Inflammation: It’s Complicated

The body’s complicated relationship to inflammation continues to  intrigue us. While inflammation is a necessary part of the healing process, it can also lead to heart disease, stroke, arthritis and, recent evidence suggests, even Alzheimer’s.

Inflammation is not all bad. It is a necessary part of the immune system and promotes bodily health. But just as a fire can provide good (warmth, light, etc.), the inflammation that helps heal us, when left unchecked, becomes analogous to a devastating wildfire, ravaging tissues, joints and blood vessels in its path and causing significant damage.

Acute inflammation is the necessary fire that surrounds and protects cuts, bruises and fractures as the body sends white blood cells rushing in to protect the area and red blood cells begin to repair the damage. This type of inflammation also occurs when you have the flu or pneumonia, offering protection from infection by battling invaders that may otherwise cause it, as well as contributing to the general healing process. Acute inflammation is characterized by the familiar sensation of heat, along with redness and swelling.

Chronic inflammation is the unchecked wildfire that can occur when the body’s immune response consistently overreacts. “Autoimmune disease” is the catchall term for a state of immune-system overreactivity. (“Immune deficiency disease,” by contrast, refers to an underperforming immune system. All are “immune system disorders.”)

 Autoimmune diseases are thought to have a variety of causes, but in many cases the cause is poorly understood. Environmental toxins have at times been implicated; inheritance of certain genes is also a factor. In the next issue we’ll explore an alternate theory of autoimmune disease causation that is gaining acceptance among a growing body of scientists.

In any case, chronic inflammation is the result of autoimmune disease, but the latter is not always the cause of chronic inflammation. This is clear simply from the fact that chronic inflammation does not always produce autoimmune disease-type symptoms. Examples of problems unrelated to autoimmune disease that chronic inflammation can cause include Alzheimer’s, stroke, cancer and heart disease.

Common autoimmune diseases include: rheumatoid arthritis, lupus, ulcerative colitis and Crohn's disease, multiple sclerosis, type 1 diabetes, Guillain-Barre syndrome (attacks on the nerve cells), psoriasis, Graves' disease (causing hyperthyroidism), and vasculitis (attacks on the blood vessels).

Cytokines and chronic inflammation
It is with regard to chronic inflammation that the complex role of cytokines enters the picture. Cytokines are small secreted proteins released by cells have a specific effect on the interactions and communications between cells. The term “cytokine” is a general one—there are many different types.

Specific inflammatory responses vary. It is common for different cell types to secrete the same cytokine or for a single cytokine to act on several different cell types. Sometimes problematically, cytokines are redundant in their activity—similar functions can be stimulated by different cytokines.

Additionally, they are often produced in a cascade, as one cytokine stimulates its target cells to make even more cytokines. For example, white blood cells (specifically, macrophages) are among the first types of cells on the scene, and they (among other functions) produce cytokines, which in turn (among other functions) regulate the behavior of yet more white blood cells (specifically, lymphocytes).

When white blood cells are directed to flood into, and then overstay their welcome in, an area of the body, they can begin to attack nearby healthy tissues and organs. Certain pro-inflammatory cytokines in spinal cord, dorsal root ganglion, injured nerve or skin are known to be associated with pain behaviors. They are also thought to generate abnormal spontaneous activity from injured nerve fibers or compressed or inflamed dorsal root ganglion neurons. These pro-inflammatory cytokines are among the type produced by the above mentioned macrophages that initiate the cascade of white blood cell-cytokine production. Cytokines therefore play a key role in the development and persistence of many pathological pain states.

Chronic inflammation due to obesity and overweight
If you are overweight and have more visceral fat cells—the kind of fat that builds up in your abdomen and surrounds your organs—the immune system sees those fat cells as a threat and pumps out more white blood cells. The longer you stay overweight, the longer your body remains in a state of inflammation.

Losing extra pounds, especially around the belly, can lower your risk. Other preventive steps include fighting gum disease (bleeding gums indicate inflammation), treating high cholesterol and quitting smoking. The toxins from smoking have a direct link to inflammation.

Dietary steps
Which foods are considered the best for reducing inflammation? A study published this spring in the British Journal of Nutrition found that polyphenols from onions, turmeric, red grapes and green tea lowered a marker for inflammation in the body. All types of berries are also rich in polyphenols, as are cherries and plums. Dark green, leafy vegetables like spinach and kale are also good choices. Olive oil, flaxseed oil, salmon, sardines and mackerel offer healthy doses of omega-3 fatty acids, which have long been shown to reduce inflammation. Note that many of these foods also promote weight loss and healthy weight maintenance.

Harvard Men's Health Watch, Sep. 2016, "Playing with the fire of inflammation," delivra&utm_medium=email&utm_campaign=GB20160914-DOH&utm_id=251440&dlv-ga-memberid=10660158&mid=10660158&ml=251440

Cleveland Clinic, Chemocare, The Immune System: Information about Lymphocytes, Dendritic Cells, Macrophages, and White Blood Cells, http://chemocare.com/chemotherapy/what-is-
chemotherapy/the-immune-system.aspx

University of Rochester Medical Center, How Wounds Heal, https://www.urmc.rochester.edu/Encyclopedia/Content.aspx?ContentTypeID=134&ContentID=143

Int Anesthesiol Clin, 2007, Vol. 45, No. 2, pp. 27–37, https://www.ncbi.nlm.nih.gov/pmc/articles/P
MC2785020/

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