It’s the buzz word for all the magic pills and potions. When unchecked, it’s the underlying mechanism for most chronic diseases and the reason why long-term stress contributes to so many of them. Know what it is? It’s inflammation. This means that your chronic red, hot, joint could be signaling an underlying process that is spreading throughout your whole body. How?
A recent article in July’s Integrative Practitioner by Lise Alschuler, ND, FABNO sheds light on how inflammation contributes to the other symptoms that seem to pop up more with your chronic joint pain (fatigue, digestive disturbances, ect.):
Chronic inflammation is a complex prolonged internal response to a tissue insult. This response involves the immune and endocrine systems.The initial tissue insult results in a massive release of powerful chemical messenger molecules (cytokines, enzymes, interleukins and prostaglandins). These chemicals stimulate specific activities such as blood vessel growth and also bind to cellular membrane receptors and create cell division and anti-apoptotic signals. A powerful mediator of these reactions is nuclear factor kappaB (NF-kB). NF-kB engages the inflammatory response, stimulates cell division, alters immunity and decreases apoptosis.
Huh, Dr. Sarah? In English- an inflammatory response triggers a massive release of chemicals that can enter the body systemically. If your body doesn’t have the resistance to put out the fire, these mediators could damage various organs, tissues, and cause changes in our DNA structure (cancer).
How do we control inflammation? What could prevent our resistance and cause low immunity? Stress is a big factor, along with many other environmental and lifestyle choices. The stress mechanism signals a whole array of events from inflammatory mediators, blood sugar deregulation, hormonal imbalances, changes in digestive processes and circulatory functions.
According to the American Institute of Stress, stress contributes to 70-90% visits to primary care doctors and the American Psychological Association reports the following:
More than half of working adults-and 47 percent of all Americans-say they are concerned with the amount of stress in their lives, according to a new telephone survey conducted…Moreover, the survey finds that people experiencing stress are more likely to report hypertension, anxiety, depression or obesity.
Here is a review on some of these conditions associated with chronic inflammation (and probably linked to stress):
The American Heart Association– Heart Disease
C-reactive protein (CRP) is one of the acute phase proteins that increase during systemic inflammation. It’s been suggested that testing CRP levels in the blood may be an additional way to assess cardiovascular disease risk. A more sensitive CRP test, called a highly sensitive C-reactive protein (hs-CRP) assay, is available to determine heart disease risk.
A role for inflammation has been well established over the past decade or more in describing the artherogenic process.
Neurobiology Aging Journal [abstract] – Alzheimer’s disease
Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder
Nature Journal [abstract] – Cancer
Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signaling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
European Journal of Endocrinology [abstract] Metabolic Syndrome & Hormonal Effects
Low testosterone and SHBG levels were strongly associated not only with components of the metabolic syndrome, but also with the metabolic syndrome itself, independently of body mass index. Furthermore, sex hormones were associated with inflammation and body iron stores. Even in the absence of late-stage consequences such as diabetes and cardiovascular disease, subtle derangements in sex hormones are present in the metabolic syndrome, and may contribute to its pathogenesis.
So, my beautiful patients, you now know why the mind-body approach is so important. It’s not so much the event, but our perception and reaction that contribute to stress. So what do we do about this? Here are some simple tips to quench inflammation and calm the stress response:
1.Eat real, whole, organic, unprocessed foods.
2.Exercise in a way that is enjoyable for you
3.Drink plenty of filtered water to dilute toxins
4.Take a good multivitamin (see my webpage on supplement quality) and any lacking nutrients in your diet.
5.Supplement your many colorful vegetables with spices which down-regulate inflammatory mediators.
6.Most importantly, breathe and find relaxation therapies that work for you, such as yoga, deep breathing, or google techniques from the heartmath institute.
7.Get sleep
References:
AHA. http://www.americanheart.org/presenter.jhtml?identifier=4648
Circulation. http://circ.ahajournals.org/cgi/content/full/107/3/499
Neurobiology and Aging. PMID: 108586
Nature. 2002. http://www.ncbi.nlm.nih.gov/pubmed/12490959
America’s No. 1 Health Problem. American Institute of Stress. http://www.stress.org/americas.htm.
Brain and Cognition. Volume 65, Issue 3, December 2007, Pages 209-237
The American Psychological Association. Stressed out Nation. http://www.apa.org/monitor/apr06/nation.aspx
European Journal of Endocrinology. 2003. http://www.eje-online.org/cgi/content/abstract/149/6/601