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Osteoarthritis
Michael Lam, MD, MPH
www.DrLam.com
(READING TIPS: For
fast reading, scan through the topic headings in BOLD BLACK, important conclusions
BOLD BLUE, and " Must Know " in BOLD RED. To jump to specific sections in this article, click on the LINKS
| Before You Begin
Information presented here is for general
educational purposes only. Each one of us is biochemically and metabolically
different. If you have a specific health concern and wish my personalized
nutritional recommendation, write to me by clicking
here. |
Contents
Introduction
Primer on Osteoarthritis (OA)
Anti-Arthritic Drugs
Side Effects of Drugs
Osteoarthritis Supplementation
Protocol
1. Glucosamine Sulfate (GS)
2. Chondroitin Sulfate (CS)
3. Methylsulfonylmethane (MSM)
4. Bromelain
5. Phenylalanine (DPLA)
6. Collagen type I and II
7. Sea Cucumber
8. Cetyl Myristoluate (CMO)
9. Essential Fatty Acids
10. S-adenolsyl-methione (SAMe)
11. Antioxidants - Vitamins C , E and Others
Discussion
Introduction
Arthritis refers to inflammation of
the joint. There are various forms, including rheumatoid arthritis, an autoimmune
disorder that affects primarily young women. Osteoarthritis (OA) is a
disorder caused by the wear and tear of joint due to the natural results
of aging. OA characteristically affects middle age and elderly populations.
Over 40 million American have some form of
OA, including 80% of those over 50. The disease is more common
in men under age 45 and in women over age 45.
This Research Brief examines the current medical thinking on this common
and debilitating disease and explores alternative strategies for alleviating
osteoarthritis.
Primer on Osteoarthritis (OA)
Osteoarthritis (also known as degenerative joint disease) is the localized
degeneration of joint cartilage. It affects mainly the weight-bearing joints
(e.g. knee, hip, spine). OA results from the repetitive use of the joints
resulting in wear and tear, and from the normal results of aging without
precise etiology. This is called primary OA. Secondary OA, on the other
hand, could be the result of many factors such as sports injuries, inherited
abnormalities in joint structure, continuous repetitive use over a long
period of time, trauma, previous inflammatory disease of joints, etc.
OA is caused by the breakdown in the cellular processes that manufacture,
maintain, and repair cartilage. Cartilage covers the ends of our bones.
It is present in our joints and contains chondrocytes. Chondrocytes manufacture
proteins known as proteoglycans that consist of chondroitin and keratin
sulfate that are strung on core proteins. The proteoglycans hold joint fluid
within the joint and, in conjunction with the joint cartilage, acts as a
shock absorber for the body. Repetitive stress or trauma destroys the
proteoglycans and collagen matrix (known as glycosaminoglycans (GAG), and
inhibit the production of these substances by chondrocytes. This is how
OA starts.
OA causes achy pain in the joints, leading to limitation of movement
and loss of dexterity. Over time, osteoarthritic joints enter a vicious
cycle of progressive deterioration, as the afflicted person tends to use
the affected joints less due to pain. Symptoms generally begin in middle
age, and by age 60, most people have some degree of OA. Diagnosis is primarily
through a thorough history, physical examination, and x-ray findings, although
the correlation is not accurate. About 40% of people with the worst x-ray
classification for OA are pain-free. There is currently no reliable predictive
marker for OA.
Anti-Arthritic Drugs
Modern medicine treats OA with 3 types of drugs:
- Pain relievers, like
aspirin, that primarily act to relieve symptoms of pain.
- Non-steroidal anti-inflammatory
drugs (NSAIDs), like ibuprofen (Motrin?, which focus on the relief
of symptomatic pain with anti-inflammatory action.
- Steroidal anti-inflammatory
drugs. While these work wonders to provide short to medium-term relief,
steroids are not recommended for long-term use.
Side Effects of Drugs
While drugs do help to relieve
symptoms of OA, they have numerous adverse side effects, from relatively
minor gastric upset, dizziness, and headaches,
to severe gastric bleeding and interference with platelet function.
In addition, virtually all drugs used to treat
OA have destructive effects on the articular cartilage lining the bones
that form the joint that the drug is supposed to help.
Analgesics, like aspirin, inhibit enzymes involved in the early stages of
chondroitin sulfate biosynthesis. NSAIDs suppress proteoglycan synthesis
by the chondrocyte. The depletion of chondrocytes further weakens the joint
and exposes it to a faster deterioration cycle. Experimental studies show
that these drugs inhibit cartilage synthesis and accelerate cartilage destruction.
Steroids are the most effective anti-inflammatory agent. However, they can
also cause extensive damage to chondrocytes in long-term use. In addition,
chronic use of strong steroids leads to conditions that mimic Cushing's
Syndrome, with a number of adverse age-accelerating consequences.
Simply put,
most drugs appear to suppress the symptoms, but accelerate the progression,
of OA.
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