Everyone has experienced the feeling of an acute infection. An infection that causes a spike in your body temperature that accompanies soul-crushing fatigue, muscle pain, and brain fog.
We take it for granted when the inflammation returns to baseline and our health rebounds. But for a subset of people, the acute inflammation turns chronic, leading to symptoms of post-exertional malaise, fibromyalgia, and orthostatic intolerance (to name a few).
That’s when the panic sets in. When you realize these symptoms might be permanent.
It’s no wonder chronic inflammatory conditions increase your risk of being diagnosed with a psychiatric condition such as depression, anxiety, or a mood disorder. At least that’s what most think.
What if inflammation in the body is actually causing depression in the brain?
For decades, health professionals assumed patients were understandably distraught by the realization that their quality of life might not ever be the same. But clinical research dating back to the late 1980s paints a different picture. One where inflammation is driving debilitating mental health issues.
In this article, we will provide a brief history of modern-day antidepressants and briefly evaluate the scientific data supporting the concept of inflammation in the body causing depression in the brain.
Fluoxetine, known by the brand name Prozac, was the world’s first selective serotonin reuptake inhibitor (SSRI), introduced in 1987 by Eli Lilly and Company (1). This drug was marketed as a drug that boosts the ‘feel-good’ neurotransmitter, serotonin, in the brain of patients. Since Prozac’s market entry, many pharmaceutical companies developed their own neurotransmitter-boosting drugs.
Fast forward decades later, clever physicians realized the following problem with SSRIs: If neurotransmitter imbalance is the key to psychiatric disorders, then one would expect the explosion of new neurotransmitter modulators to dramatically reduce mental illness.
That did not happen, as we are currently experiencing a mental health epidemic in the U.S. and around the world (2). Each year is followed by an ever-increasing number of mental health conditions per capita (3). This suggests first- and second-generation psychiatric medications are not fixing the root cause of mental health conditions most patients experience.
Dr. Edward Bullmore, Professor of Psychiatry at the University of Cambridge, explains in his book The Inflamed Mind (4);
“There have been no major new advances in drug treatment, or psychological treatment come to that, for depression or any other mental health disorder [since Prozac].”
In fact, many patients report anti-depressants simply do not work for them; a phenomenon known as treatment-resistant depression.
In the late 1980s, oncologists began treating cancer patients with the pro-inflammatory cytokines interferon alpha (IFN-α) and tumor necrosis factor-alpha (TNF-α) (5). The oncologists noticed something unexpected. A subset of their patients developed severe depression soon after the cytokines were infused into their bloodstream (6).
Was this a predictable response? After all, they were diagnosed with cancer and were given what could have been toxic amounts of pro-inflammatory cytokines. Wouldn’t that also make you depressed?
Dr. Andrew Miller of Emory University was one of the first psychiatrists to interview an IFN-α-treated patient with new-onset depression. He reported in an interview,
“I really expected to see somebody under a blanket who’s shivering and shaking and miserable and toxic, and something that we typically see, and something like sepsis, where somebody’s very sick. (7)”
Instead, he observed a “woman [who] was very nicely dressed, makeup was on that looked very nice”, not a severely ill patient. Although these patients were not depressed before receiving immunotherapy, they now met the clinical definition of depression.
Furthermore, this depression could be prevented by pre-treating the cancer patients with an antidepressant two weeks before starting the immunotherapy (7).
Inflammation is a blanket term used to describe white blood cells and the molecules they release, which protect our bodies from a threat. That threat can be an infectious disease (virus, bacteria, parasite, or a prion), rogue cancer cells, or toxins in our environment.
When encountering one of these threats, a rapid spike in inflammation occurs, termed acute inflammation. In contrast, chronic inflammation is persistent inflammation that occurs when an inflammatory response remains high and does not return to baseline levels.
Many diseases cause chronic inflammation. For instance, autoimmune diseases cause chronic inflammation because the immune system attacks healthy tissues. Some infectious diseases are known to cause chronic inflammation because some pathogens are difficult to clear from the body.
The chronic inflammatory conditions associated with an increased risk of developing psychiatric conditions include, but are not limited to:
Sjogren’s disease (8,9)
Rheumatoid Arthritis (10-12)
Ankylosing Spondylitis (13,14)
Juvenile Arthritis (15,16)
Psoriatic Arthritis (17,18)
Lupus (19-21)
Psoriasis (22-24)
Celiac disease (25-27)
PANDAS/PANS (29-31)
ME/CFS (32-34)
POTS (35,36)
Inflammatory Bowel Diseases (37-41)
MCAS (42,43)
EDS (44-46)
Long COVID (47-49)
Lyme Disease (50-52)
Tuberculosis (53,54)
Chronic Sinusitis (55-60)
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