Why do we just want to be alone when we are depressed?

It's strange: when we are sick with a stomach bug, we can easily lay in bed all day and think to ourselves, “Wow, I’m really sick! Let me just sleep this one off… hopefully I’ll get back to normal by tomorrow.” No shame. No guilt. No confusion.


But, when we’re depressed, or anxious, or simply mentally and emotionally unwell, the conversation in our head sounds very different. We can instinctively look down upon ourselves for staying in bed too long (perhaps even the whole day). In this scenario, we don’t consider that rest as a good thing. We don’t think that we’re recuperating. We think we are being weak, or lazy… or that we are broken somehow.



Our ‘normal self’ would be out there in the world, mixing it up with others, working hard on things, and exploring our passions. But, when we’re depressed, we don’t have energy for any of that. Nor can we find the motivation to get moving, in hopes that the energy will eventually come. We just really don’t want to leave our bed. We definitely don’t want to be in situations where we have to talk to others. We don’t feel like ourselves. Our days moving through the sludge can be confusing, soul-aching, and filled with shame.


That shame is why we try to keep all this a secret. All this hiding under the covers doesn’t fit the typical narrative we try to put out there - that we are capable, fun, interesting, calm, happy, & normal. It’s not the same as a bout with a stomach bug. Think about it. How many times have you explained to your co-workers, in graphic detail ( and without any explicit invitation), all the gritty ins and outs of your vomit session on the first day back to work after a ‘stomach bug’? No shame there, huh?


What we need to realize is that this reaction— wanting to go away, sleep all day, avoid everything, and just recede from the world— is actually biologically driven. It’s not a character trait/flaw.


This drive to isolate is common for many people experiencing depression. And, it’s also common in other inflammatory states - including the seasonal flu, that infamous stomach bug, or periodic accidental hangover.


Somehow, in our modern-day society, we have determined that there is a difference. It feels different when we are choosing to stay in bed because we are ‘legitimately’ sick versus choosing to stay in bed because we’re depressed. It feels as if one is excusable, the other is not. As if physical illness is real and chemically mediated, and the other is not.


In reality, when we are sick, our immune system is in overdrive. We are inflamed. Our body is awash with “cytokines”. These cytokines are inflammatory messengers triggered by reactions to infections, stress, and other insults. For many experiencing depression (and other mental illnesses), the cytokines released are the same exact ones that circulate around when we are physically ill. For many (but not all) with mental illness, it’s just that these cytokines have migrated from the body into our brain (Kuhlman 2018, Felger et al. 2020)!


So, in a way, it’s the same thing. Researchers have a name for this observed decrease in energy and drive to isolate that occurs when we are sick,whether it's from an infection or depression. It’s called sickness behavior (Dantzer 2008).


Here’s a rundown of how it all goes down in our bodies:


Stress (mental, physical, emotional, even existential) begins to add up. At some point, we become overwhelmed. It’s more than we can take. In addition, there’s a possibility that our diet is “not the best.” Maybe we fail to exercise and end up being sedentary most of our days. Perhaps we smoke cigarettes (because we’re so dang stressed). Likely, we don’t get enough quality sleep for one reason or another. Regrettably, our skin doesn’t see the light of day, other than the short walk to our car before our daily commute.


Next, our body begins to respond to these insults. Our blood sugar levels sink and surge greater than before. Similarly, our hormonal secretions slosh back and forth in an effort to try to reestablish inner balance. Our digestive tract starts getting out of whack - there’s too much bad bacteria, not enough good, and the lining of our intestine loses its ability to keep toxins and undigested food particles from being absorbed into our system. And then, our immune system wakes up, and joins the party. Our body will react to all those stressors with a dose of inflammation (Berk 2013).


What is inflammation again? It starts out local, but can progress to a whole-body, coordinated response. Inflammation is our body fighting back against what is perceived as foreign. The kind of inflammation we are talking about here is chronic (all the time), low-grade (steady faucet rather than flood), systemic (all over the body) inflammation. It is often triggered by our not-so-good-for-us habits and environmental stressors described above.


Ever hear the saying, “the best defense is a good offense”? The sentiment is a close relative to the timeless sports coach refrain, “defense wins championships.” The overall point here is that inflammation is a concerted effort to protect the body. That protection has to be big, and comes at a cost.


When that inflammation reaches the brain, it’s called neuroinflammation (Calcia et al. 2016).

At the most basic level, however, after inflammation is triggered, those cytokines are released and begin to circulate throughout the body. These cytokines all have their characteristic Latin, scientific sounding names - Interleukin-1 beta, Interleukin-6, TNF-alpha, interferon - among many others (Raison et al. 2006). The end result? The release of cytokines prepares the body to defend itself— to get ready to attack what’s attacking you. As woo woo as it sounds, even psychological stress (daily life stress) can create inflammation, as the body thinks it’s under attack (Rohleder 2014).


Let’s look at one cytokine (inflammatory messenger) in particular to illustrate what’s going on. Interleukin-1 beta is a commonly secreted cytokine that can aggravate the brain in two key ways.


First, it can over excite a really important nerve that runs from the base of the brain down into the gut. IThat’s called the vagus nerve, and it sends messages back and forth between the brain and gut. Once stimulated by Interleukin-1 beta, the vagus nerve will signal the brain to focus strongly on the social environment (Dantzer 2009). That cues the brain to scan for threats, as well as supportive connections (Eisenberger et al. 2017). This heightens our awareness of threats, as well as safe supports,in our immediate environment. Our brain is now dialed in. Our radar is keyed up and on high alert for what can hurt us and what can help us.


Second, cytokines, like Interleukin-1 beta, can bypass the brain’s barrier. Once inside, these cytokines can activate receptors in the amygdala - the brain’s fear center (Eisenberger et al. 2017). This colors our experience with a shade of “I suck... they’re gonna hate me… this is all going to end poorly.”


So, in an inflammatory state (meaning higher than normal levels of circulating cytokines), we first become sensitive to all the bad out there in the world that for sure/definitely/but actually not really awaits us. Then we begin to isolate. We avoid interactions with others, basically, because we’re afraid (Hafner et al. 2011, Eisenberger et al. 2017).


Faced with that heightened awareness and flood of negativity, we shrink backwards. We try to find some safety at home, often under the covers. At the same time, we wish we had a friend or loved one with whom we could connect (Eisenberger et al. 2017). Part of us is hiding, the other part is seeking connection… with someone that could relieve us of that loneliness that makes us feel hollow inside.


Perhaps that sounds too dramatic, but the connection between inflammation and what we feel is definitely there. A few recent studies have uncovered that the higher the level of circulating inflammatory cytokines, the greater degree to which subjects rated depressive symptoms like poor motivation, lack of joy, and social drive (Hafner et al. 2011, Felger et al. 2020).


If any of this relates to you, realizing a few points may help as you’re working through these feelings and experiences. First, it may be your body that is overreacting, not you or your mind. Second, this overreaction (AKA inflammatory response) is still you trying to protect you. Third, this inflammatory response can make you (and possibly others) conclude that you’re just being lazy or weak. Not true. Fourth, some people in your life may be the cause of your stress, and thus, your extra inflammation, but connection and support is part of the answer. Get what you can from those that can’t give you more than what they’re able to give. Seek out and gravitate towards those that can offer support, connection, and the gift of listening.


Although it may not seem like it, there are others out there that do care, and can be there for you. Boundaries are always important, and we have to play it cool to some degree in order to avoid clinging on too tight, too quick. Yet, being open and sharing is always the first step.

Think about the people in your life. Who do you have that you KNOW they care about you? If you are isolating a lot, maybe it’s time to take that leap of faith and open up about what really is going on and how you really feel. Talking now is always better than later, as these feelings tend to just balloon when kept under wraps. Decide who feels safe, and then let them know what’s happening for you. Without doing anything heroic, just the ability to say it out loud to another is huge. Sandwich it with small talk if needed. Give it a try.


If family or friends are not an option for you, there are so many people out there who would be honored to help. In urgent situations, there’s the suicide hotline - 1-800-273-8255 https://suicidepreventionlifeline.org/


Otherwise, there are so many caring and talented professionals out there to help. It’s just one google search away from someone near you. And, there are those people out there, who may not be a clinician, but have been through it before, and they are usually the best listeners.


All you have to do is reach out and ask. Others may be able to lend you an ear. Give them a shot, they may just be there when you need them most— in the biggest way. All you have to do is reach out and ask. We are here for you!



References:

Kuhlman, K. R., Robles, T. F., Dooley, L. N., Boyle, C. C., Haydon, M. D., & Bower, J. E. (2018). Within-subject associations between inflammation and features of depression: Using the flu vaccine as a mild inflammatory stimulus. Brain, Behavior, and Immunity, 69, 540–547. http://doi.org/10.1016/j.bbi.2018.02.001


Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008). From inflammation to sickness and depression: when the immune system subjugates the brain. Nature Reviews. Neuroscience, 9(1), 46–56. http://doi.org/10.1038/nrn2297


Berk, M., Williams, L. J., Jacka, F. N., O’Neil, A., Pasco, J. A., Moylan, S., et al. (2013). So depression is an inflammatory disease, but where does the inflammation come from? BMC Medicine, 11(1), 200. http://doi.org/10.1186/1741-7015-11-200


Rohleder, N. (2014). Stimulation of Systemic Low-Grade Inflammation by Psychosocial Stress. Psychosomatic Medicine, 76(3), 181–189. http://doi.org/10.1097/PSY.0000000000000049


Raison, C. L., Capuron, L., & Miller, A. H. (2006). Cytokines sing the blues: inflammation and the pathogenesis of depression. Trends in Immunology, 27(1), 24–31. http://doi.org/10.1016/j.it.2005.11.006


Calcia, M. A., Bonsall, D. R., Bloomfield, P. S., Selvaraj, S., Barichello, T., & Howes, O. D. (2016). Stress and neuroinflammation: a systematic review of the effects of stress on microglia and the implications for mental illness. Psychopharmacology, 233(9), 1637–1650. http://doi.org/10.1007/s00213-016-4218-9


Dantzer, R. (2009). Cytokine, Sickness Behavior, and Depression. Immunology and Allergy Clinics of North America, 29(2), 247–264. http://doi.org/10.1016/j.iac.2009.02.002


Eisenberger, N. I., Moieni, M., Inagaki, T. K., Muscatell, K. A., & Irwin, M. R. (2017). In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 42(1), 242–253. http://doi.org/10.1038/npp.2016.141


Häfner, S., Emeny, R. T., Lacruz, M. E., Baumert, J., Herder, C., Koenig, W., et al. (2011). Association between social isolation and inflammatory markers in depressed and non-depressed individuals: Results from the MONICA/KORA study. Brain, Behavior, and Immunity, 25(8), 1701–1707. http://doi.org/10.1016/j.bbi.2011.06.017


Felger, J. C., Haroon, E., Patel, T. A., Goldsmith, D. R., Wommack, E. C., Woolwine, B. J., … Miller, A. H. (2020). What does plasma CRP tell us about peripheral and central inflammation in depression? Molecular Psychiatry, 25(6), 1301–1311. https://doi.org/10.1038/s41380-018-0096-3



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