In the past several years, a quiet revolution has been happening in molecular psychiatry. Study after study has shown that numerous mental illnesses are associated with inflammation that can be tracked using assays developed for studying inflammation in cardiovascular medicine. One recent paper simply declared in its title "So depression is an inflammatory disease, but where does the inflammation come from?"
Cells of the immune system and some other kinds of cells make molecules called cytokines many of which signal the immune system to ramp up its response -- i.e. to produce inflammation. Immune cells of the types called macrophages are activated and stimulated to multiply by cytokines such as interleukins; these macrophages not only "ingest" foreign substances and microbes but attack them with a variety of powerful chemical weapons. These chemical weapons can cause collateral damage to healthy cells as well as damage to infected cells and pathogens.
In the brain, the cells that play the roll of macrophages are called microglia. Microglia also respond to cytokines and can mount immune responses inside the brain, even damaging neural tissue at times.
It's been recognized for many years that the incidence of autoimmune disorders has been increasing in industrialized regions. The Hygene Hypothesis states that the immune system must receive a certain level of microbiological challenge during childhood in order to develop correctly; if it does not, autoimmune disorders may develop.
What we are seeing in the many recent studies of inflammation and mental illnesses is increasing evidence that many mental illnesses, including depression, OCD, autism spectrum, schizophrenia and others, are inflammatory illnesses -- i.e. they are disorders of the immune system, working havoc on the brain. If they are increasing in incidence in the US and other developed countries, that may be part of an overall pattern of increasing incidence of immune disorders.
Since there is absolutely no evidence that specific pathogens cause specific mental illnesses or autoimmune disorders, this cannot be due to novel disease organisms appearing in industrial counties. The causes must be environmental.
But what are these environmental factors? There are a long list of candidates, and it is likely that certain gene variants can increase one's susceptibility to them. Nevertheless, there is reason to suspect that if diseases such as depression or autism spectrum are increasing in the US, it is most likely because of some environmental conditions or substances that are also increasing, exactly as is the case with well-established immune disorders such as asthmas and hay fever.
Something about life in the US, and other industrialized countries, is environmentally unhealthy in ways that are producing mental illnesses. Note that "environment" here does not refer only to pollutants or toxic substances or medical practices such as overuse of antibiotics; it also includes the social environment, which can produce stresses and sleep deficiencies that are also known to promote inflammatory responses. And it includes the microbiological environment within us that results in part from the foods we eat: commensal gut microbiota interact with the human immune system and can moderate or aggravate its response, even inducing bowel diseases and cancer. Conversely, mental illnesses such as depression can promote inflammation that affects cardiovascular health. The body, including the brain, is an integrated system linked by chemical signals.
References:
Baumeister et al. Inflammatory biomarker profiles of mental disorders and their relation to clinical, social and lifestyle factors.
Brod et al. 'As above, so below' examining the interplay between emotion and the immune system.
Copeland et al. Childhood bullying involvement predicts low-grade systemic inflammation into adulthood.
Dieset et al. Association between altered brain morphology and elevated peripheral endothelial markers - Implications for psychotic disorders.
Hayes et al. Inflammatory molecular signature associated with infectious agents in psychosis.
Hughes et al. Social support predicts inflammation, pain, and depressive symptoms: longitudinal relationships among breast cancer survivors.
Muscatell et all. Greater amygdala activity and dorsomedial prefrontal-amygdala coupling are associated with enhanced inflammatory responses to stress.
Rosenblat et al. Inflamed moods: a review of the interactions between inflammation and mood disorders.
Selhub et al. Fermented foods, microbiota, and mental health: ancient practice meets nutritional psychiatry.