Inflammatory response linked to depression

[David Baxter PhD]

Inflammatory response linked to depression
September 4th, 2006

ATLANTA, Sept. 1 (UPI) ? People with major depression have an exaggerated inflammatory response to psychological stress compared to those without depression, says a U.S. study.

Study leaders Dr. Andrew Miller and Christine Heim of Emory University School of Medicine say the findings suggest that increased inflammatory responses to stress in depressed patients may be a link between depression and other diseases, including heart disease, as well as contributing to depression itself.

Twenty-eight medically healthy male participants, half of whom were diagnosed with major depression and half of whom were not depressed, were exposed to two moderately stressful situations during a 20-minute time period. Blood was collected every 15 minutes to test to check for key indicators of inflammation.

While at rest ? before the stress challenge ? the depressed patients had increased inflammation relative to the control group.

Both the depressed and the healthy groups showed an inflammatory response to the stress challenge, but people who were currently depressed exhibited the greatest increases, according to the findings published in the American Journal of Psychiatry.

 

[Kanadiana]

I certainly know that stress, as well as improper or lack of sleep, always means I suffer more inflammatory and pain symptoms, so I won't argue with this idea at all

 

[Holly]

Hi Everyone,
I have one question, what does a exaggerated inflammatory response specially mean?

People with major depression have an exaggerated inflammatory response to psychological stress compared to those without depression, says a U.S. study.

Very interesting article I just do not fully understand the meaning!
Thank you for the post, take care

 

[Daniel E.]

On the positive side, some of the things that lessen inflammation like omega-3s, exercise, and a healthy diet also help mitigate depression.

How your diet can help fight inflammation - MSNBC

 

[foghlaim]

Hi Holly,
I'm so glad you asked the question... i was going to but left it hoping some one would... Thank you!!

Now all we need is the explaination.. lol

I understand inflamation in rhumatism and arthritis..(sp) but not in this article as no meaning given.

nsa

 

[Into The Light]

from wikipedia:

Inflammation is the first response of the immune system to infection or irritation and may be referred to as the innate cascade. Inflammation is characterised by the following quintet: redness (rubor), heat (calor), swelling (tumor), pain (dolor) and dysfunction of the organs involved (functio laesa).

so it sounds like i suspected - your immune system is oversensitive or overactive when suffering from depression.

i also suspect it makes you mentally more sensitive to events around you as well. anyone any thoughts on this?

 

[healthbound]

Here's an article with a few more details. From HealthyPlace.com.

(September 4, 2006) -- Individuals with major depression have an exaggerated inflammatory response to psychological stress compared to those who do not suffer from depression, according to a study by researchers at Emory University School of Medicine. Because an overactive inflammatory response may contribute to a number of medical disorders as well as to depression, the findings suggest that increased inflammatory responses to stress in depressed patients may be a link between depression and other diseases, including heart disease, as well as contributing to depression itself.

"Several examples of increased resting inflammation in depressed patients already exist in the literature, but this is the first time anyone has shown evidence to suggest that the inflammatory response to stress may be greater in depressed people," says Dr. Miller.

The study included 28 medically healthy male participants, half of whom were diagnosed with major depression and half of whom were not depressed. The participants were exposed to two moderately stressful situations during a 20-minute time period. Blood was collected every 15 minutes starting immediately before and then up to an hour and a half after the test to check for key indicators of inflammation. The researchers measured levels of a pro-inflammatory cytokine (a regulatory protein secreted by the immune system) called interleukin-6, and the activity of a pro-inflammatory signaling molecule in white blood cells called nuclear factor-kB.

While at rest (before the stress challenge), the depressed patients had increased inflammation relative to the control group. Both the depressed and the healthy groups showed an inflammatory response to the stress challenge, but people who were currently depressed exhibited the greatest increases of interleukin-6 and nuclear factor-kB.

"While inflammation is essential for us to fight bacterial and viral infections, too much inflammation can cause harm," says Dr. Miller. "There's always some collateral damage when the immune system gets fired up, and we now believe that too much inflammation, either at rest or during stress, may predispose people to become depressed or stay depressed." In addition, medical research over the last decade has shown that runaway inflammation may play a role in a number of disorders, including heart disease, cancer, and diabetes, all of which have been associated with depression.

People in the study who suffered from depression also had higher rates of early life stressful experiences. "We have found that this kind of personal life history may make people more likely to develop major depression and is actually common in depressed patients," says Dr. Heim.

It was part of a larger project at the Emory Conte Center for the Neuroscience of Mental Disorders led by Charles B. Nemeroff, MD, PhD, Reunette W. Harris Professor and Chair of Emory's Department of Psychiatry and Behavioral Sciences. The Conte Center is dedicated to understanding the contribution of early life abuse and neglect to the neurobiology of adulthood psychiatric disorders. Ongoing studies by Dr. Miller's team of researchers will attempt to determine how early life experiences contribute to excessive inflammatory stress responses.

"According to the Depression and Bipolar Support Alliance, major depression is the leading cause of disability worldwide and costs the U.S. economy $70 billion annually in medical expenditures, lost productivity, and other expenses," says Thaddeus Pace, PhD, lead author on the paper. "This study is leading us toward finding out what actually causes depression and to identifying what aspects of immune system function are abnormal in depressed people. The goal is to find potential targets within the molecular machinery of the immune system so we can better treat major depression and minimize its consequences on health."

 

[Retired]

People in the study who suffered from depression also had higher rates of early life stressful experiences. "We have found that this kind of personal life history may make people more likely to develop major depression and is actually common in depressed patients," says Dr. Heim.

Is this a commonly held belief among therapists?

What role do genetic factors play in a person's predisposition to suffer a depressive episode.

Is the childhood stress considered the trigger that leads to depression in later life, or is childhood stress the foundation for the later depression?

So I am wondering how much genetics affects a person's risk for depression, compared to the events in their childhood.

 

[David Baxter PhD]

I think that, like almost everything, it's clearly a combination of physiological (possibly genetic) vulnerability and life experience.

 

[Daniel E.]

Brain Cells Taken From Patients With Bipolar Disorder Malfunction

Researchers have shown that an inflammation-promoting molecule called interleukin-6 (IL-6), which is secreted by astrocytes, may contribute to defects associated with bipolar disorder. The results highlight the potential role of astrocyte-mediated inflammatory signaling in the psychiatric...

www.technologynetworks.com

"At this moment, direct extrapolation of the results to patients remains challenging," Gage says. "Despite these limitations, our findings elucidate aspects of the understudied role of astrocytes in neuroinflammation in psychiatric disorders."

Astrocyte - Wikipedia

en.wikipedia.org

Research since the mid-1990s has shown that astrocytes propagate intercellular Ca2+ waves over long distances in response to stimulation, and, similar to neurons, release transmitters (called gliotransmitters) in a Ca2+-dependent manner.[5] Data suggest that astrocytes also signal to neurons through Ca2+-dependent release of glutamate.[6] Such discoveries have made astrocytes an important area of research within the field of neuroscience.

 

[Daniel E.]

Anti-Inflammatory Treatments for MDD: Update and Expert Interview - Psychiatry Advisor

Dr Jha provided discussion regarding the use of anti-inflammatory therapies for depression.

www.psychiatryadvisor.com

January 15, 2020

Several subsequent studies have found favorable results for anticytokine treatments in reducing depressive symptoms in patients with chronic inflammation. For example, one study found that brodalumab, an anti-interleukin 17 (IL-17) receptor antibody, was associated with remission rates of from 43% to 47% (vs 9% with placebo) in patients with moderate to severe symptoms at baseline.

 

[Daniel E.]

Antidepressant activity of anti-cytokine treatment: a systematic review and meta-analysis of clinical trials of chronic inflammatory conditions - Molecular Psychiatry

Inflammatory cytokines are commonly elevated in acute depression and are associated with resistance to monoaminergic treatment. To examine the potential role of cytokines in the pathogenesis and treatment of depression, we carried out a systematic review and meta-analysis of antidepressant...

www.nature.com

18 October 2016

These results suggest inflammatory cytokines may have a key role in the pathogenesis of depression and that anti-cytokine drugs may be effective for some patients with depression, particularly treatment-resistant cases characterised by increased inflammation.

 

[Daniel E.]

Inflammation Theory in Depression Still Elusive as Infliximab Trial Poses New Questions

A study designed to see if infliximab could reduce depression symptoms did not show statistically significant results, except for participants who had a history of childhood physical abuse.

www.centerforbiosimilars.com

May 8, 2019

Other than certain oncology examples, precision medicine has failed to live up to its hype, and this study is no different, the editorial said.

 

[Daniel E.]

Efficacy of Adjunctive Infliximab in the Treatment of Adults With Bipolar I/II Depression

This randomized clinical trial compares the efficacy of infliximab therapy vs placebo in improving depressive symptoms among adults with bipolar depression in Canada and the United States.

jamanetwork.com

May 8, 2019

Infliximab therapy is not efficacious at improving depressive symptoms in patients with bipolar depression.

 

[stillKaty09]

COVID-19 Psychosis: A Potential New Neuropsychiatric Condition Triggered by Novel Coronavirus Infection and the Inflammatory Response?​

Psychosomatics. 2020 September-October; 61(5): 551–555.
Published online 2020 May 19. doi: 10.1016/j.psym.2020.05.012

Despite the presence of multiple potential stress-related and physiological causes of psychosis in these COVID-19–positive patients, we report that a new-onset psychosis associated with COVID-19 infection and the potential immune-mediated neuropathogenesis described here warrant further investigation. In particular, we are interested in further investigating clinical characteristics, cognitive abnormalities, onset, course and prognosis, and their association to peripheral and central inflammatory markers, including CRP, IL-6, and others. If a COVID-19-psychosis relationship exists, treatment of the psychotic symptoms with antipsychotic medication, while potentially effective for treating symptoms, would likely be obviated or mitigated by effective treatments of the underlying COVID-19 infection and its associated inflammation.