In the last article, we began discussing how brain inflammation is indicated in the formation of severe mental illnesses. Today we are going to explore two major mental illnesses, major depression, and schizophrenia, and how brain inflammation has become implicated in their formation.

What is Inflammation?

Inflammation is one of the body’s defense responses to injury or invasion by pathogens (viruses and bacterium). Inflammation has two basic types, acute and chronic.

Acute inflammation involves warmth, pain, and swelling activating leukocytes (white blood cells), increased blood supply to the area, and permeation of blood vessels to allow molecules readily leave blood vessels and enter the injured tissue.

With the inflammatory response, a complex molecular structure becomes activated including a specialized type of proteins that kill the pathogens called Cytokines. Cytokines are produced to regulate inflammation and to control the immune response. More about cytokines next week.

Chronic inflammation involves disease processes such as cardiovascular disease, cancer, and diabetes. Chronic brain inflammation is related to microglial cell activation that plays a protective function as cells play in the rest of the body.

Microglial cells are important for the brain for maintaining and pruning away synapses (links between brain cells), eating phagocytes (cell fragments from dead or damaged cells), and the distribution of neurotransmitters. However, activated microglia produce cytokines and proteins also increase inflammation.

All the inflammation damages vital portions of the brain including the prefrontal cortex (the seat of reasoning and impulse control), the hippocampus (necessary for making new and maintaining old memories), and the amygdala (important for recognizing the danger and involuntarily reacting to it. 

A Recap of What We Have Already Discussed About Brain Inflammation

To recap the information we have already shared, I am going to quote the last part of my previous article.

Viruses are very clever.

The whole purpose of invading the body of a human by a virus is survival. They need a compatible host so they can breed more virus cells and continue their species. When the virus invades the mother, it does a remarkable thing. It mutates to mimic the white blood cells the mother’s body is producing to kill them.

It has been known for many decades that bacteria in our digestive tract are necessary for humans to correctly digest the food we eat. Without them, we could not gain nutrients and lipids from some types of food including plant matter. However, recently researchers have discovered a direct link between the microbes living in our digestive tracts and serious mental health issues.

To repeat what was stated above; viruses were always thought to barred from the brain via the blood/brain barrier, a membrane that isolates the blood of an individual’s body from brain tissue. However, we now know that some viruses are capable of camouflaging themselves as the white blood cells of an individual’s body and are allowed to pass through the blood/brain membrane.

Interestingly, we also thought until recently, that a baby in its mother’s womb was safe from viral or bacterial infection from the mother. However, we now understand that since viruses can camouflage themselves that they can and do enter the body of unborn infants and reach their brains via the same route they would in the mother.

Both viruses and bacterium, after entering the brain of the mother causes inflammation in the brain that persists long after the pathogen has been destroyed. This breaching of the blood/brain barrier by a virus or bacteria may explain post-partum depression and problems later in life with major depressive disorder.

The same is true of an infant who becomes infected with a pathogen via its mother, only the inflammation that occurs in the infant persists after birth. The inflammation is not noticeable upon delivery and may silently destroy brain tissue unnoticed for decades until, in young adulthood, the person is diagnosed with schizophrenia or other inflammation-related disorders.

The Inflammation and the Major Depression Conundrum

Up until the past few years, inflammation was not a suspect the cause of the major depressive disorder. Viruses and bacteria were thought to only affect the body, not the mood. However, burgeoning research has found a direct link between inflammation caused by a viral or bacterial infection and life-changing and disabling disorders such as major depression.

In an article, published on the website Modern Medicine Network, Dr. Charles Raison, MD explains the connection between depression and severe mental health issues. 

“inflammation turned out to be a common denominator and likely risk factor for every manner of psychiatric disturbance, from schizophrenia to obsessive-compulsive disorder, from mania to depression”

Dr. Raison goes on to explain that physicians and psychiatrists face a conundrum because while inflammation can be a cause for depression, it is not the only one. Also, in people who have a limited amount of inflammation but a great deal of depression, attempting to lower inflammation in their bodies makes matters worse for them.

Clearly, humanities old nemesis, major depression, is more complicated than someone having increased biomarkers for inflammation.

One possible answer for this conundrum is related to genetics. Some people are genetically engineered to respond badly to inflammation and others less so. This leads to folks having inflammation with some depression while others suffer major depressive episodes while their bodies and brains are inflamed.

Another possibility is the life cycle that the individual is in at the time of the onset of their major depression. In young adults, one must pitch into the pot of possible factors hormones and becoming a parent, while other individuals may experience other life changes such as childhood or old age.

Yet another reason for the conundrum could be that environmental stresses lead to inflammation and the inflammation leads to major depressive episodes.

Finally, most mental illnesses are not inflammatory diseases, but rather possible triggers to them. We have much to learn before we totally understand the inflammation/major depression connection.

Schizophrenia and Inflammation

With schizophrenia, one deals with both acute and chronic inflammation. At first, the person may experience before birth acute inflammation that later becomes chronic then slowly destroys vital brain tissue. The tissue damage builds until, normally in late adolescence or early adulthood, a stressor such, as moving away to college, tips the scales and the person experiences their first psychotic break.

Although I used the term “psychotic break”, that not only pertains to severe mental illnesses such as schizophrenia. For others, it may first appear as a severe episode of depression or other manifestations of mental health issues that had not previously affected survivors.

It is also important to note that viruses are not the only pathogens to use camouflage to enter the brain. Some bacteria can also do this and are responsible for many mental health challenges.

An article appearing in the Schizophrenia Bulletin, (2, 3)  stresses early intervention when someone has their psychotic episode to prevent the complete taking over of the person’s life. The authors went on to state that although long-term interventions for primary and secondary treatment to prevent psychosis is necessary, treating someone early can be a vital step to recovery.

The paper proposed three key elements to an early prevention approach including:

  • Early detection of detrimental mental states
  • Prompt treatment at the first psychotic episode
  • Interventions during the early phase of psychosis which is a critical period for a good outcome from treatment

However, the biggest obstacle to getting early detection and treatment for schizophrenia is the lack of psychiatrists. Many communities in the U.S. do not have access to a psychiatrist at all, and those who do will have to wait sometimes for months to get in to have an office visit. By that time, the person suffering from schizophrenic symptoms has passed the most critical phase where medical intervention can keep them from suffering a poor outcome from treatment.

Unfortunately, the only option becomes hospitalization and even then the hospital staff may not be capable or informed about the latest research on the link between inflammation and schizophrenia. Many hospitals will use chemical restraints to control psychotic patients instead of listening to the loved ones of the person and trying other interventions. This behavior on the part of hospital staff isn’t malicious, instead, they are often understaffed and must use medications to help them assist their patients.

All Is Not Lost

Reading this piece may have left you feeling depressed or at least unhappy. Please, do not give up yet as we have some wonderful news to share with you in part four of our series on inflammation and major mental health disorders. The information we will share with you next time will put a smile on your face and give you hope, perhaps for the first time since you or your loved one fell ill.

Keep your chin up and know there IS hope on the horizon and come back to read our piece next week.

“Our greatest weakness lies in giving up. ~ Thomas Edison

“You may not always have a comfortable life and you will not always be able to solve all of the world’s problems at once but don’t ever underestimate the importance you can have because history has shown us that courage can be contagious and hope can take on a life of its own.” ~ Michelle Obama

References   

  1. Laison, C., (2018). Introduction: The Inflammation Connection. Modern Medicine Network. Retrieved from: https://www.psychiatrictimes.com/special-reports/introduction-inflammation-connection
  2. Kirkpatrick, B., & Miller, B. J. (2013). Inflammation and schizophrenia. Schizophrenia Bulletin, 39(6), 1174-1179.
  3. Birchwood, M., McGorry, P., & Jackson, H. (1997). Early intervention in schizophrenia. The British Journal of Psychiatry, 170(1), 2-5.
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