January 2019

The Invisible Effect of Body Weight on Tendons

iStockphoto.com 1044399170

While the predominant view on the relationship between an elevated body weight and its effect on tendons, muscles, bones, and joints is grounded in the physical stress effects of body weight, the role of inflammation is becoming better understood.

By Robert Creighton, DPM

While the amount of body weight being physically applied to tendons, muscles, bones, and joints is certainly a factor in the development of a tendonitis, there are other consequences from excess abdominal fat on the health of the musculoskeletal system. Excess abdominal fat is not simply a storage depot of excess calories from overeating: There are inflammation-producing consequences that must be considered.

Body mass index (BMI) is a common measure of body fat based on height and weight; however, BMI by itself is not necessarily a reliable measure of a person’s metabolic health or their level of inflammation. Simply having an elevated BMI does not mean a person will automatically have chronic inflammation. There are many muscular people with an elevated BMI who are perfectly healthy. Indeed, waist circumference may be a better reflection of the volume of health-damaging visceral fat a person may have compared to BMI.1

Visceral fat is the deep fat found in the abdominal midsection; when excessive, it contributes to what is sometimes described as “central obesity.” Visceral fat may act as an overactive hormone-producing organ that promotes chronic inflammation through the production of signaling molecules that are sent throughout the body via the bloodstream. The systemic inflammation promoted by accumulated visceral fat can negatively affect any tendon, muscle, bone, or joint and its ability to heal promptly and efficiently.

Figure 1. Prevalence of metabolic syndrome among US adults, National Health and Nutrition Examination Survey (NHANES), 1988–2012. Metabolic syndrome was defined by using the criteria agreed to jointly by the International Diabetes Federation; the National Heart, Lung, and Blood Institute in the United States; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Abbreviation: SE, standard error. Reprinted from reference 4.

When excess fat becomes inflammation-producing, the term adiposopathy has been proposed (see Adiposopathy Defined, page 42).2,3 This term describes the ill-health from sick fat. While the damage caused by sick abdominal fat (think inflammation and disease) has been more fully investigated in the context of cardiovascular disease,3 we are beginning to understand its role in the health and potential disability of tendons, muscles, bones, and joints.

Systemic inflammation and the metabolic syndrome

So-called sick fat is closely associated with metabolic syndrome, a cluster of cardiometabolic risk factors associated with increased risk of multiple chronic diseases, including cancer, diabetes, and cardiovascular disease.4 According to the most recent report from the Centers for Disease Control and Prevention on the prevalence of metabolic syndrome, more than a third of all US adults met the definition and criteria for metabolic syndrome. The researchers found that prevalence increased from 25.3% in 1988 to 34.2% in 2012 (Figures 1 and 2), the most recent year for which data is available.

Earlier researchers had found that approximately 25% of people age 40–49, 35% of people age 50–59, and 43% of those over 60 years of age had some level of inflammation caused by the waistline fat that occurs in metabolic syndrome.5 This means nearly 25% to 45% of the adult population is chronically inflamed. Using cardiovascular study results, still other researchers found that while the average middle-aged American is moderately inflamed, approximately 25% of the US population has high levels of chronic inflammation.6

Chronic systemic inflammation and tendon problems

The inflammation brought about by a poor metabolism promotes several medical challenges, not the least of which are pain and negative effects on muscles and tendons.

Figure 2. Prevalence of metabolic syndrome among US adults over time by race/ethnicity–sex and age group, National Health and Nutrition Examination Survey (NHANES), 1988–2012. Metabolic syndrome was defined by using the criteria agreed to jointly by the International Diabetes Federation; the US National Heart, Lung, and Blood Institute in the United States; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Abbreviation: SE, standard error. Reprinted from reference 4.

One study looking at the patellar tendon suggested waist girth not only has a biomechanical influence on the development of knee pain in volleyball players, but a biochemical one as well.7 Other research has shown that Achilles tendon8 and elbow tendon9 problems are associated with metabolic syndrome and, generally speaking, local and widespread musculoskeletal pains are more common in patients with metabolic syndrome.10-12

The emerging belief is that the chronic low-grade systemic inflammatory environment as a result of metabolic syndrome becomes superimposed over areas of strain or injury, reducing tissue healing and/or perpetuating ongoing discomfort.13

This line of thinking is also supported in a study published in Arthritis & Rheumatology, where the investigators examined the relationships between fat mass, muscle mass, fat/muscle mass ratio, metabolic syndrome, and musculoskeletal (tendon/muscle/bone/joint) pain in a community of more than 1,500 adults.14 They found that total fat mass and fat/muscle ratio were significantly and positively associated with musculoskeletal pain among females. Widespread pain was more prevalent among those with metabolic syndrome in both normal- and high-BMI subjects, especially among females. Widespread pain was significantly associated with a high fat/muscle ratio after adjusting for confounding variables. The authors concluded that understanding the relationship between fat mass and pain may provide insights into preventative measures and therapeutic strategies for musculoskeletal pain.14

While accumulation of excess fat at the midsection is known to be harmful to tendons, it is unlikely that increased loading by itself sufficiently explains the development of tendon problems in many people. Notably, Gaida and colleagues observed that lipid deposition occurs in tendons, high cholesterol levels have been found among individuals with Achilles tendon rupture, and biopsies from Achilles tendinopathy patients have elevated esterified fractions of cholesterol.8

Many are now wondering whether increased physical load from a high BMI is the main cause of tendon problems, or are the local and/or systemic influences of body fat on tendons making tendons more vulnerable? Researchers are just now beginning to examine the effects of certain diets on tendon, muscle, bone, and joint pain. Scott and colleagues argue that excessive blood lipids may be an important factor for future clinical investigations.15

In many cases, it is likely there is a pro-inflammatory metabolic component to tendon problems and other musculoskeletal conditions associated with an elevated BMI. In other words, the structural anatomy, and thus, the integrity of the musculoskeletal system, is altered by inflammation-producing body fat buildup at the waistline, which may make one more susceptible to injury from the increased stress being applied by increased body weight. It has been suggested that, just as in cardiovascular disease, the mitigation of cardiometabolic risk factors that result from weight loss may benefit diseases of the tendons, muscles, bones, and joints beyond the reduced mechanical physical load.

Explaining the role of invisible inflammation promoted by excess body fat on tendons, muscles, bones, and joints to overweight patients with chronic tendinopathies may help them better understand the need to reduce their waistline and improve their body composition.

Robert Creighton, DPM, is a podiatrist and foot surgeon in Tampa Bay, Florida. He is also a ACSM certified personal trainer and publisher/editor at Nutrientology (http://nutrientology.com). An earlier version of this article appeared on his blog there.

Adiposopathy Defined: An Excerpt

“Adiposopathy is a disease characterised by pathogenic adipose tissue that is promoted by positive caloric balance and sedentary lifestyle in genetically and environmentally susceptible patients. Adiposopathy is anatomically manifested by adipocyte hypertrophy, visceral adiposity and/or ectopic fat deposition, which physiologically results in adverse endocrine and immune consequences leading to metabolic disease. During positive caloric balance, initial adipocyte hypertrophy optimally signals the recruitment, proliferation and differentiation of additional adipocytes in order to store energy (as fat) while maintaining normal adipose tissue functionality. However, if excessive fat cell enlargement occurs, such as when adipogenesis is impaired, then derangements of adipocyte and adipose tissue metabolic and immune responses may lead to metabolic disease.

“Anatomic manifestations of adiposopathy include adipocyte hypertrophy and visceral adiposity, which may lead to pathogenic metabolic and immune responses that promote metabolic disease. Positive caloric balance results in increased energy storage, which is initially manifested by mild adipocyte hypertrophy. This normally promotes paracrine signaling for adipogenesis (recruitment of new fat cells). Particularly when adipogenesis is impaired, continued positive caloric balance may worsen adipocyte hypertrophy, causing adipocytes to become dysfunctional and potentially pathogenic. Similarly, if excessive calories are stored in the visceral region, then this also is potentially pathogenic, and promotes metabolic disease. Excessive body fat may not be ‘healthy’ because of pathologic mass effects. However, accumulation of adipose tissue through adipocyte proliferation in the subcutaneous peripheral region may have less potential for promotion of metabolic disease, and may therefore be metabolically ‘healthier’. If during weight loss, subcutaneous peripheral adipose tissue is diminished and the proportion of visceral adipose tissue is increased, then this can also result in adiposopathy and promote metabolic disease, as is found with some cases of hypercortisolaemia and human immunodeficiency virus‐associated lipodystrophy.”

Reproduced from Int J Clin Pract. 2008;62(10):1474-83, with permission of John Wiley & Sons.

REFERENCES
  1. Nazare JA, Smith J, Borel AL, et al. Usefulness of Measuring Both Body Mass Index and Waist Circumference for the Estimation of Visceral Adiposity and Related Cardiometabolic Risk Profile (from the INSPIRE ME IAA Study). Am J Cardiol. 2015;115(3):307-315.
  2. Bays HE, González-Campoy JM, Bray GA, et al. Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity. Expert Rev Cardiovasc Ther. 2008;6(3):343-68.
  3. Bays HE, González-Campoy JM, Henry RR, et al. Is adiposopathy (sick fat) an endocrine disease? Int J Clin Pract. 2008 Oct;62(10):1474-83.
  4. Moore JX, Chaudhary N, Akinyemiju T. Metabolic Syndrome Prevalence by Race/Ethnicity and Sex in the United States, National Health and Nutrition Examination Survey, 1988–2012. Prev Chronic Dis 2017;14:160287.
  5. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults. Findings from the third national health and nutrition survey. JAMA. 2002;87(3):356-359.
  6. Pidker PM. C-Reactive Protein: A simple test to help predict risk of heart attack and stroke. Circulation. 2003;108:e81-e85.
  7. Malliaras P, Cook JL, Kent PM. Anthropometric risk factors for patellar tendon injury among volleyball players. Br J Sports Med. 2007;41(4):259-63.
  8. Gaida JE, Alfredson L, Kiss ZS, Wilson AM, Alfredson H, Cook JL. Dyslipidemia in Achilles tendinopathy is characteristic of insulin resistance. Med Sci Sports Exerc. 2009;41(6):1194-7.
  9. Shiri R, Viikari-Juntura E, Varonen H, Heliövaara M. Prevalence and determinants of lateral and medial epicondylitis: A population study. Am J Epidemiol. 2006;164(11):1065-1074.
  10. Mäntyselkä P, Miettola J, Niskanen L, Kumpusalo E. Persistent pain at multiple sites–connection to glucose derangement. Diabetes Res Clin Pract. 2009;84(2):e30-2.
  11. Mäntyselkä, J. Miettola, L. Niskanen, E. Kumpusalo. Glucose regulation and chronic pain at multiple sites. Rheumatology. 2008;47(8):1235–1238.
  12. Afifi AEA, Shaat RM, Gharbia OM, Boghdadi YE, Eshmawy MME, El-Emam OA. Osteoarthritis of knee joint in metabolic syndrome. Clin Rheumatol. 2018;37(10):2855-2861.
  13. Berenbaum F. Osteoarthritis as an inflammatory disease (osteoarthritis is not osteoarthrosis!). Osteoarthritis and Cartilage. 2013;21(1):16-21.
  14. Yoo JJ, Cho NH, Lim SH, Kim HA. Relationships between body mass index, fat mass, muscle mass, and musculoskeletal pain in community residents. Arthritis & Rheumatology. 2014;66(12):3511-3520.
  15. Scott A, Zwerver J, Grewal N, et al. Lipids, adiposity and tendinopathy: is there a mechanistic link? Critical review. Br J Sports Med. 2015;49(15):984-8.
(Visited 1 times, 1 visits today)

Leave a Reply

Your email address will not be published. Required fields are marked *

Spam Blocker * Time limit is exhausted. Please reload CAPTCHA.