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Mind and body: Scientists identify immune system link to mental illness

natasa778

Senior Member
Messages
1,774
The study, published today in JAMA Psychiatry, indicates that mental illness and chronic physical illness such as coronary heart disease and type 2 diabetes may share common biological mechanisms...

http://www.cam.ac.uk/research/news/...identify-immune-system-link-to-mental-illness


another article on the same story


Kids' responses to infections linked with depression risk


Kids with immune systems that react strongly to infections could have a higher risk of depression, a new study suggests.

Researchers studied a group of healthy children over nine years and found that those whose immune systems reacted more forcefully in response to infection were more likely to develop depression and psychosis, compared with those with immune systems that were less reactive.

The findings show that because exercise and a healthy diet help the immune system to function properly, they could help in preventing both physical and mental illness, the researchers said.

"We're showing that how our immune system responds how it works and whether it's slightly more keyed up than other people's, clearly has implications for our risk for depression and psychosis," said Golam Khandaker, a neuroscientist at the University of Cambridge in England and lead author of the new study.

One immune system response, high inflammation, has previously been linked to physical maladies like heart disease and diabetes, but the new findings could explain why patients with heart disease and diabetes also face a greater risk of depression, Khandaker told Live Science. High inflammation acts as the common mechanism, he said. [11 Surprising Facts About the Immune System]

The researchers looked at blood samples from 4,500 healthy kids when they were 9 years old, and divided them into three groups high, medium and low inflammation based on the levels of two proteins in the blood that are markers of inflammation.

When the children turned 18, the researchers examined their mental health and found that those who were in the high-inflammation group were more likely to have developed depression or symptoms of psychosis when compared with those who were in the low-inflammation group.

In explaining the link, Khandaker compared the immune system to a thermostat. Though all the children in the study were healthy, some of their "thermostats" or immune systems were set at a slightly higher level, meaning that their systems would react more strongly than those of other children to infections and stressors.

The study supports an established body of research that shows that people and animals with symptoms of depression or schizophrenia have higher levels of inflammatory markers. But the new study is the first to look at the immune system before depression has developed, and suggests that the surge in inflammation that comes in response to an infection could affect mental health, said Georgia Hodes, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York.

Hodes previously conducted a study that found the inflammatory marker IL-6 which was one of the proteins the researchers looked at in the new study was found at higher levels in mice with depression.

But besides proteins found in the blood, there are also more obvious signs of increased inflammation. Those signs may include obesity, asthma and allergies, said Dr. Andrew Miller, a psychiatrist at Emory University.

And Judy Van der Water, an immunologist at the University of California, Davis, said that kids who get fevers more often and for longer periods of time may also have higher levels of inflammation.
http://www.foxnews.com/health/2014/...eed:+foxnews/health+(Internal+-+Health+-+Text
 

A.B.

Senior Member
Messages
3,780
This has been known for a while. I always link to http://www.cytokines-and-depression.com/ when it comes up. The article is extremely interesting, and the material was written in the 90's!

Some excerpts:

McDonald, Mann and Thomas9 published a paper in 1987 in the Lancet titled 'Interferons as Mediators of Psychiatric Morbidity'. This was a controlled trial of 43 hepatitis B patients, in which 29 patients were given INFα three times weekly for up to six months. Most of the patients on INFα reported fatigue, loss of interest, lack of concentration, anxiety and depression. Control patients not given INFα did not report these symptoms. An amazing 63% of the volunteers on interferon became psychiatric patients! Depressive symptoms did not remit immediately after discontinuing INFα. Symptoms usually lingered with reduced intensity for one to three weeks.

The recently discovered anticytokine and cytokine suppressing properties of antidepressants is of fundamental importance to any theory of depression, especially a cytokine theory of depression. In sharp contrast to the rapid effects of antidepressants on neurotransmitter systems, antidepressants have a slow effect on cytokine systems. This fits beautifully with the slow therapeutic action of antidepressants on depressed patients. Indeed, the slow therapeutic action of antidepressants has been the fundamental problem with the neurotransmitter theory of depression.

HPAaxis hyperactivity in depressed patients is one of the most extensively documented physical abnormalities in biological psychiatry. So what is the cause? This question has been stumping biological psychiatry for years. Since external stessors can only account for a small percentage of HPA overactivity, they have looked elsewhere for the cause. Neurotransmitters are involved in regulating the HPAaxis, so they have been examined.51 It is reasonable to suspect that neurotransmitter dysfunctions could be causing the HPA dysfunction. But then, what causes the neurotransmitter dysfunctions? Biological psychiatry (since they are oblivious to cytokines) draws a blank. So we are back to square one, no known cause. The other area exhaustively searched is the HPAaxis itself.52 The defect or defects in the HPAaxis are sought. And what if they are found? The next question would be, what caused the HPAaxis defects? Again no answer, so back to square one, that is, no known cause.

Cytokines to the rescue. We know that HPAaxis activation is caused by either external or internal stressors. In the case of depression, external stressors have been eliminated as the key factor, so this leaves internal stressors (ie infection, trauma, autoimmune disease, cancer, dying tissue and organ dysfunction) as the cause. Internal stressors are well established causes of immune system activation and activated immune systems secrete much higher amounts of IL1, IL2, IL6 and TNF. These same cytokines profoundly activate the HPAaxis53,54

A century ago, when fever was viewed as a disease rather than a sign of disease, fever was blamed for complications and death in sick people. And why not? Patients with the highest temperatures had the highest death rates and most complications. A nice correlation: higher fever, higher death. Blaming fever for deaths based on correlations is an example of flawed scientific thinking, because correlations do not give information on cause and effect. Correlations merely indicate that there may be a relationship between death and fever, but it doesn't reveal the nature of the relationship, if any.

Today, no medical professional would suggest that fever kills patients because we know that fever is not a disease. It is a sign of acute immune system activation, an indicator of the intensity of the war going on inside the body. In like fashion, depression is not a disease, but rather a multifaceted sign of chronic immune system activation, an indicator of disease severity. Nevertheless, medical professionals continue to view depression as a disease, and therefore lay the blame on depression for the higher deaths and increased complications in physically ill patients. Blaming depression is another example of flawed scientific thinking.
 
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natasa778

Senior Member
Messages
1,774
yes, this has been known for a while, but this to my knowledge the first longitudinal study of the kind, looking at underlying risk/predisposition etc
 
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