Depression is a very common illness. About 17 percent of the population will have at least one episode in their lifetime. WHO predicts that by 2030, depression will cause more disability and mortality than any other illness including cancer, cardiovascular disease, accidents and war! It has been known for a number of years that antidepressants are no better than placebo for mild or moderate depression and only about 10 percent more effective for the severely depressed. In fact, a good clinical rule of thumb is that SSRI’s get about 50 percent of patients about 50 percent better. However, these facts do not discourage clinicians and patients from using antidepressants. 250 million prescriptions are written a year – that translates into one out of every ten patients in the US being handed an antidepressant prescription.

Our treatment of depression by manipulating neurotransmitters has remained fundamentally unchanged for the last decades. In fact, there is no data demonstrating that any of the antidepressants developed since imipramine in the 50’s WORK ANY BETTER in both achieving full remission and preventing relapse. 50 percent of patients relapse after their first episode, which mean SSRI’s don’t do anything actually to cure depression. In short, we have a very common and debilitating illness – some would say an epidemic – and our treatment modalities remain stuck in an ineffective paradigm.

A more fruitful approach is to approach depression with fresh eyes. As humans, we find it very easy to find meaning in the cluster of symptoms we label depression. Loss of interest in usual activities, withdrawal from the world, inability to find pleasure in ordinary pursuits, low energy, aches and pains changes in sleep and appetite – that must be from grief, or sadness, feelings of guilt or reaction. There must be an emotional reason for these behaviors. However, when we observe the same behaviors in an animal, we recognize the presence of a physical illness and take our pet to the vet. In humans, psychological meaning is attached to the behaviors, and therapy or antidepressants are prescribed, while in animals we simply call it sickness behavior and test for infectious disease.

There is lots of good research to suggest that animals and humans are not very different and that what we call depression is highly associated with the presence of inflammatory cytokines (Dowlati et al. 2010). Even more exciting news is recent research showing that inflammation probably precedes the development of depression (Hodes et al. 2014). Mice were checked for the presence of Interleukin 6, an inflammatory cytokine, and then placed in cages with physically bigger mice. Some mice lost their taste for sugar water and sex, and began to avoid the other mice. This is considered similar to a depressive state. What the researchers found was that the mice that developed “depression” had the higher IL-6 beforehand. In other words, the presence of inflammation made the mice less resilient in the face of stress. A similar finding was recently demonstrated in children. IL-6 levels were measured in 9 year olds and again when the children were 18. The levels of IL-6 at age 9 were positively correlated with the development of depression and psychosis at age 18 (Khandaker et al. 2014)

What causes the increase in IL-6? The precise causes are not yet known. However, proposed candidates include infectious elements such as viruses, parasites and bacteria, inflammagens such as biotoxins, and stress. In children, early abuse has been correlated with increasing IL- 6 by 2.35 percent (Gouin et al.. 2012). One common parasite found in cats, toxoplasmosis, is linked with increased suicides, and has also been proposed as a causative agent for neuroinflammatory depression (Canli 2014) I suggest watching Dr. Canli’s TED talk for more insight into infectious causes of depression (

Putting all this research together then allows us to rephrase the dramatic WHO prediction that in 2030 the leading cause of disability and mortality will be depression. No, what WHO is acknowledging is that by 2030 NEUROINFLAMMATION, caused by inflamagens such as biotoxins, Lyme, viruses, poor diet, bad fats, lack of exercise and child abuse, will be the leading cause of disability and mortality.  It will be , at least, if new approaches to treatment are not researched and applied.

The exciting news about inflammation and depression is that there are many more ways to treat neuroinflammation than simply popping SSRI’s. Possible treatments include diet, exercise, anti-inflammatory supplements and of course diagnosing and treating the underlying cause of inflammation such as mold or Lyme. For more information about these topics, I suggest browsing through other blog pieces. In addition, if you read last month’s blog on fermented foods you may also enjoy reading this well researched article on fermented foods and mental health (Selhub, Logan, and Bested 2014).


Canli, Turhan. 2014. “Reconceptualizing Major Depressive Disorder as an Infectious Disease.” Biology of Mood & Anxiety Disorders 4 (1). BioMed Central Ltd: 10. doi:10.1186/2045-5380-4-10.

Dowlati, Yekta, Nathan Herrmann, Walter Swardfager, Helena Liu, Lauren Sham, Elyse K Reim, and Krista L Lanctôt. 2010. “A Meta-Analysis of Cytokines in Major Depression.” Biological Psychiatry 67 (5): 446–57. doi:10.1016/j.biopsych.2009.09.033.

Gouin, Jean-Philippe, Ronald Glaser, William B Malarkey, David Beversdorf, and Janice K Kiecolt-Glaser. 2012. “Childhood Abuse and Inflammatory Responses to Daily Stressors.” Annals of Behavioral Medicine : A Publication of the Society of Behavioral Medicine 44 (2): 287–92. doi:10.1007/s12160-012-9386-1.

Hodes, Georgia E, Madeline L Pfau, Marylene Leboeuf, Sam A Golden, Daniel J Christoffel, Dana Bregman, Nicole Rebusi, et al. 2014. “Individual Differences in the Peripheral Immune System Promote Resilience versus Susceptibility to Social Stress.” Proceedings of the National Academy of Sciences of the United States of America 111 (45): 16136–41. doi:10.1073/pnas.1415191111.

Khandaker, Golam M, Rebecca M Pearson, Stanley Zammit, Glyn Lewis, and Peter B Jones. 2014. “Association of Serum Interleukin 6 and C-Reactive Protein in Childhood with Depression and Psychosis in Young Adult Life: A Population-Based Longitudinal Study.” JAMA Psychiatry 71 (10). American Medical Association: 1121–28. doi:10.1001/jamapsychiatry.2014.1332.

Selhub, Eva M, Alan C Logan, and Alison C Bested. 2014. “Fermented Foods, Microbiota, and Mental Health: Ancient Practice Meets Nutritional Psychiatry.” Journal of Physiological Anthropology 33 (1): 2. doi:10.1186/1880-6805-33-2.

  1. Dr. Canli’s TED talk on depression as an infectious disease can be viewed here: (