Osteoarthrosis; Natural supplements; Botanical medicine; Diet
Osteoarthrosis (OA) is sometimes referred to as osteoarthritis,
degenerative arthritis, or degenerative joint disease. It is
characterized by degeneration of the articular cartilage and
subchondral bone. It can result in joint deformities, with
characteristic Bouchard’s nodes in the proximal phalangeal joints
of the fingers and Heberden’s nodes in the distal joints of the
fingers. The predictable symptoms include joint pain and stiffness,
becoming more chronic over time. Other symptoms commonly
included joint swelling, weakness and/or paresthesias in the
extremities and decreased range of motion. Typically, joints in the
fingers, thumb, knees, spine, and hips can be involved. It can also
be the result of trauma to a single joint leading to degeneration of
the joint years later. Abnormal cartilage, congenital deformities
of joint(s), infection of a joint, crystal deposition and/or other
arthritic conditions can lead to OA of the joint.
Approximately 27 million people in the U.S. suffer from OA . As
people age, the prevalence of OA increases. In people under 45,
it’s more common in men. After 45, it is more common in women.
The knee is the most common joint to be affected. Conventional
treatments include exercise, acetaminophen, NSAIDs, opioids,
injecting anesthetics, hyaluronan (hyaluronic acid), or plateletrich
plasma, or joint replacement. One peculiar finding is the lack
of correlation between the severity of the disease as seen on
radiographs and the patient’s symptoms.
Conventional treatment includes non-steroidal anti-inflammatory
drugs. While their use is widespread, there is some evidence that long-term use may inhibit the synthesis of the cartilage matrix
and accelerate the deterioration of cartilage [2-5]. However,
there is some evidence that is contradictory. There are some
studies that demonstrate that the anti-inflammatory effects of
low-dose aspirin slow the progression on cartilage loss in OA .
Additionally, there are significant risks associated with the use
of NSAIDs; including gastrointestinal bleeding and cardiovascular
Musculoskeletal joint derangement and misalignments have
been demonstrated to play a role in the development of OA. In
one study involving 230 patients with varus deformities of the
knee, the was a four-fold increase in degenerative arthritis in
the knee when compared to the general population . Joint
alignment, muscle strength nutritional status, previous trauma
and mid-stance loads all seem to contribute to the development
of OA [8,9]. Manipulative and manual therapy has both been
shown to increase range of motion, decrease pain, and decrease
the need for pain medicine [10-12]. One study concluded that
the cost of treatment was reduced when manual therapy and
exercise were integrated into the treatment plan . Swimming
and isometrics have been identified as superior to other types
of exercise for the treatment of OA [14-15]. Decreased stability
and balance have been demonstrated to have a negative effect
on OA, particularly in the knee . Conversely, strengthening
the muscles controlling the hip and knee is an effective way to
mitigate some of the disabling symptoms associated with OA in
the lower extremity .
Diet should focus on the decrease of inflammation, as well as
improving insulin sensitivity and achieving ideal body weight.
Obesity is a major risk factor for the development of OA in the
knees and hips. There is considerable evidence linking metabolic
syndrome (syndrome X) with inflammatory cytokines implicated
in OA [18-21]. Insulin stimulates chondrocytes and chondroblasts
to secrete proteoglycans, which are essential to the proper
function of cartilage. Decreased sensitivity to insulin has a
detrimental effect on cartilage . Combining weight loss and
exercise is known to decrease the risk of developing OA, as well
as reducing the symptoms of OA and improving function .
General guidelines for diet include a plant-based diet, relying
on fresh fruits and vegetables, as well as whole grains, fatty fish
and lean meats. Dairy products and gluten-containing grains are
known to be allergenic in many people, and therefore should be
minimized or eliminated from the diet. The Mediterranean diet
has been show to significantly improve the symptoms of OA .
Certain individuals may benefit from eliminating nightshades
(tomatoes, white potatoes, peppers, and eggplant) from the
diet, most likely because of an individual’s sensitivity to these
plants. One study looked at Diosgenin, a steroidal saponin found
in nightshades. Diosgenin possesses diverse biological activities
including anti-inflammatory properties. It has been shown
to inhibit the synthesis of inflammatory mediators, such as
prostaglandin E2 and interleukins. Therefore, there is a possibility
that these plants may actually be beneficial for OA .
Glucosamine sulfate is a relatively small molecule, consisting of
glucose and an amine. One of the most common monosaccharaides,
it is found in the exoskeletons of crustaceans and arthropods, and
in the cell walls of fungi. It is known to stimulate the production
of Glycosaminoglycan’s (GAGs), a major component of cartilage.
Aging appears to reduce the individual’s ability to manufacture
glucosamine [26,27]. Oral supplementation with derivatives
of N-acetyl glucosamine has been shown to have superior
cartilage protection over glucosamine sulfate supplements .
Glucosamine sulfate supplements have demonstrated efficacy in
treating OA, as well as a wide-margin of safety . While not all
studies have proven the positive effects of glucosamine sulfate
supplementation , the overwhelming majority of the studies
support its use for treatment of OA [26-29,31-32], especially the
crystalline form .
Chondroitin sulfate is a high molecular weight GAG, found
naturally as a component of cartilage. It is composed of repeating
units of glucosamine sulfate, a GAG that is much smaller than
chondroitin sulfate and much better absorbed. Chondroitin
sulfate is generally poorly absorbed, anywhere from 0-18% of
what is ingested. The research is mixed as far as the results of oral
chondroitin sulfate on OA since it has to be partially digested to be absorbed. Administration of low-molecular weight chondroitin
sulfate has been demonstrated to have beneficial effects on the
alternative complement pathway, thus preserving chondrocytes
and preventing damage to cartilage . Immunoassays specific
for a peptide of the alpha-helical region of type II collagen
108HRGYPGLDG116 (Coll 2-1) were used to determine the effect
of chondroitin sulfate on OA. The authors used visual analog scale
to determine pain, and Lequesne's Index to measure function.
They concluded that chondroitin sulfate supplements positively
affected OA, reducing Coll 2-1 levels, resulting in decreased pain
and increased function . Other studies have shown that
combining chondroitin sulfate with hyaluronic acid and keratin
improved OA . Chondroitin sulfate supplements have been
shown to inhibit NF-κB activity, thus preventing further damage
to cartilage .
Hyaluronan (Hyaluronic acid or HA)
Hyaluronan is a GAG found in synovial joints, between layers of
fascia and in loose connective tissue. It allows cartilage to imbibe
water and provides an excellent medium for diffusion. By age 70,
the amount of HA found in the body is estimated to be as little
as 20% of that of a forty year old [38-40]. This is implicated in dry
skin and poor wound healing so prevalent in the elderly, as well
as accelerated rates of osteoporosis. Both oral and injectable
versions of hyaluronan have been shown to be beneficial in
treating OA [41-45]. In vitro experiments have shown that
hyaluronan has a positive effect on the growth of chondrocytes
as well .
SAMe is a combination of methionine and ATP (adenosine
triphosphate). It is important in cartilage in that a deficiency
results in a loss of the integrity of cartilage in regard to shock
absorption. Some proposed mechanisms are the decrease in
TNF-α [47,48], increasing levels of glutathione peroxidase,
signaling of proteoglycan synthesis, increased methylation of
proteoglycans, and positive effects on DNA synthesis in cartilage
by acting as a signal of sulfur availability [48,49].
There were several studies in the 1940s and 1950s by William
Kaufman that reported significant benefits from supplementing
with niacinamide in patients with OA. Niacinamide has been
shown to prevent apoptosis of chondrocytes by inhibiting
cytokine (IL-1) stimulated nitric oxide synthase . This has been
shown to be an important mechanism in the development of OA
. Administration of niacinamide in patients with OA improved
joint flexibility, reduced inflammation, and reduced the need for
pain medication . Due to the short half-life of the vitamin,
taking niacinamide in divided doses yielded the best results.
The intake of carotenoids, ascorbate and vitamin E have all
been demonstrated to improve the symptoms of OA and
even to reverse the progression of the disease [51,52]. The
odds of having hip OA were reduced by nearly two fold when the individual consumed recommended or higher amounts of
vitamin C . It has been demonstrated that vitamin C protects
chondrocytes from oxidative damage from hydrogen peroxide
by regulating multiple regulatory pathways . Astaxanthin, a
carotenoid found in a variety of marine mammals and plants,
has been shown to reduce Matrix Metalloproteinases (MMP), a
substance known to degrade cartilage [55,56]. The carotenoids
in saffron, namely crocins and crocetin, are known to prevent the
expression of MMP due to IL-1β [57,58].
According to several studies, low plasma levels of vitamin D are
associated with an increased risk of OA [59-61]. However, there
are some studies that contradict these findings [62,63]. Improved
outcomes following knee arthroplasty were noted after vitamin
D supplementation . Vitamin D has been shown to have a
positive effect on the mass of the quadriceps muscles .
It seems that inadequate levels of vitamin D contribute to the
progression of OA, but it is not clear whether supplementation
is beneficial in improving symptoms in those afflicted with the
Low vitamin K status is associated with an increased incidence
of OA [66-68]. The anti-inflammatory effects of vitamin K are
thought to play an important role in the prevention of OA. The
carboxylation of osteocalcin is dependent on vitamin K. Vitamin
K deficiency caused serum undercarboxyled osteocalcin levels
to increase. Measuring these levels has been suggested as a
marker for the potential development of OA . Mineralization
of cartilage has been observed in osteoarthritic cartilage.
Chondrocytes from osteoarthritic tissue produced significantly
less amounts of matrix GLA protein, a known inhibitor of
mineralization. This correlates with lower than normal vitamin
K status . A study that included 719 subjects looked at the
relationship between vitamin K levels and OA and concluded that
“vitamin K may have a protective role against knee OA” and that
supplementing with vitamin K “might lead to a disease-modifying
Zingiber officianalis (Ginger)
Ginger is well-known for its anti-inflammatory and anti-nausea
effects. A recent study used a combination of ginger and
Echinacea purpurea to treat OA patients that did not respond
well to NSAIDs, and demonstrated significant improvements
. In several studies, ginger was shown to inhibit inflammatory
cytokines and prevented the degradation of cartilage [73-75].
Even topical applications of ginger have been shown to be helpful
in improving the symptoms of OA .
Harpagophytum procumbens (Devil’s Claw)
Devil’s claw is a plant native to South Africa. It is known to possess
several compounds that block the expression of inflammatory
cytokines . Fewer than 30 mg per day seemed to have little
effect on OA, whereas supplements containing 60 mg or more
were mildly effective in relieving the symptoms of OA [78-80]. There was one case study reporting hypertension caused by H. procumbens, therefore caution should be exercised when
prescribing to a patient that is borderline or hypertensive .
Boswellia serrata is a tree used to treat inflammatory conditions.
Out of twelve boswellic acids purified from the resin of the
tree that have been identified, two are of particular interest in
treating chronic inflammation. KBA and AKBA have both been
shown to inhibit the secretion of a variety of pro-inflammatory
cytokines, including IL-1, IL-2, IL-6, IFN-γ and TNF-α, products of
complement and inhibition of leukotrienes . Two studies by
the same group used an extract of Boswellia called FlexiQule,
demonstrated reduction in pain and improved mobility when
compared to control groups [83,84]. Another study reviewed
several botanical medicines for the treatment of OA and
concluded that Boswellia extracts are effective in treating
OA through a number of mechanisms . Yet another study
looked at combining Curcumin and Boswellia proved to be more
effective than a COX-2 inhibitor, celecoxib. The combination of
the two herbs was without side effects .
There are a number of studies touting the anti-inflammatory
effects of C. longa [87-90]. It has been well-established that C. longa disrupts a number of inflammatory pathways. In a study
comparing C. longa to ibuprofen, the benefits were similar in
the two treatment groups, but the curcumin-treated group
had significantly less gastrointestinal symptoms . Another
multi-center study confirmed these results . Another study
deemed C. longa as an alternative to traditional pharmaceuticals
for treating OA due to its excellent safety record and low cost
. Multiple studies strongly recommend the use of C. longa
in the treatment of OA because of its long history of safety and
Papain, rutin, bromelain, trypsin and chymotrypsin are all
proteolytic enzymes that are used clinically for inflammatory
conditions. Papain, rutin and bromelain are from vegetable
sources, and trypsin and chymotrypsin are derived from bovine
or porcine pancreas. To mitigate the effects of inflammation,
proteolytic enzymes must be taken away from food. Several
studies looked at the efficacy and safety of proteolytic
enzymes and concluded that they are as good or superior to
pharmacological agents, with a superior safety record [97-101].
Two studies compared diclofenac and proteolytic enzymes
and concluded that the enzyme treatment was as effective as
diclofenac, but was safer to use and had a fewer side effects
Osteoarthritis is a debilitating disease that affects over a third of
Americans over the age of 60. Natural approaches to treatment
of the disease and its symptoms have been shown to be effective
and cost saving. Combining a diet rich in omega-3 fatty acids, flavonoids, and high in fibre with supplements and botanicals,
has the potential of halting the progression of the disease and
even reversing some of the damage to joints.
Glucosamine sulfate: 1500 mg/day;
Niacinamide: 500 mg 6x/day;
Beta-carotene: 25,000 IU/day;
Vitamin C: 1000 mg 2x/day; *Can cause loose bowels or diarrhea
in high doses;
Vitamin E: 400 IU 2x/day; *Can cause a temporary hypertension in patients who are borderline HTN;
Vitamin K: 750 μg/day;
Pyridoxine (B6): 50 mg/day;
Pantothenic acid (B5): 30 mg/day;
Hyaluronan: 60-100 mg 2x/day;
SAMe: 500 mg 3x/day;
Zinc: 50 mg/day m; *Must be taken with copper to avoid a copper
Copper: 3 mg/day;
Boron: 6 mg/day.
Ginger: 1000 mg 3x/day;
Devil’s claw: 60 mg of harpagoside/day;
Boswellia serrata: 400 mg of boswellic acids 3x/day;
Curcumin: 500 mg 3x/day;
Proteolytic enzymes: mixture of bromelain/papain/rutin/trypsin/
chymotrypsin 500 mg 3x/day on an empty stomach.
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