From stretching to disc herniation to adjustments, it’s all chemical generation and reaction
The theme of this article runs contrary to the thinking of many chiropractors. We are trained to think structurally and mechanically, without consideration for local chemical changes.
This perspective is supported by three incorrect musculoskeletal mantras that have persisted for many years:
- Annular fibers in the disc are damaged by compressive loading, which leads to circumferential tears that coalesce to form radial fissures, through which nuclear material migrates and herniates;
- Osteoarthritis is a wear-and-tear condition;
- Tendinosis is a degenerative non-inflammatory condition caused by excessive loading.
The above three views are incorrect. In order to understand the accurate view, it is helpful to appreciate that our structure and so–called “mechanical” tissues are made of chemistry. They are chemical tissues that move, and this should not be misperceived as a semantic argument.
Chemistry generation is produced in our nervous and muscular systems, which then allows for the movement of our chemical tissues, which subsequently leads to the creation of more chemistry. By appreciating these facts of physiology, it will become clear how disc herniation, osteoarthritis and tendinosis are chemical events, and help us understand why certain patients do not respond to chiropractic care.
Mechanics is chemistry in motion
Mechanics as a chemical event is rarely considered. One author even went so far as to write an article entitled, “Mechanics rules biology.” This makes no sense, as our musculoskeletal tissues are made of chemistry — proteins, fats, carbohydrates, hydrogen and oxygen (water), and vitamins and minerals. This undeniable fact of anatomy demands that we stop thinking that body mechanics is distinct from body chemistry.
Is there evidence that movement creates chemistry? In fact, we know that if fibroblasts are stretched, they release a host of chemical mediators, the degree of which is related to the intensity of the stretching ,. In the laboratory, when human subjects generated plantar flexion contractions commensurate with the force generated during normal walking, chemical mediator release has been identified via a dialysate collected in real time.
The notion that immune system activation with redness, swelling and heat is required for pain to manifest with inflammation is completely false. Fibroblasts are capable of promoting chronic inflammation without the cardinal signs of inflammation. In fact, fibroblasts regulate inflammation and can promote chronic inflammation. ,
Since we are made of chemistry, the process of healing and disease is determined by the degree to which our body is in an anti-inflammatory or pro-inflammatory state. The latter is associated with the expression of all chronic diseases, including musculoskeletal conditions such as disc herniation, osteoarthritis and tendinosis.
Disc herniation
Normally the nucleus pulposis bears the compressive load and redistributes it circumferentially, such that the annulus normally deals almost exclusively with tensile loads. Disc herniation begins when the vertebral endplate is damaged, which can set in motion a series of events that activate matrix metalloproteinases (MMPs), which are enzymes that degrade connective tissue, such as the nucleus and annulus.
This “digestive” process can stop at any point, via the activation of tissue inhibitors of metalloproteinases (TIMP). However, if MMP activity persists, the nucleus will continue to degrade, rendering it no longer able to properly deal with compressive loading.
After the nucleus is degraded, the annulus is digested next. Radial fissures begin at the nucleus and annulus interface, and progressive MMP activity leads to the formation of a radial fissure that extends from the nucleus into the annulus, which can ultimately progress to frank herniation. This sequence of events has been known for well over 25 years. Without knowing this sequence, the end-stage pathology of disc herniation can create a pathoanatomical illusion that suggests an annular tear led to a radial fissure, which is physiologically impossible.
To help put this chemical view of disc herniation into proper perspective, consider that patients with metabolic syndrome and Type 2 diabetes are more likely to herniate compared to normal individuals. The reason is because the pro-inflammatory state of these conditions involves less activity of TIMPs and therefore a lack of MMP inhibition. This allows for MMPs to progressively degrade the nucleus and then, annulus, creating the illusion that it was a mechanical process.
Osteoarthritis ‘wear and tear?’
It is rare for a patient to have only one joint that is painful that was caused by a traumatic event, such as a sporting injury, which is known as post-traumatic osteoarthritis (OA).
While post-traumatic OA represents about 10 percent of all cases, clinicians should readily recall that most of their patients with OA have pain in joints that were not overtly traumatized. These painful joints are perceived as becoming painful due to wear and tear over time, which is viewed as a purely mechanical scenario, without consideration for chemical involvement.
It is well known that chemical changes occur in OA joints before they manifest OA symptoms. For example, lipid deposition in joints occurs early in the OA process, before histological changes, which is why researchers view OA as an atheromatous-like disease. From a practical clinical perspective, the chemistry of OA is essentially the same as coronary atherosclerotic disease. ,
Tendinosis and inflammation
When the term tendinosis was introduced, it was described as a non-inflammatory degenerative process in tendons. The argument was that it was not an inflammatory or chemical problem because the cardinal signs of inflammation were not present and histological specimens did not reveal in increased population of immune cells. This perception about inflammation and chemical changes is completely inaccurate, as tendon fibroblasts called tenocytes can participate in tendon inflammation, degeneration and pain. ,
In 2007 I described how tendinosis absolutely must have an inflammatory component, as degeneration and pain require chemical changes in local tissues for them to function as pain generators. “Mechanical” thinkers rejected this as a fanciful notion on my part — they were wrong. It turns out that scientists now refer to tendinosis as a myth, because it, in fact, is associated with chronic inflammation. 14
Tendinopathy researchers are also urging us to now view it as a cardiovascular disease in tendons, and so should be treated from this perspective as well as with local therapy considerations. Just like vascular disease, tendinopathy manifests pathoanatomically, but asymptomatically, in the aging and overweight population. For example, men over 40 years of age with a waistline above 33 inches are more likely to have asymptomatic tendinopathy compared to their leaner counterparts. This means that when local treatments are unsuccessful, the inflammatory state of the patient must be considered. 7,
Treatments from a chemical view
Patients do not respond uniformly to adjustments and other treatments. Some respond as hoped, some respond less well, and some do not respond at all. Why is this? What do you do in your practice when patients do not respond as hoped?
If you view the body as a structural system, it will inevitably be very difficult to come up with an answer. To understand why patients do not always respond to various treatments that should otherwise be effective, we need to embrace a chemical view.
Since patients are made of chemistry, any treatment will have a chemical effect. When symptoms change after a treatment, it is because you changed that patient’s body chemistry. When patients do not respond to various treatments, that tells us that we are not able to adequately improve their body chemistry. When you encounter these patients, and there are lots of them, four main considerations should enter your mind: too much stress, lack of sleep, lack of fitness, and a pro-inflammatory diet. One or more of these pro-inflammatory factors will be present and needs to be addressed.
DAVID R. SEAMAN, DC, MS, DABCN, is professor of clinical sciences at National University of Health Sciences in St. Petersburg, Fla. He can be contacted at docseaman@mac.com or through nuhs.edu.
