An interesting new animal study suggests that depression may be in part caused by an overreaction to stress (as the media (1) put it, an ‘allergy to stress).’
While this is good information that elaborates on the role of immune function and inflammatory molecules, I was most struck by the comments of the researchers, who already reconciled how we might start using rheumatoid arthritis drug to treat depression. There already was a clear trajectory this animal research is headed for: to justify use of a pharmaceutical to stomp out the inflammatory response.
As I have mentioned before in this blog, studies have shown that antidepressants work no better than placebo in mild to moderate cases of depression (2). Conventional medical care focuses on drugs to suppress and cover up symptoms. Unfortunately, as more quality research comes out which helps us understand more underlying causes, researchers keep trying to figure out a way to justify more drugs for depression, instead of fixing the underlying issues of a disease. As Einstein said, “insanity is doing the same thing over and over and expecting a different result.”
Good Research in the Wrong Direction
This rodent research recently presented at the Society for Neuroscience meeting suggests that animals who produce an immune molecule called interleukin-6 are more likely to be depressed (3). Interleukin-6 is a protein that can communicate to other parts of the immune system to get stimulated, especially during infections and if the body is burned. IL-6 can also travel back to the brain, and send messages to the middle of the brain, an area called the hypothalamus, which can tell the body to feel sick and lay low. This might be the reason higher levels of IL-6 can contribute to someone having depression.
One important takeaway from this research is that inflammation in the body can clearly encourage the onset of depression come on, or make it get worse if someone is already predisposed.
The Driving Force Behind Re$earch:
The problem is, the driving force of this research is to justify the use of more drugs. This is a quote from one of the study authors: Dr. Georgia Hodes:
"To our knowledge, this is the first study showing a functional role for the peripheral immune system in an animal model of depression. This study suggests that cytokine-based antibody therapy currently approved for treatment of inflammatory illnesses such as rheumatoid arthritis and Castleman's disease in humans may have potential as an antidepressant treatment."
So, what the author of this study just said to us is that since inflammation outside the brain and nervous system might be contributing to depression, then we should begin to consider using rheumatoid arthritis drugs for depression - drugs like Tocilizumab (Actemra) for depression. Actemra has many side effects, including high cholesterol, low platelets, digestive problems, and increased cancer risk.
Drug companies love repackaging drugs they already have to sell to millions of other people with a totally different condition – it is a quicker way to make a whole lot of money.
While I do not know whether this study’s authors have ties to drug companies, I do know many, if not most, researchers doing work like this do have big pharma ties. This creates a problem, for much of the research is already geared to eventual drug use, instead of unearthing safer natural solutions to underlying problems.
What Can We Do Instead of Drugs for Allergy and Inflammation?
As a naturopathic doctor and former NIH researcher myself, I think this is a good study that helps fill some more information about what we already know about depression – that inflammation is a problem.
But, instead of using this information to recommend dangerous immunosuppressive drugs, let’s start to think more about working naturally with a person’s body to lower inflammation. Five ways to start doing this are:
1 – working on food sensitivities. Most of our immune system that makes IL-6 is in the digestive tract. In fact, most neurotransmitters are made in the digestive tract. Taking in the right food for our body can lower inflammation quite easily.
2 – relaxation work: meditation, yoga, acupuncture and other modalities which are proven to lower stress and inflammation in the body
3 – working on the negative messages we tell ourselves: Cognitive Behavior Therapy and other work can help us catch ourselves, before the negative messages gain inertia. Negative thoughts will contribute to inflammatory patterns in the brain in the body. Positive thoughts will help calm the fire.
4 – take natural anti-inflammatories: while the drugs suppress the immune system, anti-inflammatory herbs and nutrients are known to help heal and balance the immune system. Herbs like bromelain, boswellia, turmeric and quercetin can be helpful.
5 – take fish oil: essential fatty acids are a good place to start to help rebalance inflammation and keep the immune system balanced.
While drugs can have benefit in depression in certain emergency situations, we need to start using good quality research like the one mentioned to help clarify the multiple underlying factors of depression, like inflammation is identified in this case. As we understand all these factors better, we can then devise healthy ways to rebalance the body – instead of using research to justify more drugs that only cover up some symptoms.
About Dr. Bongiorno: Peter Bongiorno ND, LAc is co-director of Inner Source Health in New York, and author of How Come They're Happy and I'm Not? The complete naturopathic guide to healing depression for good. More about him can be found through www.drpeterbongiorno.com.
1. FOX News “Depression May Be Caused By an Allergy to Stress": http://www.foxnews.com/health/2012/10/15/depression-may-be-caused-by-allergy-to-stress/ accessed October 24, 2012
2. Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, et al. Antidepressant drug effects and depression severity: a patient-level meta-analysis.JAMA. 2010 Jan 6;303(1):47-53.
3. Hodge G. et al. Innate Immune System Influences Vulnerability to Anxiety or Depression in Animal Model: October 16, 2012 annual meeting of the Society for Neuroscience, New Orleans.