We see many patients, who on their first visit, have a smile on their face but an underlying concern. “Why do I feel so bad?,” they will ask. People who do not feel physically well can be sad, they can also be depressed. There is a big difference. Sadness, it is said, is a response to something bad happening in your life, the response to loss or disappointment or even medical concerns. There is a physical and emotional stimulus that makes you feel sad. If that stimulus is repaired or fades away, as the old expression goes, “time heals all wounds,” then the sadness fades away.
It is said about depression that a major characteristic of the sufferer is that they cannot overcome the physical and emotional stimulus of sadness. Why? In this brief article we are going to discuss a different theory. That a major characteristic of the depression sufferer is NOT that they cannot overcome the stimulus of sadness, but that they cannot overcome the stimulus of chronic inflammation.
Depression and the stimulus of chronic inflammation
This would seem an obvious statement to make, you are depressed because you are not well. We are going to start our research journey in 2008 where doctors at the University of Illinois helped bring us a clue that people who are not well physically, become depressed because of a phenomena called “sickness behavior.” Sickness behavior is caused by the immune system’s inflammatory response to illness. This study was published in the prestigious Nature reviews. Neuroscience.(1)
Here is a quote from the research, it will explain what sickness behavior is. You may realize as you read this that you already knew what sickness behavior is: “In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines (immune messengers) that act on the brain to cause sickness behavior. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer or autoimmune diseases, the ensuing immune signalling to the brain can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals. These phenomena might account for the increased prevalence of clinical depression in physically ill people. Inflammation is therefore an important biological event that might increase the risk of major depressive episodes, much like the more traditional psychosocial factors.”
The talking point here: “inflammation increases the risk of occurrence of major depressive episodes (in sick people).”
Can we reprogram this response to reduce inflammation and depression?
Depression is a great complexity and enigma as you will see from research in the following study. There are no easy answers but there are correct paths to treatment. This is expressed by research from the University of Illinois, published in 2013 in The Journal of experimental biology.(2) To these researchers you need to look at the way animals and humans respond to chronic illness and sickness to understand depression that comes with illness and treatment that may be more effective than traditional medications.
Symptoms of depression appear after pro-inflammatory cytokines (inflammatory cells) are produced by the body.
Immune activation can precipitate (cause an unwanted) depression.
Several symptoms of inflammation-induced depression overlap with sickness behaviors, including fatigue, changes in sleep pattern, lack of interest in daily or pleasurable activities (anhedonia), changes in appetite or body mass and unexplained aches and pains.
Fatigue, sleep disorders, changes in eating habits, and pain associated with depression in humans are also found in sick animals. This is “natural programming,” that needs to be unprogrammed in people.
The key to this research is that the fatigue, sleep disorders, changes in eating habits, and pain associated with depression in humans are also found in sick animals. These symptoms are Nature’s way to protect the survival of the animal by making itself (the host) undesirable to the disease that is trying to kill it.
The researchers suggest that by making the body an undesirable host, no food, no sleep, the animal is in “survival mode.” For human beings, depressive thoughts are added for greater impact on the illness. Depressive thoughts are created by and rebroadcast through cellular signalling. The expression of chemicals that initiate cellular response. The chemical environment in the body is being altered to attack the illness.
The talking point here: “inflammation increases the risk of occurrence of major depressive episodes as a survival mechanism.” If you treat the problems that are convincing your body that you need to be in survival mode, that is a state of chronic inflammation, your body may find it may not need to be depressed.
Depression can be managed with wellness
In this simple article we can see the extreme complexity of dealing with just one factor in treating depression, inflammation. So what are we to consider from these two studies and ongoing research into the connection between inflammation and depression.
Nature’s response to illness is inflammation.
Chronic, unabated inflammation leads to continuous symptoms of “unwellness” including depression.
Depression is one factor that the body utilizes to make itself unappealing to viral, parasitic, infectious disease and immune disorders.
From surviving to thriving
When you treat the cause of chronic inflammation, such as diabetes, such as cholesterol issues, such as environmental illness, such as obesity and weight issues and others, you make yourself unappealing to these diseases and your inflammation goes away.
If you would like to explore more information, please contact our office so we can start a conversation with you.
Depression and Anxiety Discussion at Magaziner Center For Wellness
1 Dantzer R, O’Connor JC, Freund GG, Johnson RW, Kelley KW. From inflammation to sickness and depression: when the immune system subjugates the brain. Nat Rev Neurosci. 2008;9(1):46-56.
2 McCusker RH, Kelley KW. Immune-neural connections: how the immune system’s response to infectious agents influences behavior. J Exp Biol. 2013;216(Pt 1):84-98.