Your Tendons on Cake

 


Take Home Points…

  1. Long-term dietary behaviors play a pivotal role in maintaining healthy tendons
  2. People with diabetes are prone to poor tendon health due to accumulation of advanced glycation end products, collagen cross links, inflammation and oxidative damage
  3. Higher average blood glucose levels, still considered in the normal range, are associated with other chronic diseases and increased risk for rotator cuff tendon tears
  4. High body fat percentage, particularly abdominal fat, is associated with developing degenerative tendinopathies
  5. The non-diabetic population can likely improve tendon-health by improving their glycemic control
  6. Other foods added to a lower-carbohydrate diet may improve tendon health including turmeric, green tea, and glycine-rich foods

This was written in 2015. I will try to update this post if new information comes out since this was written, but please be aware that this a information may become outdated before I am able to do so.

Tendinopathy

Tendinopathy (a chronic tendon injury characterized by degenerative tissue, pain and impaired performance) is one of the most common problems managed in sports medicine. It causes mobility deficits, pain, and decreased performance.  Degenerative tendonopathy presents in a wide variety of individuals from highly active athletes to the more sedentary population. It is accumulative and can eventually progress to complete tendon ruptures. I feel strongly that we should be considering preventative lifestyle strategies due to a paucity of highly effective treatment options. Mechanical loads and genetics are important contributors in the pathophysiology of the degeneration of connective tissues. There appears to be an equally important systemic input that is often neglected in the context of tendon health.

Tendon tissue consists of tendon cells (tenocytes) and extracellular matrix (ECM). Tendon ECM consists of Type 1 collagen, proteoglycans, and glycosaminoglycans and contributes greatly to tendon biomechanical properties [1]. The ECM is continuously remodeled and an equilibrium between synthesis and degradation is achieved when in homeostasis (healthy) [2]. Much like bone, mechanical forces are necessary to maintain homeostasis [3, 4] and tendons that experience higher mechanical loads experience accelerated ECM turnover [3, 5]. Aberrant ECM turnover likely contributes to the progression of chronic tendinopathies [6]. Though stem cells have been demonstrated [7], tendons lack the same degree of regenerative capacity that is present in many other tissues. Highly active individuals experience accelerated ECM turnover in a tissue that has a lower regenerative capacity and is continuously exposed to the body’s extracellular fluids. This vulnerability to accumulative damage highlights the importance of maintaining long-term homeostasis in tendon tissue.

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The mechanisms contributing to the development of tendinopathies are poorly understood. In degenerative tendon tissue the ECM becomes disorganized with less parallel structure of collagen, and has changes in the proteoglycan content with increased blood vessel growth (neovascularization) [8, 9]. It is a common assumption that inflammation’s role in tendinopathy is minimal, though this is now being re-evaluated as it likely does contribute to the degenerative process [10].

Now we will discuss some dietary interventions that likely improve tendon health by helping to slow degenerative change.

1.) Low carbohydrate diet (Low blood glucose / insulin levels)

Diabetes is an independent risk factor for degenerative tendon pathology. Tendons of diabetics are thicker, have more disorganized ECM, and more aberrant calcification which increases the risk of tears [11-14]. The tendons are mechanically different with increased stiffness and decreased elasticity [13, 15, 16]. These differences appear to stem from chronic hyperglycemia which leads to an accelerated accumulation of advanced glycation endproducts (AGE’s), collagen cross links and elevated systemic inflammation with oxidative stress [17, 18]. The heightened inflammatory state further accelerates collagen cross linking in a feed forward cycle of damage [19].

Tendon ECM remodeling is also significantly altered by a hyperglycemic environment [15]. Consistently elevated glucose concentration appears to up-regulate certain proteins involved in ECM turnover (matrix metalloproteinases) [20] which may push the equilibrium more towards degradation further contributing to damage.

AGE-mediated collagen cross links negatively impact tendon biomechanics [21] and tendon stiffness is increased proportional to the amount of accumulated cross links [22-24]. Tendons of diabetics also have reduced proteoglycan levels which likely alters biomechanical properties even further [25]. This process appears to be independent of AGE accumulation, supporting the idea that there are multiple pathways through which consistent hyperglycemia can impact tendon.

You don’t have to have to meet the diagnostic criteria for diabetes to have elevated serum AGE levels [26, 27] and AGE accumulation is important in the development of many other chronic diseases. A recent study demonstrated that higher average blood glucose levels, still below the diabetic range, were associated with increased risk for dementia [28]. Elevated serum levels of AGE’s are predictive of all cause mortality, cardiovascular mortality and the severity of coronary artery disease in people without diabetes [29, 30].

A study in the British Journal of Sports Medicine examined fasting glucose levels in a non-diabetic population and its association with rotator cuff tears. They found that patients with statistically higher fasting glucose levels, still within the normal range (defined as <100mg/dL), was a significant risk factor for rotator cuff tears [31].

Reducing simple processed sugar and acellular carbohydrate intake will likely reduce the accumulation of AGE’s and therefore reduce the associated collagen cross linking, inflammation and oxidative damage. Optimizing your fasting blood sugar levels and improving insulin sensitivity, through reduced consumption of highly process carbohydrate, is likely one of the most potent anti-inflammatory ‘medications’ one can take, not to mention with improvements to your gut microbiome adding greater improvements in systemic inflammation levels [32].

What’s the right dose? The healthiest amount of human carbohydrate intake is a source of great contention on the interwebs. For some reason this topic gets people very fired up! Carb intake should be determined on a case-by-case basis, considering many variables such as your carbohydrate sources, activity levels, genetics, stress levels, sleep habits, insulin sensitivity, etc., and more discussion regarding this is beyond the scope of this blog post. The main point here is that the quantity of highly processed carbohydrate and sugar in a standard Western Diet is not just harmful to your cardiovascular and endocrine systems, but likely to your connective tissues as well. This is accelerated by two main systemic inputs as we currently understand it; hyperglycemia and oxidative stress (inflammation) though they are both interrelated. If your glucose levels are in the high-normal range (fasting or postprandial or both), you likely have some room for improvement. This will likely improve your cardiovascular health and the health of your connective tissue which translates to better mobility later in life…and therefore indirectly…cardiovascular health!

2.)  Body composition (especially central adiposity)
There is evidence that higher body fat percentage is an independent risk factor for developing tendinopathies. Waist-to-hip ratios and increased waist circumference [33-35] are associated with tendinopathies independent of diabetes. It is believed that this is due to both increased mechanical loading and a heightened inflammatory state. This is particularly true for abdominal fat deposition [34] and may involve some of the same cytokines that are involved in the associated cardiovascular disease risk [36]. More often than not, central obesity and insulin resistance coincide and likely provide a double hit to connective tissues. Optimizing insulin sensitivity and improving body composition also go hand-in-hand and may go a long way for tendon health.

3.)  Turmeric

turmericCurcumin, the principle curcuminoid of the plant turmeric, has significant antioxidant and anti-inflammatory properties [37] and appears to down regulate genes that are associated with ECM degradation, and apoptosis in human tendon cells [38].  In a hyperglycemic environment, Curcumin can significantly reduce the accumulation of AGE’s and cross links in tendon cells [39]. This likely occurs through reduced oxidative damage as it appears to not improve hyperglycemia. Important to note, Curcumin may be much more effective at preventing AGE accumulation rather than treating AGE’s that already exist [39].

Turmeric is a member of the ginger family and is a commonly used spice in Indian cuisine.  Increasing Turmeric in your diet, or curcumin through supplementation, may slow the accumulation of AGE’s and collagen cross linking over time.  More research is needed to better characterize this relationship, but It tastes great and has minimal downsides. It is important to remember that it is a supplement and not a substitute for a high quality whole food diet with well thought out carbohydrate consumption.


4.) Green Tea

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Green tea (Camellia sinesis) has many anti-inflammatory properties [40, 41] and appears to improve insulin sensitivity [42, 43]. Green tea is also shown to reduce AGE accumulation and cross linking in rat tendon exposed to a hyperglycemic environment [44, 45]. When combined with Glycine (see below), it accelerated ECM remodeling following tendon damage [46]. Green tea is delicious and soothing, so go ahead and use it to wash down that nutrient dense diet. Just avoid the high-sugar versions as consuming these would be missing the point!

5.) Glycine:

bone broth 2Glycine makes up 35% of a collagen molecule and is a non-essential amino acid, meaning that your body can synthesize it.  The body’s ability to make glycine, however,  may not be efficient enough to maintain healthy collagen, so sufficient dietary intake remains important [47]. This may be more important in highly active athletes with larger amounts of ECM turnover. Glycine is also an important modulator of systemic inflammation [48-50]. A higher-glycine diet has been shown to increase tendon glycosaminoglycan content, improve collagen organization, accelerate ECM remodeling, and is associated with improved mechanical properties of the Achilles’ tendon [51].

One of my favorite glycine-rich foods, which is gaining in popularity, is bone broth, oxtail and tendon soups. Bone broth also contains a lot of proline, proteoglycans, glycosaminoglycans, chondroitin and glycoproteins, all compounds that can support healthy connective tissues (52). Even Kobe Bryant consumes bone broth for improved recovery.

I personally like Dr. Colin Champ’s recipe for breakfast found here, and Michele Tam’s slow cooker recipe found here.

Taking it home…
Chronic degenerative tendon injuries are incredibly common and there are many variables contributing to the pathological processes. Bio-mechanics, mobility, muscle strength and endurance, mechanical loading patterns, training regimen, and genetics all contribute. There also appears to be a large systemic component to the pathological process. This input that can be modulated with long term dietary habits, giving practitioners yet another important reason to discuss healthy diet with patients.

Much like many other components of human health, diet is a feed-forward system of dominoes that can fall in the direction of better health if managed well, or in the opposite direction toward chronic disease if managed poorly.  For tendon health, like many other chronic diseases, diet should be considered one of the lead dominoes.

More studies are still needed to better characterize the fascinating relationship between blood sugar levels, AGEs, collagen cross links, ECM turnover and tendon health.

Thanks for reading!

References:

  1. Nourissat, G., F. Berenbaum, and D. Duprez, Tendon injury: from biology to tendon repair. Nat Rev Rheumatol, 2015. 11(4): p. 223-233.
  2. Rees, S.G., et al., Catabolism of aggrecan, decorin and biglycan in tendon. Biochemical Journal, 2000. 350(Pt 1): p. 181-188.
  3. Heinemeier, K., Kjaer, M. , In vivo investigation of tendon responses to mechanical loading. Journal of musculoskeletal & neuronal interactions, 2011. 11(2): p. 115-23.
  4. Humphrey, J.D., E.R. Dufresne, and M.A. Schwartz, Mechanotransduction and extracellular matrix homeostasis. Nature reviews. Molecular cell biology, 2014. 15(12): p. 802-812.
  5. Shwartz, Y., E. Blitz, and E. Zelzer, One load to rule them all: Mechanical control of the musculoskeletal system in development and aging. Differentiation, 2013. 86(3): p. 104-111.
  6. Karousou, E., et al., Collagens, Proteoglycans, MMP-2, MMP-9 and TIMPs in Human Achilles Tendon Rupture. Clinical Orthopaedics and Related Research, 2008. 466(7): p. 1577-1582.
  7. Salingcarnboriboon, R., et al., Establishment of tendon-derived cell lines exhibiting pluripotent mesenchymal stem cell-like property. Experimental Cell Research, 2003. 287(2): p. 289-300.
  8. Sharma, P. and N. Maffulli, Tendon Injury and Tendinopathy: Healing and Repair. Vol. 87. 2005. 187-202.
  9. Åström, M. and A. Rausing, Chronic Achilles Tendinopathy: A Survey of Surgical and Histopathologic Findings Mats. Clinical Orthopaedics and Related Research, 1995. 316: p. 151-164.
  10. Rees, J.D., M. Stride, and A. Scott, Tendons – time to revisit inflammation. British Journal of Sports Medicine, 2014. 48(21): p. 1553-1557.
  11. Akturk, M., et al., Thickness of the Supraspinatus and Biceps Tendons in Diabetic Patients. Diabetes Care, 2002. 25(2): p. 408.
  12. Jim, Y., et al., Coexistence of calcific tendinitis and rotator cuff tear: an arthrographic study. Skeletal Radiology, 1993. 22(3): p. 183-185.
  13. Akturk, M., et al., Evaluation of Achilles Tendon Thickening in Type 2 Diabetes Mellitus. Exp Clin Endocrinol Diabetes, 2007. 115(02): p. 92-96.
  14. Grant, W.P., et al., Electron microscopic investigation of the effects of diabetes mellitus on the Achilles tendon. The Journal of Foot and Ankle Surgery, 1997. 36(4): p. 272-278.
  15. Reddy, G.K., L. Stehno-Bittel, and C.S. Enwemeka, Glycation-Induced Matrix Stability in the Rabbit Achilles Tendon. Archives of Biochemistry and Biophysics, 2002. 399(2): p. 174-180.
  16. de Oliveira, R., et al., Mechanical Properties of Achilles Tendon in Rats Induced to Experimental Diabetes. Annals of Biomedical Engineering, 2011. 39(5): p. 1528-1534.
  17. Kislinger, T., et al., N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene Expression. Journal of Biological Chemistry, 1999. 274(44): p. 31740-31749.
  18. Sybille Franke, M.S., Christiane Rüster, Tzvetanka Bondeva, Julia Marticke, Gunther Hofmann, Gert Hein, and Gunter Wolf, Advanced glycation end products induce cell cycle arrest and proinflammatory changes in osteoarthritic fibroblast-like synovial cells. Arthritis Research & Therapy, 2009. 11(R136).
  19. Abate, M., et al., Occurrence of tendon pathologies in metabolic disorders. Rheumatology, 2013. 52(4): p. 599-608.
  20. Tsai, W.-C., et al., High glucose concentration up-regulates the expression of matrix metalloproteinase-9 and -13 in tendon cells. BMC Musculoskeletal Disorders, 2013. 14: p. 255-255.
  21. Menzel, E.J. and R. Reihsner, Alterations of biochemical and biomechanical properties of rat tail tendons caused by non-enzymatic glycation and their inhibition by dibasic amino acids arginine and lysine. Diabetologia, 1991. 34(1): p. 12-16.
  22. Andreassen, T.T., H. Oxlund, and C.C. Danielsen, The Influence of Non-Enzymatic Glycosylation and Formation of Fluorescent Reaction Products on the Mechanical Properties of Rat Tail Tendons. Connective Tissue Research, 1988. 17(1): p. 1-9.
  23. Andreassen, T.T., K. Seyer-Hansen, and A.J. Bailey, Thermal stability, mechanical properties and reducible cross-links of rat tail tendon in experimental diabetes. Biochimica et Biophysica Acta (BBA) – General Subjects, 1981. 677(2): p. 313-317.
  24. Reddy, G.K., Cross-Linking in Collagen by Nonenzymatic Glycation Increases the Matrix Stiffness in Rabbit Achilles Tendon. Experimental Diabesity Research, 2004. 5(2): p. 143-153.
  25. Burner T, G.C., Mitton-Fitzgerald E, Rosenthal AK., Hyperglycemia Reduces Proteoglycan Levels in Tendons. Connective Tissue Research, 2012. 53(6): p. 535-41.
  26. Tan, K.C.B., et al., Serum advanced glycation end products (AGEs) are associated with insulin resistance. Diabetes/Metabolism Research and Reviews, 2011. 27(5): p. 488-492.
  27. Takahiro Yoshikawa, A.M., Shigeo Fujimoto, Decrease in serum levels of advanced glycation end-products by short-term lifestyle modifi cation in non-diabetic middle-aged females Med Sci Monit, 2009. 15(6): p. 65-73.
  28. Crane, P.K., et al., Glucose Levels and Risk of Dementia. New England Journal of Medicine, 2013. 369(6): p. 540-548.
  29. Semba, R.D., et al., Advanced glycation end products and their circulating receptors predict cardiovascular disease mortality in older community-dwelling women. Aging clinical and experimental research, 2009. 21(2): p. 182-190.
  30. Kanauchi, M., N. Tsujimoto, and T. Hashimoto, Advanced Glycation End Products in Nondiabetic Patients With Coronary Artery Disease. Diabetes Care, 2001. 24(9): p. 1620-1623.
  31. Longo, U.G., et al., Higher fasting plasma glucose levels within the normoglycaemic range and rotator cuff tears. British Journal of Sports Medicine, 2009. 43(4): p. 284-287.
  32. Spreadbury, I., Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 2012. 5: p. 175-189.
  33. Gaida, J., et al., Are unilateral and bilateral patellar tendinopathy distinguished by differences in anthropometry, body composition, or muscle strength in elite female basketball players? British Journal of Sports Medicine, 2004. 38(5): p. 581-585.
  34. Malliaras, P., J.L. Cook, and P.M. Kent, Anthropometric risk factors for patellar tendon injury among volleyball players. British Journal of Sports Medicine, 2007. 41(4): p. 259-263.
  35. Visnes, H. and R. Bahr, Training volume and body composition as risk factors for developing jumper’s knee among young elite volleyball players. Scandinavian Journal of Medicine & Science in Sports, 2013. 23(5): p. 607-613.
  36. Park, H.S., J.Y. Park, and R. Yu, Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-α and IL-6. Diabetes Research and Clinical Practice. 69(1): p. 29-35.
  37. Reddy, A.C.P. and B. Lokesh, Studies on the inhibitory effects of curcumin and eugenol on the formation of reactive oxygen species and the oxidation of ferrous iron. Molecular and Cellular Biochemistry, 1994. 137(1): p. 1-8.
  38. Buhrmann, C., et al., Curcumin Modulates Nuclear Factor κB (NF-κB)-mediated Inflammation in Human Tenocytes in Vitro: ROLE OF THE PHOSPHATIDYLINOSITOL 3-KINASE/Akt PATHWAY. Journal of Biological Chemistry, 2011. 286(32): p. 28556-28566.
  39. Sajithlal, G.B., P. Chithra, and G. Chandrakasan, Effect of curcumin on the advanced glycation and cross-linking of collagen in diabetic rats. Biochemical Pharmacology, 1998. 56(12): p. 1607-1614.
  40. Adcocks, C., P. Collin, and D.J. Buttle, Catechins from Green Tea (Camellia sinensis) Inhibit Bovine and Human Cartilage Proteoglycan and Type II Collagen Degradation In Vitro. The Journal of Nutrition, 2002. 132(3): p. 341-346.
  41. Ahmed, S., et al., Green tea polyphenol epigallocatechin-3-gallate inhibits the IL-1β-induced activity and expression of cyclooxygenase-2 and nitric oxide synthase-2 in human chondrocytes. Free Radical Biology and Medicine, 2002. 33(8): p. 1097-1105.
  42. Wu, L.-Y., et al., Effect of Green Tea Supplementation on Insulin Sensitivity in Sprague−Dawley Rats. Journal of Agricultural and Food Chemistry, 2004. 52(3): p. 643-648.
  43. Kobayashi, Y., et al., Green Tea Polyphenols Inhibit the Sodium-Dependent Glucose Transporter of Intestinal Epithelial Cells by a Competitive Mechanism. Journal of Agricultural and Food Chemistry, 2000. 48(11): p. 5618-5623.
  44. Babu, P.V.A., K.E. Sabitha, and C.S. Shyamaladevi, Effect of green tea extract on advanced glycation and cross-linking of tail tendon collagen in streptozotocin induced diabetic rats. Food and Chemical Toxicology, 2008. 46(1): p. 280-285.
  45. Rutter, K., et al., Green Tea Extract Suppresses the Age-Related Increase in Collagen Crosslinking and Fluorescent Products in C57BL/6 Mice. International journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition, 2003. 73(6): p. 453-460.
  46. Vieira, C.P., et al., Green tea and glycine aid in the recovery of tendinitis of the Achilles tendon of rats. Connective Tissue Research, 2015. 56(1): p. 50-58.
  47. Enrique Melendez-Hevia, P.D.P.-L., Athel Cornish-Bowden and Maria Luz Cardenas, A weak link in metabolism: the metabolic capacity for glycine biosynthesis does not satisfy the need for collagen synthesis. J. Biosci, 2009. 34: p. 853-872.
  48. Hartog, A., et al., Anti-inflammatory effects of orally ingested lactoferrin and glycine in different zymosan-induced inflammation models: Evidence for synergistic activity. International Immunopharmacology, 2007. 7(13): p. 1784-1792.
  49. Wheeler, M.D., et al., Glycine: a new anti-inflammatory immunonutrient. Cellular and Molecular Life Sciences CMLS, 1999. 56(9-10): p. 843-856.
  50. Stoffels, B., et al., Anti-inflammatory role of glycine in reducing rodent postoperative inflammatory ileus. Neurogastroenterology & Motility, 2011. 23(1): p. 76-e8.
  51. Vieira, C.P., et al., Glycine Improves Biochemical and Biomechanical Properties Following Inflammation of the Achilles Tendon. The Anatomical Record, 2015. 298(3): p. 538-545.
  52. http://www.westonaprice.org/health-topics/why-broth-is-beautiful-essential-roles-for-proline-glycine-and-gelatin/

5 thoughts on “Your Tendons on Cake

  1. Been on strict lchf (<50g/day) for 3 years. Prior to that lived on carbs, sugars & isotonic/soda for 25 year triathlon age group level training & competition including Ironman.

    2 year ago left foot broke down with plantar facsiitis after excessive lsd ultra running (& anti inflammatory meds) and although still on lchf never really got better.

    I'm 52 year old and almost decided will never get better but also thinking how it could har been on lc.
    No… I dont miss them and feel bettet without them.

  2. Great article. I would urge any and all suffering lots of tendinitis and tendonopathies to also look into Ehlers-Danlos Syndrome, especially if you are also pre-diabetic or have any form of dysautonomia, food & drug intolerances/sensitivities, IBS, easy bruising, weak teeth, fallen (or falling) arches, hernias, prolapses, aneurysms and myopia. It is really not rare and is now believed to be as high as 2% of general population (1 in 50 people!) – just rarely diagnosed as doctors have only been told about the grossest signs (super bendiness, frank dislocations, ruptures) of the rarest types. Up to 75% are not getting properly diagnosed. It comes with myriad comorbidities, and often secondary autoimmune disorders which do get diagnosed, masking the underlying connective tissue disorder. I DO agree a low sugar diet is best for everyone, but even more so for those with EDS for all the reasons you mentioned. More info on when to suspect and how to diagnose can be found here: http://ohtwist.com

  3. Hi,

    Thanks for the info. I have been suffering on and off with Achilles tendinitis/tendinopathy for 5 years. I have been vigilant in taking care of it but it has slowed me down a bit (I play rugby, not LSD running). I have a pretty solid diet (not perfect) and have recently started the green tea + glycine. So the point of all this is where can I get a full copy of reference #51. “Glycine Improves Biochemical and Biomechanical Properties Following Inflammation of the Achilles Tendon”

    Thanks,

    Chris

    • Hi Chris,
      Thanks for the comment. You actually need full access to the journal since it is not an open access article.

      The abstract, however, can be found here

      I hope that helps!
      James

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