The prevalence of inflammation and associated health conditions is increasing in the developed world.
Inflammation has become the subject of intense scientific research in recent years, as an increasing number of conditions and diseases are shown to involve inflammatory processes.
These conditions and diseases include everything from common ailments you may see in your practice, such as trauma or musculoskeletal pain, to cardiovascular disease, type 2 diabetes, cancer and overall mortality.
Inflammation is the body’s natural attempt at self-protection and self-healing by removing harmful stimuli, microorganisms or pathogens. When inflammation persists, however, tissue damage can result.
This in turn leads to the production of molecules that re-stimulate inflammation. This negative loop can promote tissue and organ dysfunctions, especially if the lymphatic system is deficient.1, 2, 3
The question, in terms of client care, is how do we keep inflammation below the threshold at which it becomes damaging and self-sustaining? The solution may be found within the lymphatic system, our bodies’ mechanism for draining fluids, regenerating tissues, filtering out toxins and foreign substances, and maintaining a healthy immune system.
What Type of Inflammation?
Let’s look at the pathophysiology of inflammation. When addressing inflammation in a client, it is important to know the type of inflammation with which you’re dealing. All inflammations are not created equal, nor are the approaches you’ll take.
Inflammation is a complex, nonlinear process that involves a cascade of events mediated by numerous cells such as mast cells, macrophages, neutrophils, and T- and B-lymphocytes, and molecules such as inflammatory cytokines and free radicals.4
The word inflammation derives from the Latin word inflammo, meaning “I ignite; I set on fire.” Classic signs of the presence of inflammation include heat, redness, swelling, pain and inhibited or lost function. All of these indicators are not necessarily present in every type of inflammation; they are typically more often present when the inflammation is acute and on or very close to the skin.
In 1993, researchers discovered a different type of prolonged, dysregulated inflammatory response that was later termed metaflammation.5 This chronic inflammation differs from classic inflammation in a number of ways.
Chronic Inflammation
Metaflammation is low-grade, causing only a small rise in immune system markers. (In other words, a fourfold to sixfold increase vs. a several hundredfold increase.) It is persistent and results in chronic rather than acute allostasis. It appears to perpetuate rather than resolve disease, and is also associated with a reduced rather than increased metabolic rate.6
Scientific research shows chronic inflammatory processes are implicated in the pathophysiology of a wide range of acute and chronic diseases, including cardiovascular disease7, metabolic syndrome7 and type 2 diabetes8 as well as overall mortality9.
Chronic inflammations are also related to common problems presented by massage clients. These may include local trauma, chronic fascia or musculoskeletal pain, chronic wounds, rheumatologic disorders, asthma, allergy and autoimmune diseases.10
Chronic inflammation can last for several months or several years and will affect your client’s health and well-being. These inflammatory responses need to be reduced on a regular basis. Lymph drainage techniques are at the top of the list of manual approaches that can directly and efficiently decrease chronic tissue inflammations.
The Role of Lymph Drainage
Now let us explore lymph drainage to resolve inflammation. Acute and chronic inflammatory processes usually are associated with the growth or enlargement of lymphatic vessels.11
The initial phase of acute inflammation includes blood vessel vasodilation and consequent fluid leakage to the interstitial compartment. Lymphatic vessel activation limits acute inflammation via promotion of fluid drainage from the skin and reduction of edema formation.
Specifically, lymph drainage can remove fluid, extravasated cells, including neutrophils, macrophages and lymphocytes; and inflammatory factors such as bradykinin, histamine and prostaglandins from the site of inflammation to the lymph nodes and to secondary lymphoid organs.
The lymphatic system thereby contributes to the decrease of inflammatory response. In cases of chronic inflammation, lymphatic vessels help to resolve proinflammatory cells from the site of inflammation.12
As with any technique, contraindications must always be carefully observed. With lymph drainage, this includes acute infectious and early-onset inflammatory disease. Cases of chronic infection or inflammation should be treated with caution since the disease can become reactivated into an acute state.
Edema and lymphedema may be either a good indication for lymphatic drainage or a contraindication, depending on the etiology of the edema, its complications and the therapist’s level of training.
Be Part of the Solution
We know science is uncovering increasingly strong evidence that points to acute and chronic inflammation as being a major constituent of disease. We also know lymphatic drainage is instrumental in limiting these detrimental inflammatory processes.
Contraindications withstanding, the gentle strokes of lymphatic drainage therapy attenuate local edema, inflammation and pain without irritating or re-traumatizing the tissue.
With proper training, therapists can easily and effectively incorporate lymph drainage techniques into their practice regimen for numerous kinds of acute, chronic and low-grade inflammation.
The award-winning research of Bruno Chikly, M.D., D.O., led to important innovations in the development of lymphatic drainage therapy. He is the founder of the Chikly Health Institute, which offers lymphatic drainage therapy and brain workshops worldwide.
Footnotes
1. Vodovotz, Y., Constantine, G., Rubin J., Csete, M., Voit, E.O., An G. “Mechanistic simulations of inflammation: Current state and future prospects,” Mathematical Biosciences. 2009; 217:1–10.
2. Vincent, J.L., Ferreira, F., Moreno, R. “Scoring systems for assessing organ dysfunction and survival,” Critical Care Clinics. 2000; 16:353–366.
3. Rosenberg, A.L. “Recent innovations in intensive care unit risk-prediction models,” Current Opinion in Critical Care. 2002; 8:321–330.
4. Brown, K.L., Cosseau, C., Gardy, J.L., Hancock, R.E. “Complexities of targeting innate immunity to treat infection,” Trends in Immunology. 2007; 28:260–266.
5. Hotamisligil, G.S., Shargill, N.S., Spiegelman, B.M. “Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance,” Science. 1993; 259(5091):87-91.
6. Egger, G. “In Search of a Germ Theory Equivalent for Chronic Disease,” Preventing Chronic Disease. 2012; 9:E95.
7. Ridker, P.M., Buring, J.E., Cook, N.R., Rifai, N. “C-reactive protein, the metabolic syndrome, and risk of incident cardiovascular events: An 8-year follow-up of 14,719 initially healthy American women,” Circulation. 2003; 107:391–397.
8. Pradhan, A.D., Manson, J.E., Rifai, N., Buring, J.E., Ridker, P.M. “C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus,” Journal of the American Medical Association. 2001; 286:327–334.
9. Jenny, N.S., et al. “Inflammation biomarkers and near-term death in older men,” American Journal of Epidemiolgy. 2007; 165:684–695.
10. Mathur, N., Klarlund, Pedersen B., “Exercise as a Mean to Control Low-Grade Systemic Inflammation,” Mediators of Inflammation. 2008; 2008:109502.
10. Halin, C., Detmar, M. “Inflammation, angiogenesis, and lymphangiogenesis,” Methods in Enzymology. 2008; 445:1–25.
12. Huggenberger, R., et al. Blood. 2011, April 28; 117(17).