Tissue Recovery

Where Recommendations are Based on Scientific Evidence  
All the explanations and recommendations are based on published research and clinical experiences. You can even click on the references and it will take you to the original abstracts.

If you don’t want to read the scientific explanations documenting why the recommendations are effective, click here on summary which lists an easy way to implement the information.

Osteoarthritis

Science has not been able to explain all aspect of arthritis yet, but we know that systemic low grade inflammation increases joint pain (Fernandes EM, et al, 2007). The inflammatory mediators matrix metalloproteinases (MMPs) promote joint pain by increasing prostaglandin E2, a major pain producing prostaglandin triggered by an increase of the COX2 enzymes. Low grade systemic inflammation may not have any visible signs like a swollen joint, but contributes to pain and tissue degeneration, interfering with healing and normal function. It is a risk factor for most chronic diseases and one way to detect systemic inflammation is by testing the level of C-reactive protein (CRP) one of the inflammatory markers (Haheim LL, et al, 2009). Patients with osteoarthritis and higher levels of highly sensitive C-reactive protein (hs-CRP) experienced more severe pain when compared with patients having lower levels of hs-CRP (Sturmer T, et al, 2004).

Causes of systemic inflammation


Anything that consistently activates the immune system can cause systemic inflammation.

Some of the reasons are chronic bacterial or viral infection, chronic allergies, and gastrointestinal dysfunction caused by food allergies, food sensitivities, pathogens or anti-inflammatory drugs.

Overweight and obesity also increases systemic inflammation (Lee YH, Pratley RE, 2005., Ramano M, et al. 2003., Rexrode KM, et al. 2003., Pannacciulli N, et al. 2001., Visser M, et al. 1999).

A major trigger of inflammation for many people is insulin resistance.


Insulin resistance triggers inflammatory cytokines and has shown to increase C-reactive protein (CRP), one of the inflammatory markers (Clifton PM, 2003., Lee WY, et al. 2004., Wannamethee SG, et al. 2005).

Eating high glycemic index foods, such as foods that elevate the blood sugar high, and not getting enough physical activity make the tissue less sensitive to insulin. The insulin is then not able to transfer the blood sugar into the cells as efficiently as it used to. This is called insulin resistance. There are different degrees of insulin resistance and it develops gradually. Severe insulin resistance leads to type 2 diabetes.

We know that pentosidine, an advanced glycation end product, contribute to the disease process of osteoarthritis and increased pentosidine levels were detected in patients with osteoarthritis
(Senolt L, et al. 2005). Advanced glycation end products are produced when glucose (sugar) reacts with protein causing tissue destruction as in insulin resistance. Advanced glycation end products decrease the proteoglycan synthesis (building material for cartilage) and reduce the maintenance and repair capacity of the cartilage (DeGroot J, et al. 2001).

Glycation contributes to stiffer and more brittle cartilage with advancing age (Verzijl N, et al. 2001).

We know that extracellular superoxide dismutase (SOD) is the major scavenger of free radicals in cartilage and it is decreased in people with osteoarthritis
(Regan E, et al. 2005). Inadequate control of free radicals plays a role in the disease process of osteoarthritis.

We know that science has documented that increased bone formation may protect against cartilage loss
(Wang Y, et al. 2005).

Recommendations

The following describes a sensible and effective approach to support joint health and decrease pain and dysfunction if you are uncomfortable and have some degenerative changes. These suggestions also make sense if you like to do what you can to avoid joint dysfunction and pain in the future.

Follow a low glycemic index diet, high in nutrients with the right ratio of omega 3 to 6 fatty acids. This will help reduce inflammation, increase insulin sensitivity and subsequently help reduce pain and increase your energy.

Research has documented that immune responses to food, food allergies will increase inflammatory markers like CRP, TNF-alpha and erythrocyte sedimentation rate (Karatay S, et al. 2004, Hvatum M, et al. 2006, Hafstrom I, et al. 2001). The same research shows that these inflammatory markers and pain decrease when avoiding the allergy triggering foods. When patients with rheumatoid arthritis were put on a fast followed by a vegetarian diet, they showed significant improvement in number of swollen joints, pain score, duration of morning stiffness, grip strength, erythrocyte sedimentation rate (an inflammatory marker), C-reactive protein (an inflammatory marker), white blood cell count and a health assessment questionnaire score (Kjeldsen-Kragh J, et al. 1991., Muller H, et al. 2001).

While it is not necessary to be a vegetarian it is important to follow a low glycemic index, high nutrient food plan, eliminating certain foods commonly triggering immune responses (allergies). In the book “Effective Nutrition for Effective Healing” you will find explanations and recommendations with references to the research. The book also includes a lot of easy to make recipes, click here.

It is also important to support the joint cartilage and other connective tissue with the right nutrients.


Joint cartilage is made up of cells called chondrocytes, which are surrounded by extracellular matrix. The matrix is made up of collagen and proteoglycan. Synovial fluid provides lubrication of the joint. One of the constituent of synovial fluid is lubricin, which is also made up of proteoglycan.

Glucosamine sulfate
Glucosamine sulfate has shown to cause a significant stimulation of proteoglycan production by chondrocytes from human osteoarthritic cartilage (Bassleer C, et al. 1998).

Glucosamine sulfate has been documented to also inhibit the production and enzymatic activity of matrix-degrading MMP-3 in chondrocytes from osteoarthritic cartilage. This provides a mechanism to support clinical observation suggesting glucosamine sulfate may have a beneficial effect in prevention of cartilage loss in some patients with osteoarthritis (Dodge GR, Jimenez SA, 2003).

Numerous studies have shown glucosamine sulfate to be safe and effective in decreasing osteoarthritic pain, and two studies in which participants took 1500 mg of glucosamine sulfate per day for 3 years revealed that further cartilage degeneration stopped in the treatment group, while the control group experienced further degeneration (Reginster JY, et al. 2001, Pavelka K, et al. 2002).

Free Radicals


It is important to protect the joints from free radical damage. Patients with osteoarthritis had approximately a 4 fold lower level of extracellular SOD (superoxide dismutase), the body’s own antioxidant enzymes, a constituent of cartilage (Regan E, et al. 2005). Zinc, copper and manganese are necessary for the formation of SOD.

Bone metabolism


Research also shows that support of bone metabolism is important for cartilage integrity. Higher baseline serum osteocalcin a marker of bone metabolism has been found to be associated with a decreased rate of cartilage loss (Wang Y, et al. 2005).

Calcium, magnesium, zinc, copper, manganese and vitamin D
are important for bone formation (Elders PJ, et al. 1994, Weaver CM, et al. 1995, Dimai HP, et al. 1998, Strause L, et al. 1994, Biscoff-Ferrari HA, et al. 2005).

Vitamin D is one of the most important vitamins and it also plays a role in arthritis.
An increased risk for osteoarthritis of the hip and knee has been documented in people who had mid and low levels of vitamin D compared to those who had the highest level (Lane NE, et al. 1999, Bergink AP, et al. 2009).

For easy implementation of all these nutrients, click here.


Fat as an anti-inflammatory


The type of fat we eat is also important since fatty acids are incorporated into the cell membranes and are involved in the immune and inflammatory process.

Omega 6 fatty acids are involved in the production of arachidonic acid, a precursor of prostaglandins and leukotrienes which are inflammatory and pain producing agents.

Ingesting omega 3 fish oil results in a partial replacement of arachidonic acid in the cell membranes by EPA which is a component of omega 3 fat (Calder PC, 2003). This has a beneficial anti-inflammatory effect. In addition, omega 3 fatty acids have shown to inhibit the inflammatory cytokines IL-1 (interleukin-1), IL-2 (interleukin-2) and TNF-alpha (tumor necrosis factor-alpha) (Adam O, 2003, Kang JX, Weylandt KH. 2008, Rennie KL, et al. 2003)

The ingestion of omega 3 fatty acid supplements has consistently shown to reduce both the number of tender joints and morning stiffness in patients with rheumatoid arthritis (Kremer JM. 2000). A decreased synthesis of the proinflammatory eicosanoids prostaglandin E2 and leukotriene B4 has been documented after the inclusion of omega 3 fatty acids in the diet (James MJ, et al. 2000).

Healthy dietary habits should include omega 3 fatty acids. For easy implementation, click here.


Additional inhibition of inflammation


There are also additional things you can do to reduce inflammation and pain if needed. There are several plant compounds that have shown to have an anti-inflammatory effect. One of the most effective and safe combination of plant derived compounds according to research are a mixture of rho iso-alpha acids from hops, rosemary leaf extract and oleanolic acid from olive leaf extract (Hall AJ, et al. 2008, Minich DM, et al. 2007, Hougee S, et al. 2006).

According to the research, a specific combination of these compounds reduced osteoarthritic pain and inhibited prostaglandin E2 effectively. Prostaglandin E2 is one of the major pain and inflammatory producing chemicals in the body.

For easy implementation, click here.

 

Summary

Osteoarthritis

Follow the dietary recommendations in the book “Effective Nutrition for Effective Healing.”

Be strict for 4 weeks for best results.

BMJ – Take 4 tablets twice daily.

The BMJ is the most important formula for support of the musculoskeletal system and should be your first choice.

Better Fish Oil – Take 2 capsules twice daily.

ComFol – Take 1 tablet 3 times daily.

Take all supplements with food.

 

Rheumatoid arthritis

Follow the dietary recommendations in the book “Effective Nutrition for Effective Healing.”

Be strict for 4 weeks for best results.

BMJ – Take 4 tablets twice daily.

The BMJ is the most important formula for support of the musculoskeletal system and should be your first choice.

Better Fish Oil – Take 2 capsules twice daily.

ComFol EX – Take 1 capsule twice daily.

Take all supplements with food.

 

References:

Adam O. Dietary fatty acids and immune reactions in synovial tissue. Eur J Med Res. 2003 Aug 20;8(8):381-7.

Bassleer C, Rovati L, Franchimont P. Stimulation of proteoglycan production by glucosamine sulfate in chondrocytes isolated from human osteoarthritic articular cartilage in vitro. 1998 Nov;6(6):427-34.

Bergink AP, Uitterlinden AG, Van Leeuwen JP, Buurman CJ, Hofman A, Verhaar JA, Pols HA. Vitamin D status, bone mineral density, and the development of radiographic osteoarthritis of the knee: The Rotterdam Study. J Clin Rheumatol . 2009 Aug;15(5):230-7.

Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with vitamin D supplementation: a meta-analysis of randomized co ntrolled trials. JAMA. 2005 May 11;293(18):2257-64.

Calder PC. N-3 polyunsaturated fatty acids and inflammation: from molecular biology to the clinic. Lipids. 2003 Apr;38(4)343-52.

Clifton PM. Diet and C-reactive protein. Curr Atheroscler Rep. 2003 Nov;5(6):431-6.

DeGroot J, Verzijl N, Jacobs KM, Budde M, Bank RA, Bijlsma JW, TeKoppele JM, Lafeber FP. Accumulation of advanced glycation endproducts reduces chondrocyte-mediated extracellular matrix turnover in human articular cartilage. Osteoarthritis Cartilage. 2001 Nov;9(8):720-6.

Dimai HP, Porta S, Wirnsberger G, Lindschinger M, Pamperl I, Dobnig H, Wilders-Truschnig M, Lau KH. Daily oral magnesium supplementation suppresses bone turnover in young adult males. J Clin Endocrinol Metab. 1998 Aug;83(8):2742-8.

Dodge GR, Jimenez SA. Glucosamine sulfate modulates the levels of aggrecan and matrix metalloproteinase-3 synthesized by cultured human osteoarthritis articular chondrocytes. Osteoarthritis Cartilage. 2003 Jun;11(6):424-32.

Elders PJ, Lips P, Netelenbos JC, van Ginkel FC, Khoe E, van der Vijgh WJ, van der Stelt PF. Long term effect of calcium supplementation on bone loss in perimenopausal women. J Bone Min Res, 1994; 9:963-70.

Fernandes CM, Pereira Teixeira Cde F, Leite AC, Gutiérrez. The snake venom metalloproteinase BaP1 induces joint hypernociception through TNF-alpha and PGE2-dependent mechanisms. Br J Pharma co l. 2007 Aug;151(8):1254-61. Epub 2007 Jun 25.

Hafstrom I, Ringertz B, Spangberg A, von Zweigbergk L, Brannemark S, Nylander I, Ronnelid K, Laasonen L, Klareskog L. A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis co rrelate with a reduction in antibodies to food antigens. Rheumatology (Oxford). 2001 Oct;40(10):1175-9.

Hĺheim LL, Nafstad P, Olsen I, Schwarze P, Rřnningen KS. C-reactive protein variations for different chronic somatio disorder. Scand J. Public Health. 2009 Apr 16.

Hvatum M, Kanerud L, Hallgren R, Brantzaeg P. The gut-joint axis: cross reactive food antibodies in rheumatoid arthritis. Gut. 2006 Sep;55(9):1240-7. Epub 2006 Feb 16.

Hall AJ, Babish JG, Darland GK, Carroll BJ, Konda VR, Lerman RH, Bland JS, Tripp ML. Safety, efficacy and anti-inflammatory activity of rho iso-alpha-acids from hops. Phytochemistry . 2008 May;69(7):1534-47. Epub 2008 Mar 20.

Hougee S, Faber J, Sanders A, Berg WB, Garssen J, Smit HF, Hoijer MA. Selective inhibition of COX-2 by a standardized CO2 extract of Humulus lupulus in vitro and its activity in a mouse model of zymosan-induced arthritis. Planta Med . 2006 Feb;72(3):228-33.

James MJ, Gibson RA, Cleland LG. Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr. 2000 Jan; 71(Suppl):343S-8S.

Kang JX, Weylandt KH. Modulation of inflammatory cytokines by omega-3 fatty acids. Subcell Biochem . 2008;49:133-43. Review.

Karatay S, Erdem T, Yildirim K, Melikoglu MA, Ugur M, Cakir E, Akcay F, Senel K. The effect of individualized diet chanllenges co nsisting of allergic foods on TNF-alpha and IL-1beta levels in patients with rheumatoid arthritis. Rheumatology (Oxford). 2004 Nov;43(11):1429-33. Epub 2004 Aug 10.

Kjeldsen-Kragh J, Haugen M, Borchgrevink CF, Laerum E, Eek M, Mowinkel P, Hovi K, Fřrre O. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet . 1991 Oct 12;338(8772):899-902.

Kremer JM. n-3 fatty acid supplements in rheumatoid arthritis. Am J Clin Nutr. 2000 Jan;71(1 Suppl):349S-51S.

Lane NE, Gore LR, Cummings SR, Hochberg MC, Scott JC, Williams EN, Nevitt MC. Serum vitamin D levels and incident changes of radiographic hip osteoarthritis: a longitudinal study. Arthritis Rheum. 1999;42(5):854-860.

Lane NE, Gore LR, Cummings SR, Hochberg MC, Scott JC, Williams EN, Nevitt MC. Serum vitamin D levels and incident changes of radiographic hip osteoarthritis: a longitudinal study. Study of Osteoporotic Fractures Research Group. Arthritis Rheum. 1999 May;42(5):854-60.

Lee WY, Park JS, Noh SY, Rhee EJ, Sung KC, Kim BS, Kang JH, Kim SW, Lee MH, Park JR. C-reactive protein concentrations are related to insulin resistance and metabolic syndrome as defined by the ATP III report. Int J Cardiol. 2004 Oct;97(1):101-6.

Lee YH, Pratley RE. The evolving role of inflammation in obesity and the metabolic syndrome. Curr Diab Rep. 2005 Feb;5(1):70-5.

McAlindon TE, Felson DT, Zhang Y, Hannan MT, Aliabadi P, Weissman B, Rush D, Wilson PW, Jacques P. Relation of dietary intake and serum levels of vitamin D to progression of osteoarthritis of the knee among participants in the Framingham Study. Ann Intern Med. 1996 Sep 1;125(5):353-9.

Minich DM, Bland JS, Katke J, Darland G, Hall A, Lerman RH, Lamb J, Carroll B, Tripp M. Clinical safety and efficacy of NG440: a novel combination of rho iso-alpha acids from hops, rosemary, and oleanolic acid for inflammatory conditions. Can J Physiol Pharmacol . 2007 Sep;85(9):872-83.

Müller H, de Toledo FW, Resch KL. Fasting followed by vegetarian diet in patients with rheumatoid arthritis: a systematic review. Scand J Rheumatol. 2001;30(1):1-10.

Pannacciulli N, Cantatore FP, Minenna A, Bellacicco M, Giorgino R, De Pergola G. Urinary albumin excretion is independently associated with C-reactive protein levels in overweight and obese nondiabetic premenopausal women. J Intern Med. 2001 Dec;250(6):502-7.

Pavelká K, Gatterová J, Olejarová M, Machacek S, Giacovelli G, Rovati LC. Glucosamine sulfate use and delay of progression of knee osteoarthritis: a 3-year, randomized, placebo-controlled, double-blind study. Arch Intern Med. 2002 Oct 14;162(18):2113-23.

Regan E, Flannelly J, Bowler R, Tran K, Nicks M<, Carbone BD, Glueck D, Heijnen H, Mason R, Crapo J. Extracellular superoxide dismutase and oxidant damage in osteoarthritis. Arthritis Rheum. 2005 Nov;52(11):3479-91.

Reginster JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giaco velli G, Henrotin Y, Dacre JE, Gossett C. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo- controlled clinical trial. Lancet. 2001 Jan 27;357(9252):251-6.

Rennie KL, Hughes J, Lang R, Jebb SA. Nutritional management of rheumatoid arthritis: a review of the evidence. J Hum Nutr Diet. 2003 Apr;16(2):97-109.

Rexrode KM, Pradhan A, Manson JE, Buring JE, Ridker PM. Relationship of total and abdominal adiposity with CRP and IL-6 in women. Ann Epidemiol. 2003 Nov;13(10):674-82.

Romano M, Guagnano MT, Pacini G, Vigneri S, Falco A, Marinopiccoli M, Manigrasso MR, Basili S, Davě G. Association of inflammation markers with impaired insulin sensitivity and coagulative activation in obese healthy women. J Clin Endocrinol Metab. 2003 Nov;88(11):5321-6.

Senolt L, Braun M, Olejárová M, Forejtová S, Gatterová J, Pavelka K. Increased pentosidine, an advanced glycation end product, in serum and synovial fluid from patients with knee osteoarthritis and its relation with cartilage oligomeric matrix protein. Ann Rheum Dis . 2005 Jun;64(6):886-90.

Strause L, Saltman P, Smith KT, Bracker M, Andon MB. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr. 1994 Jul;124(7):1060-4.

Stürmer T, Brenner H, Koenig W, Günther KP. Severity and extent of osteoarthritis and low grade systemic inflammation as assessed by high sensitivity C reactive protein. Ann Rheum Dis. 2004 Feb;63(2):200-5.

Verzijl N, DeGroot J, Bank RA, Bayliss MT, Bijlsma JW, Lafeber FP, Maroudas A, TeKoppele JM. Age-related accumulation of the advanced glycation endproduct pentosidine in human articular cartilage aggrecan: the use of pentosidine levels as a quantitative measure of protein turnover. Matrix Biol. 2001 Nov;20(7):409-17.

Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999 Dec 8;282(22):2131-5.

Wang Y, Ebeling PR, Hanna F, O'Sullivan R, Cicuttini FM. Relationship between bone markers and knee cartilage volume in healthy men. J Rheumatol. 2005 Nov;32(11):2200-4.

Wannamethee SG, Lowe GD, Shaper AG, Rumley A, Lennon L, Whincup PH. Insulin resistance, haemostatic and inflammatory markers and coronary heart disease risk factors in Type 2 diabetic men with and without coronary heart disease. Diabetologia. 2004 Sep;47(9):1557-65. Epub 2004 Sep 9.

Weaver CM, Martin BR, Plawecki KL, Peacock M, Wood OB, Smith DL, Wastney ME. Differences in calcium metabolism between adolescent and adult females. Am J Clin Nutr . 1995 Mar;61(3):577-81.

 

 

 

 

 

 

 

 

 

 

The information on this website is provided for informational purposes only and is not intended as a substitute for the advice provided by your physician or other healthcare professional. The information and products on this website are not intended to diagnose, treat, cure or prevent any disease.