Body Mass Index and Musculoskeletal Pain: is there a Connection?

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Body Mass Index and Musculoskeletal Pain: is there a Connection?


Body Mass Index and Musculoskeletal Pain: is there a Connection?

David R. Seaman; Chiropractic & Manual Therapies, 2013, 21:15.

Now that I have spent a number of weeks reviewing Dr. Houston’s Functional Medicine approach to cardiovascular disease, let’s get back to more of a structural focus. This article explores the concept that adiposity can act as an overactive immune/endocrine organ that can generate chronic systematic inflammation which then causes physical pain. The objective of this article is to describe how an elevated BMI can be associated with chronic systemic inflammation and pain expression.

The author points out that overweight and obese individuals are more likely to suffer from tension-type or migraine headaches, fibromyalgia, abdominal pain, and chronic widespread pain.

For example: “Studies have implicated an elevated BMI as a promoter of low back pain. Obese subjects with hsCRP levels above 3mg/dL are more likely to report low back pain; compared to obese subjects with normal levels. Studies have also demonstrated that local and widespread musculoskeletal pains are more common in patients with metabolic syndrome.”

All of the following have been found to be more prevalent in people with metabolic syndrome:

Neck pain

Shoulder pain

Achilles, patella, and elbow tendinopathy

Risk of lumbar disc herniation

Low back and radiating pain


The concept is that adiposopathy, or “sick fat”, is associated with a non-resolving systemic inflammation that is a pathophysiologic state that promotes nociception in injured or dysfunctional musculoskeletal tissues and prevents healing and pain resolution.

The author specifically discusses osteoarthritis and that it is still characterized as a non-inflammatory, wear and tear condition; but that evidence over the last several decades has been indicating that it actually is a chronic inflammatory condition similar to the inflammatory chemistry found to cause atherosclerotic vessels.

“As adiposity increases, there is a fundamental change in the metabolic activity of adipose tissue. In lean individuals, adipocytes exert an anti-inflammatory function by releasing adiponectin and anti-inflammatory interleukin-10, which are associated with health promotion and body repair. Adiponectin supports insulin sensitivity and mitochondrial biogenesis in skeletal muscle and interleukin-10 has analgesic and anti-inflammatory immune modulating properties.

In contrast, as adipocytes increase in size, which is associated with an increase in BMI, a metabolic shift can occur in adipose tissue, such that a systemic chronic inflammatory state develops in certain patients. Indeed, circulating inflammatory mediators, such as hsCRP, TNF, and IL-6, were measured in obese individuals and non-obese controls. In obese individuals, an increase in weight, BMI, waist circumference, hip circumference, and waist-hip ratio was correlated to increased levels of inflammatory mediators.

There also is normally a small population of macrophages in lean adipose tissue and they exist in their M2 or non-activated state. However, as adipocytes grow in size, mast cells, lymphocytes, and macrophages can actively enter adipose tissue, which leads to the transformation of macrophages from M2 to the M1 or activated state. This combination of immune cells causes adipose tissue to behave as an overactive immune organ that promotes chronic systemic inflammation.”

Thus, there is a similar pathophysiology behind chronic musculoskeletal pain and cardiovascular disease and most chronic disease states for that matter. Based on this concept, those working in the structural medicine world need to think beyond the musculoskeletal system in their treatment paradigms and help patients make changes in their lifestyle to decrease inflammation to address their pain.