Functional Neurology: Brain Inflammation and Depression

According to the World Health Organization, depression is one of the main causes of disability worldwide. Moreover, approximately 30 percent to 60 percent of patients don’t respond to the currently available antidepressant treatments. That means that about 40 percent to 70 percent of patients aren’t being helped by existing antidepressant treatments. One region of research studies can ultimately shed some light on why many patients are not helped by antidepressants.  

 

Neuroinflammation and Mood Changes

 

Increasing evidence from these research studies shows that brain inflammation can aggravate or even increase symptoms of depression. Inflammation is a fundamental part of the immune system. When the human body is affected by toxins, bacteria, viruses, or parasites, the immune system recruits cells, proteins, and other structures, to attack these invaders. The main purpose is to indicate the injured body parts so that we can pay more attention. Inflammation makes affected body parts reddish, swollen, and hot. After the injury isn’t localized, then the nervous system can become inflamed. Neuroinflammation can ultimately contribute to “mood changes.” These can also include cognitive, physical, and behavioral changes.  

 

Generally, people with depression experience sleepiness, fatigue, slow response time, cognitive impairments, and loss of sexual desire. This collection of changes causes people to want to get more sleep to heal themselves and remain isolated so as to not spread infections. However, prolonged inflammation can wreak havoc in the human body and it can increase the risk of depression and other illnesses. Increased evidence shows the link between brain inflammation and depression.  

 

By way of instance, markers of inflammation are increased in people who suffer from depression in contrast to non-depressed types, according to research studies. Furthermore, indicators of inflammation may also predict the intensity of gastrointestinal tract symptoms associated with depression. A research study that examined twins which share 100 percent of the same genes found that the twin who had a greater CRP concentration, a common measure of inflammation, was more prone to develop depression five years later. Doctors also noticed that cancer and Hepatitis C patients treated with IFN-alpha treatment, which increases the human body’s inflammatory response, also suffered from depression later in life.  

 

This treatment increased the discharge of pro-inflammatory cytokines, which increased the reduction of appetite, sleep disturbances, anhedonia or lack of enjoyment, cognitive impairment, and suicidal ideation, according to research studies. The incidence of depression in these patients has increased. Additionally, these results provided further evidence for the connection between inflammation and depression. Subsequent, careful research studies also demonstrated that the increase in the prevalence of depression in patients treated with IFN-alpha was not only due to the previously presented problem.  

 

Depression and Brain Inflammation in Functional Neurology

 

Utilizing a very simple way of injecting healthy subjects with immune system invaders, researchers found higher levels of depressive symptoms from the ones who were more vulnerable compared to the placebo group. The subjects that were provided with an inflammatory response complained of symptoms, such as negative mood, anhedonia, sleep disturbances, social withdrawal, and cognitive impairments. The link between inflammation and depression is much more powerful for patients that don’t respond to current antidepressant treatments. Various studies have revealed that treatment-resistant patients tend to have elevated inflammatory aspects circulating at baseline compared to responsive ones.  

 

This is clinically significant because a clinician can utilize CRP levels, which are part of a regular physical exam, to predict the treatment response to antidepressants. In one research study, they found that increased levels of an inflammation molecule before treatment predicted poor response to antidepressants. There are environmental factors that cause inflammation and increase the risk of depression, including stress, low socioeconomic status, or even a troubled childhood. Additionally, an increased inflammatory response leads to greater sensitivity to stress. The result was reported in research studies in mice.  

 

By way of instance, mice that have gone under chronic unpredictable stress have higher levels of inflammation markers. Surprisingly, there are individual differences that make some mice resistant to stress, therefore, initiating a calmer immune response. Depression is a heterogeneous disorder. Each individual’s struggle is unique given their youth, genetics, the sensitivity of their immune system, other existing bodily illnesses, and their current status in society. Being around the disadvantageous end of the dimensions disrupts our immune system and causes chronic inflammation.  

 

The mind is very responsive to those circulating inflammatory markers and initiates “illness behavior”. When the inflammation is prolonged by stressors or other vulnerabilities, the illness behavior becomes depression. If you are a healthcare professional working with people that have depression, it’s fundamental to look at the health of the patients’ immune systems. If you are a patient experiencing an exaggerated immune disorder (e.g., arthritis), don’t discount the depressive symptoms that you might be experiencing. If you are currently suffering from depression, prevent anything that might exacerbate your reaction. After all, treating the root of the health issue may ultimately improve depression.  

 

Brain inflammation has been associated with a variety of signs and symptoms, including mood changes like anxiety and depression. Inflammation in the brain can also cause a variety of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. Inflammation is an essential function of the immune system, however, excess brain inflammation, can cause anxiety, depression, and other health issues. In the following article, inflammation and mood changes, such as depression, can cause a variety of symptoms, including fatigue and cognitive impairment. – Dr. Alex Jimenez D.C., C.C.S.T. Insight

 

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Metabolic Assessment Form

 

The following Metabolic Assessment Form can be filled out and presented to Dr. Alex Jimenez. Symptom groups listed on this form are not intended to be utilized as a diagnosis of any type of disease, condition, or any other type of health issue.  

 

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In honor of Governor Abbott’s proclamation, October is Chiropractic Health Month. Learn more about the proposal.  

 

According to the World Health Organization, depression is one of the main causes of disability worldwide. Moreover, approximately 30 percent to 60 percent of patients don’t respond to the currently available antidepressant treatments. That means that about 40 percent to 70 percent of patients aren’t being helped by existing antidepressant treatments. One region of research studies can ultimately shed some light on why many patients are not helped by antidepressants. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .  

 

Curated by Dr. Alex Jimenez  

 

References:  

1. Haapakoski, R., Mathieu, J., Ebmeier, K.P., Alenius, H., Kivimäki, M., 2015. Cumulative meta-analysisofinterleukins6 and 1?,tumournecrosisfactor? and C-reactive protein in patients with major depressive disorder. Brain Behav.Immun. 49,206.  
2. 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.  
3. Krishnan V, Nestler EJ (2008). The molecular neurobiology of depression. Nature 455: 894–902.  
4. Lotrich, F.E., Rabinovitz, M., Gironda, P., Pollock, B.G., 2007. Depression following pegylated interferon-alpha: characteristics and vulnerability.J.Psychosom.Res.63, 131–135.doi.org/10.1016/j.jpsychores.2007.05.013.  
5. O’Brien, S.M., Scully, P., Fitzgerald, P., Scott, L.V., Dinan, T.G., 2007a. Plasma cytokine profiles in depressed patients who fail to respond to selective serotonin reuptake inhibitor therapy. J. Psychiatr. Res. 41, 326e331.  
6. Tianzhu, Z., Shihai, Y., Juan, D., 2014. Antidepressant-like effects of cordycepin in a mice model of chronic unpredictable mild stress. Evid. Based Complement. Altern. Med. 2014, 438506.

 

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Additional Topic Discussion: Chronic Pain

 

Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.

 

 

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Neural Zoomer Plus for Neurological Disease

 

 

Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural Zoomer^TM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural Zoomer^TM Plus is designed to assess an individual’s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural Zoomer^TM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention.  

 

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