Disc Nutrition

• repairs degraded bones,
• increases the absorption and replacement of calcium,
• diminishes the disease and
• begins rebuilding the damaged area with none of the health risks of NSAIDs.

• improves mobility and relieves pain with significantly less side effects than NSAIDs
• has good tolerability
• maintains its good benefits even if there is an interruption in taking them compared with drug therapy which relieves pain only while taking the drug

Glucosamine sulfate (GS) is a naturally occurring part of joint cartilage and forerunner for and stimulant of proteoglycan synthesis and the making of GAG which is necessary for development of the white fibrocartilage of the disc. Unlike NSAIDs which relieve symptoms of and, over time, accelerate the destruction of, degenerative joint and disc disease, glucosamine has been shown in experiments to slow the progression of the degenerative disease and promote repair of affected cartilage:

Two similar yet separate experiments (6,7) were conducted and gained similar results: patients receiving glucosamine sulfate improved by 71% compared to a placebo group. (6) 

A comparison (8) of 2 groups —one receiving ibuprofen and one GS three times per day (total of 1500 mg) for 30 days—showed that the GS group reported less pain on rest, standing, and exercise. The GS group’s improvement was more pronounced, lasting for a period of 6 to 12 weeks after the treatment ended.

In a double-blind study (9) of people suffering from osteoarthritis of the knees compared a placebo group to a GS group. The GS group showed significant reduction in pain, joint tenderness, and swelling  treated with 1500 mg GS daily.

Findings by electron micrographs of cartilage of persons receiving GS compared to a placebo (10) show:

• Placebo results - typical of osteoarthritis;            
• GS results - more similar to healthy cartilage.

GS is able to stimulate proteoglycan synthesis by chondrocytes and has mild anti-inflammatory properties. In a clinical trial, GS was tested against ibuprofen. 35% of the ibuprofen group complained of adverse effects throughout the treatment, with seven dropping out of the study. Only six of the 100 patients in the GS group experienced adverse effects. Therefore, GS was as effective as ibuprofen. (18)

The absorption rate for GS is about 98%. (24,25)

GS is extremely non-toxic, and its therapeutic margin is 10-30 times better than NSAIDs (26)  When taken orally, it is more effective than placebo and at least as effective as NSAIDs in relieving the symptoms of osteoarthritis. (28)

2% of 1500 patients were unable to tolerate GS: peptic ulcer and diuretic use were associated w/increased risk of side effects, most commonly: gastric upset (3.5%), heartburn (2.7%), diarrhea and nausea (1%).  (27)

• GS HCl lacks the sulfur compound which is an essential nutrient for joint tissue. (29)
• The sulfur compound restrains the enzymes which lead to cartilage destruction in osteoarthritis. (29)
• GS has many clinical studies proving its effectiveness; GS HCl lacks such studies. (29)

Supplemented chondroitin sulfates work like naturally occurring chondroitins found in cartilage:

• stop enzyme starvation of cartilage and build proteoglycans, glycosaminoglycans, and collagen, the building blocks for healthy new cartilage. (13)
• protect existing cartilage from premature breakdown by inhibiting the action of certain “cartilage chewing” enzymes. (12)
• work synergistically with glucosamine. (14)

Results of loss or low proteoglycan or glycosaminoglycan content:

• The central event in osteoarthritis and degenerative disc disease is the loss of the proteoglycans from the disc. (32)
• Low GAG precedes degenerative disc disease; injured and adjacent discs show less GAG and increased collagen. (33)
• Osteodegenerative arthritis shows increased release of GAG. (34)
• Arthrosis shows a loss of glycosaminoglycan. (35)

Busci reports that OSTEOARTHRITIS CAN BE REVERSED by chondroprotective agents - GAGs - if use of analgesics (aspirin, non-steroidal drugs) is minimal. (1)  Further, he states that oral administration of GAGs is better than injection because constant higher levels can be maintained in the bloodstream instead of short periods of elevation by shots.

Cole, Ghosh & Taylor wrote that mature beagle dogs, when given GAG over a 26 wk period, showed cartilage improvement. (2) These  findings  were  the  first  to suggest that GAG administration might be  of value in management of  degenerative disc disease.

A 50% loss of GAG from rabbit articular cartilage when arthritis of the joint was reported in one study. This caused the cartilage matrix to be less capable of restoring the proteoglycan content of the cartilage and resulted in loss of joint stiffness and resistance to the compression. (3)

In rabbits with osteoarthritis of the knee, injection of sulfated GAG inhibited enzymes that destroy cartilage and promoted repair of the defects. GAG had been found to increase proliferation of the hyaline cartilage of the hip joint in mice and the femoral condyles, femur and tibia of rabbits. Furthermore, Puhl and Dustmann induced regeneration of damaged cartilage in rabbits. (5)

120 patients suffering from osteoarthritis of the knees and hips were either given oral chondroitin sulfates or a placebo. After three months, the group given the oral chondroitin in the morning and the evening reported a reduction in pain and pain movement. There were no reported side effects. In addition, there was a 60-day carry-over effect when administration was stopped. Results appeared within 2 to 8 weeks. (16)

50 patients suffering from osteoarthritis of the knee were given oral chondroitin sulfate or a pain medication. Cartilage tissue samples were taken after three months of therapy. Results showed that the chondroitin group had repaired the cartilage to a significant degree. (15)

Eismont showed circulation into the disc when he reported that antibiotics reach the nucleus pulposus following 8 hours of intramuscular administration. (4)

Dogs given GAG  (36) showed

• less osteophyte formation,
• less disc space narrowing,
• better disc injury repair, and
• prevention of experimental disc degeneration.

Trentham et al 19 (of Harvard University) report in Science on a new way to help rheumatoid arthritis (RA) sufferers: oral tolerization. This procedure involved a liquid solution of cartilage/collagen and orange juice. Dr. Trentham states that this seems to “teach” the body’s immune system to stop inflaming the tissue around the joints. This appears to arrest the progress of RA. In a three month trial, 28 patients — all of whom were taken off all other drugs — got relief from RA; 4 went into remission. Thirty-one patients on a placebo became worse. Basically, this study finds that the immune system can be helped to relieve joint and disc pain and inflammation with cartilage.

“Dr. Arthur Grayzel, senior vice president of medical affairs of the Arthritis Foundation, said he was quite encouraged by the [Trentham] study” that such a solution may have the potential to halt rheumatoid arthritis.  (20)

42 patients with osteoarthritis (OA) of the knee were given 800 mg of oral chondroitin sulfate. The chondroitin sulfate patients showed less pain, better mobility, stabilization of joint space narrowing whereas the placebo patients' OA progressed. (37)

A 6 month trial compared 800 mg of chondroitin sulfate and a placebo given to 80 patients with OA of the knee. Results showed that the patients had reduced use of pain medications and walked faster. (38)

Pipitone VR: Chondroprotection with chondroitin sulfate. Drugs in Experimental and Clinical Research 1991;17(1):3-7

• 50 patients with ODA of the knee were given 8-1200 mg of chondroitin sulfate daily or 500 mg of pain medication
• In 3 months, biopsy showed repair of the patients taking chondroitin sulfate.

Olivero U et al: Effects of treatment with matrix on elderly people with chronic articular degeneration. Drugs in Experimental and Clinical Research 1991;17(1):45-51

• 120 ODA of hip and knee patients given chondroitin sulfate or placebo
• 3 months, chondroitin sulfate patients had reduced pain.
• Take am and pm.
• Results in 2-8 weeks.

Bucsi L, Poor G: Efficacy and tolerability of oral chrondroitin sulfate as a symptomatic slow-acting drug for osteoarthritis in the treatment of knee osteoarthritis. Osteoarthritis and Cartilage 1998;6(A):31-6

• 6 month trial of 800 mg chondroitin sulfate versus placebo
• 80 patients with osteoarthritis of knee
• Reduced pain medication and walked faster.

• 24 patients with osteoarthritis
• Given 800 mg chondroitin sulfate a day for 10 days
• Joint aspiration showed decreased phospholipase A2, increased hyaluronic acid concentration
• Decreased collagen enzyme breakdown
• Oral chondroitin sulfate reaches target tissues in less than 2 weeks

Uebelhart D: Effects of oral chondroitin sulfate on the progression of knee osteoarthritis: a pilot study. Osteoarthritis and Cartilage.1998;6(A):39-46

• 42 patients with osteoarthritis of knee
• Given 800 mg oral chondroitin sulfate a day
• Chondroitin patients showed less pain, better mobility, stabilization of joint space narrowing
• Placebo patients progressed

Bucci LR: Reversal of osteoarthritis by nutritional intervention. ACA J Chiro 11/90

• Glycosaminoglycan is chondroprotective if aspirin and NSAIDS are minimal
• Oral administration is best as serum level is constant with GAG

Shostak NA et al: Low back pain in spinal osteochondrosis: experience of treatment with chondroprotective drug. Terapevtichjeskii Arkhiv 2002; 74(8):67-69

• 30 patients with low back pain (mean age 51)
• given chondroitin sulfate (drug name: structum) 1g/day for 24 weeks
• 73% of patients showed pain relief and improved spinal function
• included in treatment of low back pain as chondroprotective drug

Mazurov, VI; Belyaeva, IB: Structum in combined treatment of low back pain syndrome. TERAPEVTICHESKII ARKHIV 2004; 76 (8):68-71

• Aim. To assess duration of a clinical response and tolerance of structum in patients with low back pain (LBP) and co-morbid cardiovascular disease.
• Results. To the end of the first treatment months structum significantly relieved pain intensity, spinal motility, increased exercise tolerance. Excellent and good response to structum were observed in 71% patients, noresponse was in 29%. Tolerance of the drug was good in 23 (92%) patients. The effect persisted for 3 months. CHD characteristics did not change while arterial pressure went down noticibly.

DRUGS HARMFUL TO DISCS: Damaging Factors of Cartilage and Glycosaminoglycan Processing

ANTIDEPRESSANTS  ENDANGER BONE and JOINTS

• Ray: Cyclic antidepressants may increase hip fracture risk. J of Manipulative Medicine (12/91):46

STEROIDS  CAUSE BONE LOSS, INCREASE FRACTURE RISK

• Bockman RS et al: Steroid induced osteoporosis. Ortho Clin of N Amer 21(1):97
• Fries: Prednisone greatly increases fracture risk. J of Musculoskeletal Med (6/92):16
• Mitchell: Steroid use causes osteo-degenerative arthritic hips. Radiology 1987; 62(3):709
• Fessler: [Chronic steroid use leads to epidural lipomatosis.] Spine 1992; 17(2)

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)  DEPRESS GAG PRODUCTION and SYNTHESIS, DESTROY CARTILAGE

• Yoo: Suppression of proteoglycan synthesis in chondrocyte cultures derived from canine intervertebral disc. Spine 17(2):221-224
• Newman: Acetabular bone destruction due to NSAIDs. Lancet 1985; pgs. 11-14
• VanDerKraan et al: High susceptibility of human articular cartilage glycosaminoglycan synthesis to changes in inorganic sulfate availability. J of Ortho Research 1990; 8(4):565-71
• Whittaker: Arthritis drugs actually cause cartilage destruction! Health & Healing 3(6):1-4

SALICYLATES (aspirin) DEPLETE GAG SYNTHESIS in DISC, LEAD to OSTEOARTHRITIS, WEAKEN BONE

• Palmoski: Arthritis and Rheumatism 1985; 28:548;
• DeVries: Arthritis and Rheumatism 1985; 28:922-9;
• Laan: Arthritis and sciatica drug weakens vertebrae. Backletter 1994;9(2):22

CHIROPRACTIC & GLUCOSAMINE SULFATE FOR OSTEOARTHRITIS

LOSS OF GLYCOSAMINOGLYCAN FROM THE NUCLEUS PULPOSUS LEADS TO INTERNAL STRESS CHANGES IN THE DISC LEADING TO DEGENERATION