New Theory Links Depression to Chronic Brain Inflammation

[guest]

Science progresses extremely fast the last years.

http://www.sciencedaily.com/releases/2010/10/101020091857.htm

ScienceDaily (Oct. 19, 2010) — Chronic depression is an adaptive, reparative neurobiological process gone wrong, say two University of California, San Diego School of Medicine researchers, positing in a new theory that the debilitating mental state originates from more ancient mechanisms used by the body to deal with physical injury, such as pain, tissue repair and convalescent behavior.

In a paper published in the September online edition of Neuroscience and Biobehavioral Reviews, Athina Markou, PhD, professor of psychiatry, and Karen Wager-Smith, a post-doctoral researcher, integrate evidence from diverse clinical, biological and behavioral studies to create a novel theory they hope will lead to a shift in thinking about depression.

"In contrast to other biological theories of depression, we started with a slightly different question," said Wager-Smith. "Other theories address the question: 'What is malfunctioning in depression?' We took a step back and asked the question: 'What is the biology of the proper function of the depressive response?' Once we had a theoretical model for the biology of a well-functioning depressive response, it helped make sense of all the myriad differences between depressed and non-depressed subjects that the biomedical approach has painstakingly amassed."

According to the new theory, severe stress and adverse life events, such as losing a job or family member, prompt neurobiological processes that physically alter the brain. Neurons change shape and connections. Some die, but others sprout as the brain rewires itself. This neural remodeling employs basic wound-healing mechanisms, which means it can be painful and occasionally incapacitating, even when it's going well.

"It's necessary and normal so that an individual can adapt, change behavior and deal with altered circumstances," Markou said. Real problems occur only "when these restructuring processes go into overdrive, beyond what is necessary and adaptive, and for longer periods of time than needed. Then depression becomes pathological."

The theory extends findings made by other researchers that the neurobiological substrates of physical and emotional pain overlap. Just as the body's repair mechanisms for physical injury can sometimes result in chronic pain and inflammation, so too can the response to psychological trauma, resulting in chronic depression.

Markou and Wager-Smith argue that existing, conflicting views about depression actually describe different aspects of the same phenomenon. Psychoanalytic and sociological theories refer to the psychological transformation that occurs during a productive depressive episode. Biomedical theories relate to the neural remodeling that underlies this psychological change. And neurodegenerative theories account for remodeling malfunctions.

"The big question, of course, is why aren't all people affected the same way," said Markou. "Why do some people deal effectively with stress, but others perpetuate a pathological state? This is an interesting question for future research."

The researchers' findings may have clinical ramifications as well. If psychological and physical pain responses share similar biological mechanisms, then analgesic agents could be useful in treating at least some symptoms of depression. Similarly, if chronic depression is proven to be a neuroinflammatory condition, then anti-inflammatory treatments should also have some antidepressant effects. Several small trials with depressed patients have already been published that support this possibility, though Markou cautioned that much more specific research and larger clinical trials are required.
Funding for this work came from a National Institutes of Health National Research Service Award and a grant from the National Institute of Mental Health.

Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

 

[tymewarp#9]

Thanks for this, Diesel; I'm going to need to mull this over a while! Seems like it might be simple (relatively) to experiment with - tho I don't like popping ibuprofen, acetominophen, etc. Interesting, nonetheless!

 

[guest]

Thanks for this, Diesel; I'm going to need to mull this over a while! Seems like it might be simple (relatively) to experiment with - tho I don't like popping ibuprofen, acetominophen, etc. Interesting, nonetheless!

Yes, I don't like using ibuprofen etc. as well and I wonder if they meant certain anti-inflammatory drugs. Kofi just posted the pubmed abstract to the study above.

Neurosci Biobehav Rev. 2010 Sep 29

Depression: A repair response to stress-induced neuronal microdamage
that can grade into a chronic neuroinflammatory condition?

* Wager-Smith K,
* Markou A.
Department of Psychiatry, School of Medicine, University of California,
San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0603, USA.

Depression is a major contributor to the global burden of disease and
disability, yet it is poorly understood. Here we review data supporting
a novel theoretical model for the biology of depression. In this model,
a stressful life event leads to microdamage in the brain. This damage
triggers an injury repair response consisting of a neuroinflammatory
phase to clear cellular debris, and a spontaneous tissue regeneration
phase involving neurotrophins and neurogenesis.

During healing, released inflammatory mediators trigger sickness behavior and psychological pain via mechanisms similar to those that produce physical pain during wound
healing. The depression remits if the neuronal injury repair process
resolves successfully. Importantly, however, the acute psychological
pain and neuroinflammation often transition to chronicity and develop
into pathological depressive states. This hypothesis for depression
explains substantially more data than alternative models, including why
emerging data show that analgesic, anti-inflammatory, pro-neurogenic and
pro-neurotrophic treatments have antidepressant effects.

Thus, an acute depressive episode can be conceptualized as a normally self-limiting but highly error-prone process of recuperation from stress-triggered
neuronal microdamage.

Copyright (c) 2010 Elsevier Ltd. All rights
reserved.
PMID: 20883718 [PubMed - as supplied by publisher]

 

[slayadragon]

My experience is that depression is the first sign that I get that an inflammatory response (e.g. from a mold or other biotoxin exposure) is occurring.

If I feel that sensation, and then get away right away, I can keep from getting sick from the exposure.

Thus, maybe the depression is a warning sign - and thus a good, functional thing.....to help me to stay well.

Best, Lisa

 

[FancyMyBlood]

Michael Maes (also a ME/CFS researcher) has been saying this for years. He is a strong opponent of Wessely, Reeves and the Dutch psychiatric lobby (as a neuropsychiatrist himself).

And guess what happened with visionaries like him, they get reviled and ridiculed by the establishment. If only scientist would be more open-minded and would let go the old psychiatric dogmas, we'd be much further in these neurobiological diseases.

 

[pictureofhealth]

Inflammation seems to be the culprit in a lot of disease, including heart disease, autoimmune conditions, ME/CFS. But why does one person get one illness, whereas someone else gets an entirely different one? Perhaps inflammation is the key to most chronic illnesses, and the different disease names and symptoms and parts of the body in which they appear are just the 'weak link'.

 

[guest]

And here we have some more evidence, that inflammation of the brain plays an important role in disease.

http://www.sciencedaily.com/releases/2010/11/101101151310.htm

Arthritis Drugs Could Help Prevent Memory Loss After Surgery, Study Suggests
ScienceDaily (Nov. 1, 2010) — Anti-inflammatory drugs currently used to treat diseases such as rheumatoid arthritis may also help prevent cognitive problems after surgery, according to a new study by researchers at Imperial College London and University of California, San Francisco (UCSF).

The research also reveals for the first time that a specific inflammatory response in the brain may explain why many patients experience memory loss or other forms of cognitive dysfunction after surgery or critical illness.
The findings, from research in mouse models, could lead to human clinical trials within a year, the authors say. Their work is published in the journal Proceedings of the National Academy of Sciences.
For years, anesthesiologists and neurologists have struggled to explain why some patients, especially the elderly, experience confusion, learning disorders and memory loss after surgery -- a condition clinicians call post-operative cognitive decline. While typically short-term, this delirium occurs widely in intensive care units, affecting between 28 and 92 per cent of hospitalized patients, depending on their age, health status and type of surgery. It also has been linked to poorer surgical outcomes, as well as an increased risk of mortality, inability to cope and possible permanent dementia.
Until now, researchers have not clearly understood what causes the disorder or how to treat it. The new research suggests that it is caused by cell-to-cell signalling molecules called cytokines released by cells of the immune system. There are drugs already in use that target the activity of cytokines so it is possible that these drugs could be effective against cognitive decline.
The senior author of the study is Mervyn Maze, MB ChB, Professor and Chair of the Department of Anesthesiology and Perioperative Care at UCSF and a Visiting Professor in the Department of Surgery and Cancer at Imperial College London.
"Antibody therapies already are widely used against cytokines to prevent or treat inflammation, so we know that these are effective in humans," said Professor Maze, who began the research at Imperial before moving to UCSF. "This study suggests that one day we also might be able to use these therapies as a single, pre-surgical dose to prevent cognitive decline in susceptible patients."
Previous studies have linked post-operative cognitive decline with the rise in blood levels of a cytokine called interleukin-1 beta (IL-1β), which is involved in inflammation. For this study, Maze and his colleagues studied another cytokine called tumour necrosis factor (TNF-α), which is known to regulate the immune system's inflammatory response before interleukin-1 is produced.
Working with Professor Sir Marc Feldmann -- a pioneer in cytokine research in inflammatory disorders and Head of the Kennedy Institute of Rheumatology at Imperial College London -- the team gave a single dose of anti-TNF antibody to mice before giving them surgery. They found that the treatment decreased blood levels of IL-1β, limited inflammation in the brain and prevented the mice from showing behavioural signs of cognitive decline.
The research suggests that TNF acts "upstream" of IL-1 and triggers a cascade of immune responses during surgery that provokes the production of IL-1 in the brain, Professor Maze said. That in turn contributes to cognitive decline after surgery or critical illness.
"This is an important observation, as it demonstrates that cytokines are potential therapeutic targets in a wider range of diseases, not just autoimmune disease and cancer for which they are known targets," Professor Feldmann said. "Moreover, effective therapeutics already are available, with a known safety profile and modest cost if used short term."
The study was supported by the Westminster Medical School Research Trust, in London, the Mathilda and Terence Kennedy Institute of Rheumatology Trust, and Arthritis Research UK.
Arthritis Research UK-funded research at its Kennedy Institute of Rheumatology was instrumental in showing the substantial health benefits of anti-TNF therapy in patients with rheumatoid arthritis and has transformed the lives of millions of people worldwide. Medical director of the charity Professor Alan Silman said: "This research shows the potential that these drugs have in other areas of health."

 

[glenp]

Very interesting, thank you for posting. I have had some improvement in cognition - I am more able to add numbers and dont make as many mistakes paying my bills, after taking minocyclin which is also supposed to help many sufferers of rheumatoid arthritis and HIV I wonder what drugs would help more?

glen

 

[guest]

GABA is one of the most important neurotransmitters we have. Problems with GABA always seem to result in neuropsychiatric disorders like autism and schizophrenia.

http://www.sciencedaily.com/releases/2010/11/101110131155.htm

Inhibitory Neurons Key to Understanding Neuropsychiatric Disorders
ScienceDaily (Nov. 10, 2010) — The brain works because 100 billion of its special nerve cells called neurons regulate trillions of connections that carry and process information. The behavior of each neuron is precisely determined by the proper function of many genes.

In 1999, Baylor College of Medicine researcher Dr. Huda Zoghbi and her colleagues identified mutations in one of these genes called MECP2 as the culprit in a devastating neurological disorder called Rett syndrome . In new research in mice published in the current issue of the journal Nature, Zoghbi and her colleagues demonstrate that the loss of the protein MeCP2 in a special group of inhibitory nerve cells in the brain reproduces nearly all Rett syndrome features.
Children, mostly girls, born with Rett syndrome, appear normal at first, but stop or slow intellectual and motor development between three months and three years of age, losing speech, developing learning and gait problems. Some of their symptoms resemble those of autism.
These inhibitory (gamma-amino-butyric-acid [GABA]-ergic) neurons make up only 15 to 20 percent of the total number of neurons in the brain. Loss of MeCP2 causes a 30 to 40 percent reduction in the amount of GABA, the specific signaling chemical made by these neurons. This loss impairs how these neurons communicate with other neurons in the brain. These inhibitory neurons keep the brakes on the communication system, enabling proper transfer of information.
"In effect, the lack of MeCP2 impairs the GABAergic neurons that are key regulators governing the transfer of information in the brain," said Dr. Hsiao-Tuan Chao, an M.D./Ph.D student in Zoghbi's laboratory and first author of the report.
Chao made the discovery by developing a powerful new tool or mouse model that allowed researchers to remove MeCP2 from only the GABAergic neurons.
"We did this study thinking that perhaps all we would see was a few symptoms of Rett syndrome," said Chao. "Strikingly, we saw that removing MeCP2 solely from GABAergic neurons reproduced almost all the features of Rett syndrome, including cognitive deficits, breathing difficulties, compulsive behavior, and repetitive stereotyped movements. The study tells us that MeCP2 is a key protein for the function of these neurons."
Once the authors determined that the key problem rested with the GABAergic neurons, they sought to find out how the lack of MeCP2 disturbed the function of these neurons. Chao discovered that losing MeCP2 caused the GABAergic neurons to release less of the neurotransmitter, GABA. This occurs because losing MeCP2 reduces the amount of the enzymes required for the production of GABA.
Intriguingly, prior studies showed that expression of these enzymes is also reduced in some patients with autism, schizophrenia and bipolar disorder, said Chao.
"This tells us a lot about what is going on in the brains of people with Rett syndrome, autism or even schizophrenia," said Chao. "A child is born healthy. She starts to grow and then begins to lose developmental milestones. Communication between neurons is impaired, in part due to reduced signals from GABAergic neurons."
"This study taught us that an alteration in the signal from GABAergic neurons is sufficient to produce features of autism and other neuropsychiatric disorders," said Zoghbi, a Howard Hughes Medical Institute investigator and director of the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital.
Others who took part in this work include Hongmei Chen, Rodney C. Samaco, Mingshan Xue, Maria Chahrour, Jong Yoo, Jeffrey L. Neul, Hui-Chen Lu, Jeffrey L. Noebels and Christian Rosenmund, all of BCM, John L.R. Rubenstein of University of Calfornia in San Francisco, Marc Ekker of University of Ottawa in Ontario, and Shiaoching Gong and Nathaniel Heintz of The Rockefeller University in New York.
Funding for this work came from the Howard Hughes Medical Institute, the National Institute of Neurological Disorders and Stroke, the Simons Foundation, the Rett Syndrome Research Trust, the Intellectual and Developmental Disability Research Centers, the International Rett Syndrome Foundation, Autism Speaks, the National Institute of Mental Health, Baylor Research Advocates for Student Scientists and McNair Fellowships.
Editor's Note: This article is not intended to provide medical advice, diagnosis or treatment.

 

[guest]

And another study to support the headline. Blocking Interleukin 6 can help with depression.

http://www.sciencedaily.com/releases/2010/11/101116101836.htm

Immune System Involved in Depression, Animal Study Suggests
ScienceDaily (Nov. 17, 2010) — A new animal study suggests the immune system plays a role in depression. The research was presented at Neuroscience 2010, the annual meeting of the Society for Neuroscience, held in San Diego.

Activation of the immune system caused mice to learn to run less on wheels in their cages -- an activity they normally like. The mice resumed their normal activity when the action of interleukin-6, an immune hormone that carries "sickness" signals to the brain, was blocked.

"Our findings suggest that blocking the action of interleukin-6 might reduce depression symptoms, like fatigue or loss of interest in pleasurable activities, in people who are depressed and who have elevated levels of interleukin-6," said Simon Sydserff, PhD, a senior research scientist at BrainCells Inc., who conducted the research while with AstraZeneca Pharmaceuticals.

Scientists previously observed that some people became depressed due to an immune response to illness or stress. Elevated levels of immune hormones like interleukin-6 have been found in some depressed patients who are otherwise healthy. In addition, people who have never had a mental illness, but who are treated for other illnesses with immune- stimulating cytokines, often become depressed.

"These observations support the idea that depression may be caused in part by a breakdown in the normal communication between the immune system and the brain, causing people to experience the feelings associated with sickness even when they are medically healthy," Sydserff said.

Research was supported by AstraZeneca Pharmaceuticals.

_______________________________________________

IL-27 seems to block IL-6

http://www.sciencedaily.com/releases/2010/11/101108185916.htm
New Anti-Inflammatory Substance: Biochemists ID Important Messenger in
Immune System

ScienceDaily (Nov. 10, 2010) The messenger interleukin-27 plays an
important role when the human body blocks inflammations, according to
new research.

The discovery was made by an international research team, of which the
Kiel Professors Joachim Gr tzinger and Stefan Rose-John, as well as the
doctoral candidate, Bj rn Spudy, are a part of. The research findings of
the scientists from Kiel, the US and Great Britain were published Nov. 7
in the online advance edition of Nature Immunology.

The human immune system reacts to bodily injuries and infections with
inflammation. This is important for the healing process, but can result
in harmful effects if it becomes chronic. Inflammation is triggered by
messengers such as the cytokine interleukin-6 (IL-6). This peptide
hormone latches on to special receptor molecules on cells and compels
inflammation. "We observed that another cytokine, interleukin-27, can
counteract this effect," explained Professor Joachim Gr tzinger, from
the Institute of Biochemistry at Kiel University. "IL-27 latches on to
the same receptors as IL-6 and thus inhibits the inflammatory reaction."

The Kiel biochemists were able to support the international research
team with their knowledge of IL-6 in particular. According to
Gr tzinger, "We have dedicated ourselves to this topic for over 20
years." Professor Stefan Rose-John added: "We hope that these
fundamental findings will one day be able to aid the healing of chronic
inflammatory diseases."

The Christian-Albrechts-Universit t zu Kiel (CAU) has proven
international expertise as a North German research university in the
field of Life Sciences. This fact is emphasised by the cluster of
excellence Inflammation at Interfaces, with which the CAU was successful
in the first round of the national Excellence Initiative, together with
the University of L beck and the Research Center Borstel.

The Collaborative Research Centre (CRC) 877, "Proteolysis as a Regulatory
Event in Pathophysiology," whose spokesperson is Rose-John and in which
Gr tzinger is also involved, substantiates the competence of Kiel in the
field of Life Sciences as well. CRC 877 deals with signalling pathways
within and between cells, which are triggered by the fission of proteins.

Editor's Note: This article is not intended to provide medical advice,
diagnosis or treatment.

 

[guest]

Inflammation seems to be key for so many diseases.

Link Between Depression and Inflammatory Response Found in Mice: New Treatments for Mood Disorders?

http://www.sciencedaily.com/releases/2010/12/101220150946.htm

ScienceDaily (Dec. 21, 2010) — Vanderbilt University researchers may have found a clue to the blues that can come with the flu -- depression may be triggered by the same mechanisms that enable the immune system to respond to infection.

In a study in the December issue of Neuropsychopharmacology, Chong-Bin Zhu, M.D., Ph.D., Randy Blakely, Ph.D., William Hewlett, M.D., Ph.D., and colleagues activated the immune system in mice to produce "despair-like" behavior that has similarities to depression in humans.

"Many people exhibit signs of lethargy and depressed mood during flu-like illnesses," said Blakely, director of the Vanderbilt Center for Molecular Neuroscience. "Generally these have been treated as just a consequence of being physically ill, but we think there is likely to be something more brain-centric at work here."

Blakely and his colleagues previously reported that inflammatory cytokines can enhance the activity of the serotonin transporter (SERT), which regulates the supply of the neurotransmitter serotonin in the synapse, or gap between nerve cells.

Elevations in SERT activity remove serotonin from brain synapses at an enhanced rate and, based on studies in animal models and man, would be predicted to increase the risk for mood and anxiety disorders. Indeed, a class of antidepressant drugs called selective serotonin reuptake inhibitors (SSRIs) -- Prozac, Zoloft, etc. -- work by blocking the ability of SERT to eliminate serotonin.

In the current study in mice, the researchers triggered pro-inflammatory cytokine production. Within 30 to 60 minutes, SERT was activated in the brain and the animals displayed despair-like behavior.

Remarkably, this behavior was not observed when cytokine production was triggered in mice lacking the SERT gene. Similarly, a drug that blocks inflammatory molecule signaling also prevented stimulation of SERT and the despair behavior. "It's as if these inflammatory molecules are an 'anti-Prozac,'" Blakely said.

In their paper, the researchers cautioned that "we do not presume that changes in SERT activity alone are sufficient to induce the full spectrum of depression traits, nor that our animal model can reproduce all the elements of a complex neuropsychiatric disorder."
"Nonetheless, we were able to identify a mechanism that may be a engaged, even without inflammation, to impact risk for depressive illness," Blakely said.

More study is needed. Identifying genetic variations in the SERT activation pathway, for example, might suggest additional sources of genetic risk for depression. "Our work suggests that novel therapies targeting inflammation-linked pathways may be of use in the treatment of mood disorders," he said.

Zhu is research associate professor of Pharmacology, Blakely is the Alan D. Bass Professor of Pharmacology and professor of Psychiatry, and Hewlett is associate professor of Psychiatry and Pharmacology.

Other contributors were Vanderbilt research assistant Kathryn Lindler, and Lynnette Daws, Ph.D., and Anthony Owens, both at the University of Texas Health Science Center at San Antonio.

The study was supported by the National Alliance for Research on Schizophrenia and Depression (NARSAD), and by a Conte Center grant from the National Institute of Mental Health.

 

[Angela Kennedy]

Ok. This is a grand theory. BUT - lots of potential problems. 'Stress' cannot be successfully delineated between psychosocial/physical, or from each other as psychosocial events. These authors are still claiming psychogenic stresses are causing somatic illness. They may also be utilising a 'black box' theory to explain this - so people should not be seeing this as plausible yet - and it may never be so.

How are they even defining 'depression'?

 

[Angela Kennedy]

Where are they claiming that psychogenic stresses and psychogenic stresses only cause somatic illness?

The point of all this research is that inflammation of the brain is causing depression. Inflammation of the brain can be caused through psychological events but it doesn't have to. Any illness that to some extent manipulates brain chemistry and causes inflammation of the brain (including CFS) will lead to depression. No psychogenic stresses are needed! This implicates many new ways to treat people. Stop treating the last chain link (by increasing certain neurotransmitters) and start looking at the chain links before that (stop the inflammation and the depression will resolve itself alone).

From the report you've quoted (your post #1)

"According to the new theory, severe stress and adverse life events, such as losing a job or family member, prompt neurobiological processes that physically alter the brain."

This is then used to promote a theory of 'inflammation' CAUSED by 'stress and adverse events'. Direction of causation is a bit ambiguous in this piece, and this is a common phenomenon, but, sooner or later psychogenic explanations tend to be revealed, as here, for example, and in the 'childhood trauma causing neurological and immune dysfunction causing CFS' promoted by Heim et al and utilising Freudian notions as well. : (

It might look like a grand theory - but it's the links in the chain of reasoning that matter.

 

[Tia]

They're doing a study about that here where they put the worst depressed patients on though antiinflammatory tablets and see if they see a difference.
The study starts after they get it aprooved byt the healthpanel here, in the beginning of 2011.

 

[D Bergy]

I found out by accident, that my own thirty years worth of on again off again depression was caused by low grade chronic inflammation.

When I was diagnosed with Crohn's Disease, I started to quell the intestinal inflammation with anti-inflammatory supplements, such as Krill Oil, Turmeric, Ginger and others.

While this was not 100% effective in controlling the Crohn's, it did resolve my depression problem 100%.

It is easy enough to test out, and with little to no risk.

Dan

 

[Cort]

Michael Maes (also a ME/CFS researcher) has been saying this for years. He is a strong opponent of Wessely, Reeves and the Dutch psychiatric lobby (as a neuropsychiatrist himself).

And guess what happened with visionaries like him, they get reviled and ridiculed by the establishment. If only scientist would be more open-minded and would let go the old psychiatric dogmas, we'd be much further in these neurobiological diseases.

Yes, Maes just put out a paper on that. I've been trying to get an interview with him...He has been like a lone wolf for years....I'm sure he's just loving this!

I think its important stuff because of the increased incidence of depression/anxiety in CFS. For myself I would not meet the criteria for an anxiety disorder but something is definitely there. I wonder if the pathways for creating fatigue in the brain are close to those that create depression or for that matter, pain.....

Love to see them open up biological underpinnings of depression.

Neuroglial dysfunction may also be causing the pain in fibromyalgia...Thanks for posting this.

 

[Cort]

I found out by accident, that my own thirty years worth of on again off again depression was caused by low grade chronic inflammation.

When I was diagnosed with Crohn's Disease, I started to quell the intestinal inflammation with anti-inflammatory supplements, such as Krill Oil, Turmeric, Ginger and others.

While this was not 100% effective in controlling the Crohn's, it did resolve my depression problem 100%.

It is easy enough to test out, and with little to no risk.

Dan

That's great to hear - was it a combination of all of them?

 

[Cort]

From the report you've quoted (your post #1)

"According to the new theory, severe stress and adverse life events, such as losing a job or family member, prompt neurobiological processes that physically alter the brain."

This is then used to promote a theory of 'inflammation' CAUSED by 'stress and adverse events'. Direction of causation is a bit ambiguous in this piece, and this is a common phenomenon, but, sooner or later psychogenic explanations tend to be revealed, as here, for example, and in the 'childhood trauma causing neurological and immune dysfunction causing CFS' promoted by Heim et al and utilising Freudian notions as well. : (

It might look like a grand theory - but it's the links in the chain of reasoning that matter.

After I read John Falk's book I realized that some people become depressed without any psychological antecedents. The fact that cytokine production in people who come down with CFS after an infectious appears to be much HIGHER than those that don't makes me wonder if some sort of cytokine cascade get started in the brain?

I've always thought this was a great explanation for CFS since 'sickness 'behavior'' (ie flu-like symptoms) is definitely triggered by infections and infections seem to trigger many peoples cases of CFS....that's always seemed to fit and actually its a theory that the CDC, believe it or not, is very interested in.

 

[Cort]

The point of all this research is that inflammation of the brain is causing depression. Inflammation of the brain can be caused through psychological events but it doesn't have to. Any illness that to some extent manipulates brain chemistry and causes inflammation of the brain (including CFS) will lead to depression. No psychogenic stresses are needed! This implicates many new ways to treat people. Stop treating the last chain link (by increasing certain neurotransmitters) and start looking at the chain links before that (stop the inflammation and the depression will resolve itself alone).

The other thing is that they are just looking at depression! Why stop there with brain inflammation?....that's just the first stop, hopefully,for these researchers.

I think you should write an article on this Diesel

 

[Angela Kennedy]

Where are they claiming that psychogenic stresses and psychogenic stresses only cause somatic illness?

The point of all this research is that inflammation of the brain is causing depression. Inflammation of the brain can be caused through psychological events but it doesn't have to. Any illness that to some extent manipulates brain chemistry and causes inflammation of the brain (including CFS) will lead to depression. No psychogenic stresses are needed! This implicates many new ways to treat people. Stop treating the last chain link (by increasing certain neurotransmitters) and start looking at the chain links before that (stop the inflammation and the depression will resolve itself alone).

But again, what do they mean by 'depression'? This is a very important problem. AND, they cannot yet (and may never be able to) substantiate the claim that psychological events will lead to 'inflammation' of the brain, OR that 'inflammation' of the brain leads to 'depression' per se, especially because the definition of 'depression', like many mental health labels, is unstable and confused.

As for ME/CFS, the claims people have higher levels of 'depression' or 'anxiety' are themselves unsafe, and even where feelings that get labelled as 'depression' (or 'anxiety') do happen, can happen for other reasons such as the terrible situation people are in.

'Depression' claims in mental health neurology are as unsafe as those around ME/CFS.