of action of bright light is not clear, but it is hypothesized to be due to stimulation of light-sensitive retinal ganglion cells, which contain melanopsin, and project to the hypothalamus where the suprachiasmatic nucleus, the main center of regulation of circadian rhythms, is activated, primarily through inhibition of melatonin synthesis. Melatonin is a hormone involved in sleep regulation, essential for controlling mood and behavior (Figure 1). In addition, bright light influences key neurotransmitter molecules such as the serotonin transporter, a key neuromodulator in mood and behavior regulation, and may influence immune functions (7, 8).

Schematic of the melanopsin pathway through the retinal ganglion cells to the suprachiasmatic nucleus, the main center of regulation of circadian rhythms. Image obtained from: (9)

On the other hand, direct administration of melatonin, or melatonin analogues, has the capacity to reestablish altered circadian rhythms, independently or in combination with phototherapy, so they are also promising in the treatment of the seasonal affective disorder (3).

 What is the role of genetics in SAD?

In the process of regulating circadian rhythms, as in virtually all physiological processes, are involved specific proteins encoded by different genes that make up the so-called “molecular clock”. Therefore, mutations in these genes will have implications for the regulation of circadian rhythms and may lead to a greater or lesser predisposition to suffer from SAD. 

One of the proteins that forms part of the so-called molecular clock is the NPAS2 protein (Neuronal PAS domain-containing protein 2). Also, there are genome-wide association studies (GWAS) that demonstrate its association with a greater predisposition to seasonal affective disorder (10, 11). 

What can 24Genetics tell you about SAD?

The 24Genetics DNA talent and personality test can elicit your predisposition to experience seasonal variations in mood, which is also related to appetite and weight.

Bibliography

1. Blue Monday: a depressing day of pseudoscience and humiliation | Psychology | The Guardian. (n.d.). Retrieved January 5, 2023, from https://www.theguardian.com/science/blog/2012/jan/16/blue-monday-depressing-day-pseudoscience
2. Jan. 24 called worst day of the year. (n.d.). Retrieved January 5, 2023, from https://www.nbcnews.com/id/wbna6847012#.VXnhVkao1T8 
3. Kaminski-Hartenthaler, A., Nussbaumer, B., Forneris, C. A., Morgan, L. C., Gaynes, B. N., Sonis, J. H., Greenblatt, A., Wipplinger, J., Lux, L. J., Winkler, D., van Noord, M. G., Hofmann, J., & Gartlehner, G. (2015). Melatonin and agomelatine for preventing seasonal affective disorder. Cochrane Database of Systematic Reviews, 2015(11). https://doi.org/10.1002/14651858.CD011271.PUB2
4. Ciarleglio, C. M., Resuehr, H. E. S., & McMahon, D. G. (2011). Interactions of the serotonin and circadian systems: nature and nurture in rhythms and blues. Neuroscience, 197, 8–16. https://doi.org/10.1016/J.NEUROSCIENCE.2011.09.036 
5. Magnusson, A., & Partonen, T. (2005). The Diagnosis, Symptomatology, and Epidemiology of Seasonal Affective Disorder. CNS Spectrums, 10(8), 625-634. doi:10.1017/S1092852900019593 
6. Información sobre el procedimiento de fototerapia | Memorial Sloan Kettering Cancer Center. (n.d.). Retrieved January 5, 2023, from https://www.mskcc.org/es/cancer-care/patient-education/about-your-phototherapy-procedure 
7. Pjrek, E., Friedrich, M. E., Cambioli, L., Dold, M., Jäger, F., Komorowski, A., Lanzenberger, R., Kasper, S., & Winkler, D. (2020). The Efficacy of Light Therapy in the Treatment of Seasonal Affective Disorder: A Meta-Analysis of Randomized Controlled Trials. Psychotherapy and psychosomatics, 89(1), 17–24. https://doi.org/10.1159/000502891
8. Venkataramanujam Srinivasan, Domenico De Berardis, Samuel D Shillcutt & Amnon Brzezinski (2012) Role of melatonin in mood disorders and the antidepressant effects of agomelatine, Expert Opinion on Investigational Drugs, 21:10, 1503-1522, DOI: 10.1517/13543784.2012.711314
9. Awad-Alkoziv H. Melatonina y melanopsina en el ojo: ¿amigos o enemigos?. ANALES RANF [Internet]. Royal National Academy of Pharmacy; An Real Acad Farm · year 2019 · volume 85 · issue 01:49-59.
10. Kim, H. I., Lee, H. J., Cho, C. H., Kang, S. G., Yoon, H. K., Park, Y. M., Lee, S. H., Moon, J. H., Song, H. M., Lee, E., & Kim, L. (2015). Association of CLOCK, ARNTL, and NPAS2 gene polymorphisms and seasonal variations in mood and behavior. Chronobiology international, 32(6), 785–791. https://doi.org/10.3109/07420528.2015.1049613
11. Partonen, T., Treutlein, J., Alpman, A., Frank, J., Johansson, C., Depner, M., Aron, L., Rietschel, M., Wellek, S., Soronen, P., Paunio, T., Koch, A., Chen, P., Lathrop, M., Adolfsson, R., Persson, M. L., Kasper, S., Schalling, M., Peltonen, L., & Schumann, G. (2007). Three circadian clock genes Per2, Arntl, and Npas2 contribute to winter depression. Annals of medicine, 39(3), 229–238. https://doi.org/10.1080/07853890701278795