Why February Feels So Long Despite Being the Shortest Month

Why February Feels So Long Despite Being the Shortest Month

How this phenomenon can affect mood, inflammation and immunity

Each year, we deal with the excessively long, cold, and dimly lit season of winter that seems to drag on while we patiently await spring. After making it through the exhaustive 31 days of January, we get one step closer to the sunlight and warmer weather that tends to accompany the summer months.

If only we didn’t have to scrape through February…the shortest month of the year that feels like the longest.

But why does it feel so long and what are its potential effects on mood, inflammation and overall immunity?

This question has been asked over and over again by various individuals everywhere.

Some researchers believe that our sense of time can become distorted following December and into the early months of the New Year, which may be an after-effect of the countless events and relaxation that we tend to experience over the year-end holidays.

Interestingly, this “after-effect” may be attributed to the dopamine clock hypothesis1, which asserts that the neurotransmitter, dopamine, dictates our perception of time.

To put this in perspective, if we are experiencing pleasurable feelings, such as those that occur when we are socializing and relaxing over the holidays, dopamine release increases and so does our sense of time.

On the other hand, when we are deprived of the feel-good times, such as those that tend to occur in the “after-effect months” of January and February, and even within an isolation-prompting pandemic, it becomes less likely that those dopamine hits will happen, which may cause us to feel like time slows down, and is generally perceived as less enjoyable.

I guess that gives merit to the old saying, “time flies when you’re having fun”.

At the same time, we are likely to experience a variety of lifestyle stressors like work deadlines and finances as well as environmental stressors such as cold temperatures and isolation during these months.

The combination of accumulated stressors with a lack of excitement to buffer the effects of stress can have significant consequences on our mood and motivation, possibly by impacting central dopamine activity in our brains2,3.

Stress, inflammation, and mood

There is evidence that intermittent exposure to cold temperatures can sensitize our stress response system4, or make it more “reactive” than normal. Moreover, cold stress has been shown to increase depressive-like behavior5.

Together, these findings suggest an intricate link between environmental stress and mood—a very relevant topic for the winter months.

On a similar note, we tend to be deprived of natural sunlight in the winter, which is thought to contribute to seasonal depression, resulting in reduced motivation and can lead to social isolation.

Importantly, there is evidence that social isolation can be a significant stressor in and of itself 6–8, known to cause depressive-like behavior 9,10, and cause long-term deficits in mental and systemic health11.

An important consideration to keep in mind during the winter is our tendency to become sedentary, or inactive, due to a steep decline in the outdoor activities that are usually accessible during summer.

Interestingly, sedentary behavior has been found to increase inflammation in the blood12,13. Specifically, non-active individuals displayed higher levels of the inflammation proteins called c-reactive protein, TNF-α, and IL-6 in their circulating blood.

This is important to consider because several studies have shown that increased inflammation can negatively influence mood14–16.

Frequent stress exposure is associated with increased inactivity and fatigue17, and can typically result in social isolation18,19. In turn, this isolation and inactivity can fuel inflammation, which can cause changes in mood.

As you can see, stress and inflammation can influence one another in a vicious cycle, which may be influenced by the lifestyle and environmental stressors that come with the post-holiday months.

How does inflammation affect your mood?

Inflammation, in this context, can be thought of as little immune molecules in your blood that cause areas around a wound to become red and thus, “inflamed”. These molecules are commonly referred to as cytokines and chemokines.

Several studies have investigated how inflammation can negatively influence mood and have found some interesting results.

For example, one study found that participants who reported high levels of chronic psychological stress displayed abnormal activity of their stress response system, characterized by irregular cortisol activity, a hallmark stress hormone.

Moreover, immune cells that were isolated from the blood of these participants were more reactive to a chemical that causes an immune response20. Therefore, as suggested by this study, it is possible that abnormal inflammation may be a result of exposure to chronic stress.

Additional theories have suggested that inflammation directly influences mood by interacting with areas of the brain involved in mood and motivation21–23.

Importantly, researchers have suggested that long-term exposure to stress can steadily increase brain inflammation24,25, otherwise known as neuroinflammation, and may be a result of increased cytokines in the blood.

Accordingly, cytokines have been shown stimulate changes in the activity of immune cells in our brain, called microglia26.

If cytokines relay an emergency signal to these microglia, they become reactive and will typically begin to produce compounds in your brain that can become toxic in high enough concentrations27.

Interestingly, researchers have shown that several cytokines, including the ones that increase when we become inactive or when we are exposed to frequent stress, can directly increase levels of  toxic compounds produced by reactive microglia28.

A significant body of research has associated the impact of inflammation on mood and motivation with changes in dopamine activity in the brain14.

Thus, it is possible that compounding effects of life and environmental stressors, sedentary lifestyles, and increased inflammation may all be playing with our internal clock through changes in dopamine activity.

So, what does this mean?

Despite February being the shortest month, it may feel like the longest because: we have a lack of events to look forward to; we do not include enough buffers to reduce the effects of life and environmental stressors; and, simply put—we aren’t getting enough physical activity! All factors which may negatively impact our overall immunity.

In addition, the combination of isolation, cold-induced stress and its subsequent impact on inflammation and brain dopamine levels, may result in individuals experiencing negative feelings and reduced motivation during these months.

In this context, making plans to see friends and family (even virtually), starting and maintaining a workout routine, taking up an interesting and pleasurable hobby (e.g., cross-country skiing, snowshoeing, painting, writing, etc.), investing in a bright-light appliance to tackle low-light conditions, or even taking immune-boosting supplements, are all great ways to buffer lifestyle and environmental stressors and to ensure we receive those necessary hits of dopamine during the shortest, yet longest month of the year.

Of course, incorporating all of these together will surely enhance your perception and sense of time during the everlasting month of February.

Author: Brett Melanson is a PhD Candidate in Behavioral NeuroscienceHis interests primarily reside within the life sciences with an emphasis on stress-based psychopathologies.

energia+

References

  1. Simen, P. & Matell, M. Why does time seem to fly when we’re having fun? Science (2016) doi:10.1126/science.aal4021.

  2. Rincón-Cortés, M. & Grace, A. A. Sex-dependent effects of stress on immobility behavior and VTA dopamine neuron activity: Modulation by ketamine. Int. J. Neuropsychopharmacol. 20, 823–832 (2017).

  3. Rincón-Cortés, M. & Grace, A. A. Antidepressant effects of ketamine on depression-related phenotypes and dopamine dysfunction in rodent models of stress. Behav. Brain Res. 379, 112367 (2020).

  4. Morilak, D. A. et al. Role of brain norepinephrine in the behavioral response to stress. Prog. Neuro-Psychopharmacology Biol. Psychiatry 29, 1214–1224 (2005).

  5. Borsini, F., Lecci, A., Sessarego, A., Frassine, R. & Meli, A. Discovery of antidepressant activity by forced swimming test may depend on pre-exposure of rats to a stressful situation. Psychopharmacology (Berl). 97, 183–188 (1989).

  6. Campagne, D. M. Stress and perceived social isolation (loneliness). Archives of Gerontology and Geriatrics (2019) doi:10.1016/j.archger.2019.02.007.

  7. Marcolin, M. L., Hodges, T. E., Baumbach, J. L. & McCormick, C. M. Adolescent social stress and social context influence the intake of ethanol and sucrose in male rats soon and long after the stress exposures. Dev. Psychobiol. 61, 81–95 (2019).

  8. Marcolin, M. L., Baumbach, J. L., Hodges, T. E. & McCormick, C. M. The effects of social instability stress and subsequent ethanol consumption in adolescence on brain and behavioral development in male rats. Alcohol 82, 29–45 (2020).

  9. Zaletel, I., Filipović, D. & Puškaš, N. Hippocampal BDNF in physiological conditions and social isolation. Reviews in the Neurosciences (2017) doi:10.1515/revneuro-2016-0072.

  10. Fone, K. C. F. & Porkess, M. V. Behavioural and neurochemical effects of post-weaning social isolation in rodents-Relevance to developmental neuropsychiatric disorders. Neuroscience and Biobehavioral Reviews (2008) doi:10.1016/j.neubiorev.2008.03.003.

  11. Arzate-Mejía, R. G., Lottenbach, Z., Schindler, V., Jawaid, A. & Mansuy, I. M. Long-Term Impact of Social Isolation and Molecular Underpinnings. Front. Genet. 11, 1–13 (2020).

  12. Lund, A. J. S., Hurst, T. L., Tyrrell, R. M. & Thompson, D. Markers of chronic inflammation with short-term changes in physical activity. Med. Sci. Sports Exerc. (2011) doi:10.1249/MSS.0b013e3181f59dc4.

  13. Allison, M. A., Jensky, N. E., Marshall, S. J., Bertoni, A. G. & Cushman, M. Sedentary behavior and adiposity-associated inflammation: The multi-ethnic study of atherosclerosis. Am. J. Prev. Med. (2012) doi:10.1016/j.amepre.2011.09.023.

  14. Felger, J. C. & Treadway, M. T. Inflammation Effects on Motivation and Motor Activity: Role of Dopamine. Neuropsychopharmacology 42, 216–241 (2017).

  15. Wang, J. et al. The Dopamine Receptor D3 Regulates Lipopolysaccharide-Induced Depressive-Like Behavior in Mice. Int. J. Neuropsychopharmacol. (2018) doi:10.1093/ijnp/pyy005.

  16. O’Connor, J. C. et al. Interferon-γ and tumor necrosis factor-α mediate the upregulation of indoleamine 2,3-dioxygenase and the induction of depressive-like behavior in mice in response to bacillus calmette-guérin. J. Neurosci. (2009) doi:10.1523/JNEUROSCI.5032-08.2009.

  17. Strahler, J. et al. Physical activity buffers fatigue only under low chronic stress. Stress (2016) doi:10.1080/10253890.2016.1192121.

  18. Venzala, E., García-García, A. L., Elizalde, N., Delagrange, P. & Tordera, R. M. Chronic social defeat stress model: Behavioral features, antidepressant action, and interaction with biological risk factors. Psychopharmacology (Berl). (2012) doi:10.1007/s00213-012-2754-5.

  19. Golden, S. A., Covington, H. E., Berton, O. & Russo, S. J. A standardized protocol for repeated social defeat stress in mice. Nat. Protoc. 6, 1183–1191 (2011).

  20. Miller, G. E., Cohen, S. & Ritchey, A. K. Chronic psychological stress and the regulation of pro-inflammatory cytokines: A glucocorticoid-resistance model. Heal. Psychol. 21, 531–541 (2002).

  21. Tonelli, L. H., Holmes, A. & Postolache, T. T. Intranasal immune challenge induces sex-dependent depressive-like behavior and cytokine expression in the brain. Neuropsychopharmacology 33, 1038–1048 (2008).

  22. de Melo, L. G. P. et al. Shared metabolic and immune-inflammatory, oxidative and nitrosative stress pathways in the metabolic syndrome and mood disorders. Prog. Neuro-Psychopharmacology Biol. Psychiatry 78, 34–50 (2017).

  23. Fang, X. et al. Abnormalities in inflammatory cytokines confer susceptible to chronic neuropathic pain-related anhedonia in a rat model of spared nerve injury. Clin. Psychopharmacol. Neurosci. 17, 189–199 (2019).

  24. Miller, A. H., Maletic, V. & Raison, C. L. Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression. Biological Psychiatry vol. 65 732–741 (2009).

  25. Slavich, G. M. & Irwin, M. R. From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. Psychol. Bull. 140, 774–815 (2014).

  26. Nimmerjahn, A., Kirchhoff, F. & Helmchen, F. Neuroscience: Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Science (80-. ). (2005) doi:10.1126/science.1110647.

  27. Feng, W. et al. Microglia activation contributes to quinolinic acid-induced neuronal excitotoxicity through TNF-α. Apoptosis 22, 696–709 (2017).

  28. Kim, Y. K. & Won, E. The influence of stress on neuroinflammation and alterations in brain structure and function in major depressive disorder. Behav. Brain Res. 329, 6–11 (2017).

0 comments

Leave a comment

Please note, comments must be approved before they are published