I recently did a couple of webinars on the biome for practitioners down in Australia. In preparing my slides, I came across some amazing (and terrifying) statistics. According to the CDC in the US, 7.6% of Americans aged 12 and over have had moderate to severe depression in the past 2 weeks. In Australia, a million people a year (in a population of 23 million – so about 4%) suffer from depression. The numbers are staggering. And that is just depression! What about anxiety disorders: generalized anxiety disorder, PTSD, panic attacks, OCD (which is a subset of anxiety disorders), bipolar disorder, autism, ADHD, etc.?
Referring back yet again to Sid Baker’s spider web analogy – that everything in the body is interconnected – it is amazing how much information has been discovered in the last couple of years about the immune-CNS-gut connection. In 2015 an important article was published in the Journal of Experimental Medicine which, for the first time ever, showed that the central nervous system is physically tied in directly to the immune system via a previously unknown system of lymph vessels.[i]
Scientific America had a great summary article of this revolutionary finding:
“Perhaps the most commonly cited division between body and brain concerns the immune system. When exposed to foreign bacteria, viruses, tumors, and transplant tissue, the body stirs up a torrent of immune activity: white blood cells devour invading pathogens and burst compromised cells; antibodies tag outsiders for destruction. Except, that is, in the brain. Thought to be too vulnerable to host an onslaught of angry defensive cells, the brain was assumed to be protected from this immune cascade. However research published this month reported a previously unknown line of communication between our brains and immune systems, adding to a fast-growing body of research suggesting that the brain and body are more connected than previously thought.” [ii]
In a way though it’s strange that anyone would have ever thought the immune system was completely separate from the brain. Medicine has long recognized “sickness behavior,” for example: when an organism is sick, and inflammatory cytokines are released, the organism conserves energy to use it in the battle against the disease – thus appearing lethargic and enervated. Back in 2013, I remember reading this blog post from Harvard Health Publications, “Infection, Autoimmune Disease Linked to Depression,”[iii] which cited an amazing statistic based upon a study of the entire Danish population from 1945 to 1995: “People who had been treated for a severe infection were 62% more likely to have developed a mood disorder than those who never had one. An autoimmune disease increased the risk by 45%.”
And of course, the connection is bidirectional. How many of us have gotten sick after a period of extreme psychic stress? Shingles is a perfect example: the herpes virus that causes shingles lives in the nerves, but is generally kept dormant by our immune systems. Stress us out and suddenly, the virus wins out over our suppressed immune system.
So, what does all this have to do with the gut biome? 70% or more of our immune system is in our digestive system as most germs enter through our nose and mouth. And our body’s co-inhabitants are a crucial part of normal immunity…and also, talk directly to our brains. Completely coincidently, just before finishing this post, I read about the publication of a new article called “Linking the Human Gut Microbiome to Inflammatory Cytokine Production Capacity.”[iv] I’ll write more on this, the connection of the gut biome to brain development and health, and other recent research in the near future.
[i] Aleksanteri Aspelund, Salli Antila, Steven Proulx, Tine Karlsen, Sinem Karaman, Michael Detmar, Helge Wiig and Kari Alitalo. A dural lymphatic vascular system that drains brain interstitial fluid and macromolecules. The Journal of Experimental Medicine, June 2015 DOI: 10.1084/jem.20142290
[iv] Schirmer, Melanie et al.Linking the Human Gut Microbiome to Inflammatory Cytokine Production Capacity. Cell , Volume 167 , Issue 4 , 1125 – 1136.e8