The Connection Between Inflammation and Depression

Do you know the leading cause of disability in our world? Depression according to the World Health Organization (WHO). Sadly, many if not most individuals do not find help from depression medications like SSRIs. (Krishnan & Nestler, 2008).

One region of study might shed some light on why a substantial portion of clients are not helped by existing antidepressants. Recent evidence shows that inflammation can intensify or perhaps create depressive behaviors. While Major Depressive Disorder (MDD) might not be a primary “inflammatory disease” evidence has shown a close relation. Understanding this relationship can help increase the efficacy of depression and mental health treatments.

Reason For Inflammation

The inflammatory reaction is a crucial element in the body’s immune system. When our bodies are invaded by parasites, bacteria, viruses, or toxins, the immune system employs proteins, cells, and tissues to combat these intruders.

The primary strategy is to mark the damaged body parts, so we can pay more attention to them. Regional inflammation makes the wounded parts red, inflamed, and warm. When the injury is not localized, then the entire body ends up inflamed.

These proinflammatory aspects generate “sickness behaviors.” These include physical, behavioral and cognitive modifications. Normally, the sick person experiences sleepiness, tiredness, slow reaction time, cognitive impairments, and loss of appetite.

This pattern of changes that take place when we are sick actually helps us get better. It nudges us to get more sleep, recovery, and remain isolated to not proliferate the infection.

Too Much of Anything Isn’t Good

A prolonged inflammatory response can wreak havoc in our bodies and can put us at risk of clinical depression and other diseases. There is plenty of proof strengthening the link in between inflammation and clinical depression.

For instance, for people who suffer from depression, their markers for inflamation are increased compared to non-depressed (Happakoski et al., 2015). Also, signs of inflammation can anticipate the seriousness of depressive symptoms. A report that took a look at twins with a the very same genes found that the twin who had a greater CRP concentration (a measure of inflammation) was most likely to establish clinical depression 5 years later on.

Doctors observed that their cancer and Hepatitis C patients treated with IFN-alpha therapy (boosts inflammatory action) also struggled with clinical depression. This treatment increased the release of pro-inflammatory cytokines, which generated a loss of appetite, sleep disruption, anhedonia (loss of enjoyment), cognitive problems, and suicidal ideation (Lotrich et al., 2007). The prevalence of depression in these clients was high. These outcomes include confidence in the inflammation connection within the depression.

Additional studies illustrated that the rise of depression in clients treated with IFN-alpha was not just because they were sick. Utilizing a simple technique of injecting healthy patients with immune system invaders, scientists discovered greater rates of depressive manifestations in the ones who were exposed compared to the placebo group. The individuals who were induced to have an inflammatory action suffered symptoms such as unfavorable mood, sleep disruptions, social withdrawal, anhedonia, and cognitive impairments.

Lesser Response to Medications

The link between inflammation and depression is much more solid for clients who don’t respond to existing antidepressants. Studies have revealed that treatment-resistant clients tend to have elevated inflammatory aspects circulating at baseline than the responsive ones.

With this information, a clinician can measure CRP levels (which is a very common practice) and anticipate the effectiveness of antidepressants. In one research study, they discovered that increased levels of an inflammation before treatment saw poor effectiveness to antidepressants (O’Brien et al., 2007).

There are environmental elements that trigger inflammation and for that reason elevate the danger for depression: stress, low socioeconomic status, or a troubled youth. An elevated inflammatory response leads to increased sensitivity to stress. The impact has been reported in several research studies in mice. (Tianzhu et al., 2014)

Depression is a heterogeneous condition. Each client’s struggle is special given their sensitivity of their immune system, childhood, genetics, other existing bodily diseases, and their present status in society.

Being on the unfavorable end of these dimensions aggravates our immune system and causes persistent inflammation. The brain is very responsive to these circulating inflammatory markers and starts “sickness behavior.” After the inflammation becomes chronic by stressors the sickness behavior ends up being clinical depression.

If you are a specialist dealing with clients experiencing clinical depression, I prompt you to think about the health of your clients’ immune systems. If you are a patient struggling with an exaggerated immune disorder (e.g., arthritis), do not neglect the depressive manifestations that you might be experiencing. If you are experiencing clinical depression, prevent anything that may exacerbate your immune reaction. This is another example of the gorgeous dance between body and mind!

---

Haapakoski,R.,Mathieu,J.,Ebmeier,K.P.,Alenius,H.,Kivimäki,M., 2015. Cumulative meta-analysisofinterleukins6 and 1β,tumournecrosisfactorα and C-reactive protein in patients with major depressive disorder. Brain Behav.Immun. 49,206.

Hodes GE, Pfau ML, Leboeuf M, Golden SA, Christoffel DJ, Bregman D et al (2014). Individual differences in the peripheral immune system promote resilience versus susceptibility to social stress. Proc Natl Acad Sci USA 111: 16136–16141.

Krishnan V, Nestler EJ (2008). The molecular neurobiology of depression. Nature 455: 894–902.