It Isn’t All In Your Head: Depression Is Actually a Physical Illness Caused by Inflammation

According to many scientists and scientific experiments performed in recent years, it has been thought that the chemical processes that take place in the brain are the only cause of depression, but new scientific findings suggest that the immune system is the one that stimulates the onset of depression; while the feeling of hopelessness, extreme anxiety and pessimism are the result of some kind of physical problem.

The main starting point of the current scientific research on depression was the balance and the imbalance of dopamine and serotonin, and this has contributed, to some degree of success in treating depression, but the inability to stabilize and suppress the immune system after the existence of any disease or condition in recent years is considered to be a major reason for depression for which there is a lot of evidence.

From the Cambridge University, professor Ed Bullmore says that almost certainly depression can be caused by some form of inflammation but does not give clear examples of this.

According to Bullmore, “immuno-neurology” is a field to which serious attention and time should be paid. Abject doldrums experienced during depression and their association with the inflammation are a reason good enough for studying this field.

Bullmore claims that the connection that exists between the manifest signs of depression and inflammation has a significant influence on human reactions and mood.

Although there is no evidence, practice suggests that almost all people who have been vaccinated at least once in a lifetime manifest some kind of depression.

However, the question that needs to be asked is whether it is a coincidence of the occurrence of depression due to the presence of inflammation or is it vice versa, whether as a result of depression an inflammatory process occurs in the body?

If an anti-inflammatory drug such as interferon is given to healthy individuals, then depression will occur in a fairly large proportion of those individuals, and hence the clear linkage can be seen, and in one way this can be interpreted as evidence.

Immunopsychiatry together with psychoneuroimmunology provide a synergistic approach to the discovery of a drug which, although it would act against inflammation, would still be significantly effective in treating depression and thus achieve a double effect.

According to Professor Bullmoure, studies to be carried out by Wellcome Trust scientists and Cambridge University should further prove that anti-inflammatory drugs can be reliably used in the treatment of depression.

Nearly 30 per cent of people who have rheumatoid arthritis suffer from depression, and it is good enough evidence that there is a great connection between inflammatory diseases of any type and depression.

According to a number of prominent scientists, if patients with inflammatory diseases cease to be advised to fully withdraw into their homes and rest, then the number of people with depression will be significantly lower.

Although there is insufficient evidence of the linkage that exists, however, innumerable clinical cases and prevalence are here to prove the opposite, despite the fact that scientists firmly stick to the existence of a blood-brain barrier by which the immune system and brain are clearly separated.

In addition, this was explained in the Reader in Neuropsychiatry, by Dr. Alan Carson of the University of Edinburgh who explained that the brain is structurally and functionally connected and it is very difficult to clearly distinguish the functions of the anatomical structures in the brain because all social, biological and psychological actions originate primarily from it. “Yet institutionally we use an outmoded code which separates brain disorders into psychiatric ‘f’ codes and neurological ‘g’ codes which holds back both scientific and clinical progress.”

Until now it has been shown that there is ample evidence that inflammation can cause depression, but now attention should be paid to precise details in order to set up an appropriate, reliable and effective treatment of inflammation and, thus, depression.

The evidence that has so far been collected from lower-level clinical trials, nevertheless does not provide sufficient evidence of the causes of depression nor the treatment directed towards it.