Keeping Joints in Commission
By Mary Kaye Sawyer-Morse, PhD, RD, LD
For The Record
Vol. 19 No. 4 P. 34

Bone up on joint health and how proper nutrition, exercise, and weight control can aid in osteoarthritis symptom relief.

The symptoms sound familiar: You experience joint stiffness and pain when you get out of bed in the morning. You mentally shrug and attribute the discomfort to a busy weekend of gardening and yard work. You are, after all, getting older, and everyone gets a touch of arthritis.

Although we tend to associate it with the joint stiffness, aches, and pains of older adults, arthritis affects people of all ages. In fact, it is the leading cause of disability among those over the age of 15 in the United States.

So what exactly is arthritis? There isn’t one answer because arthritis involves a group of diseases, each with its own cause, symptoms, and treatments. What these diseases have in common is that they affect some part of the joint, they cause pain and potential loss of movement, and they often include some level of inflammation. The word arthritis, which literally means joint inflammation, comes from the Greek words arthros (joint) and itis (inflammation). According to the Arthritis Foundation, more than 43 million Americans—nearly one in six—suffer from the more than 100 types of arthritis.

However, a bit of creaky joint stiffness is a visitor who knocks on nearly everyone’s door sooner or later. This visitor is often a type of arthritis called osteoarthritis (OA).

The Basics of OA
OA is the most prevalent type of arthritis, afflicting more than 21 million Americans, most of whom develop the disease after the age of 45. With the aging of our population, the condition is becoming increasingly prevalent.

Diagnosis
Simply put, OA is the painful result of cartilage breakdown. When the tough, resilient substance that cushions bone ends no longer does its job effectively, the bones don’t glide across each other easily within the joint. Therefore, pain and stiffness set in and knees ache or shoulders stiffen. An OA diagnosis usually includes a review of physical findings, including bone tenderness, joint enlargement, decreased range of motion, and radiographic changes. Radiographic findings in OA frequently include osteophyte (an outgrowth of bone usually found around a joint) formation, joint space narrowing, and cysts.

Individuals with early OA typically experience localized joint pain that worsens with activity and gets better with rest, while those with more severe disease may have pain even when at rest. In addition, weight-bearing joints may “lock” or “give way” due to internal derangement, another consequence of the disease.1

Causes
So what causes cartilage to deteriorate? Sometimes we don’t know. When that is the case, the condition is called primary osteoarthritis or osteoarthritis of unknown cause. Other times, the condition can be linked to a specific health problem or issue and is known as secondary osteoarthritis.

The principal cause of primary OA is unidentified. For unknown reasons, the collagen network of the cartilage becomes jumbled; it weakens and is unable to hold its structure. As the collagen network disintegrates, proteoglycans found in all connective tissue are released and with them their water-retaining abilities. The loss of proteoglycans causes the cartilage to dry out and, over time, even crack. At the same time, the released proteoglycans draw excess fluid into the joint capsule, causing swelling.1

In contrast, the cause of secondary OA is usually straightforward. It results from various types of joint trauma—from sudden, high-velocity damage (such as a car accident) to small, repetitive insults to the joints. Specific causes of secondary OA include the following:

• Repetitive motion injury. Joints stressed over and over again in the same way are more likely to experience a cartilage breakdown.

• Joint injury. Once a joint has been injured, whether through sports or a car accident, it is much more likely to develop OA.

• Bone disease. A bone disease, such as Paget’s disease, weakens the bone structure, making it more likely to fracture and develop bony overgrowth.

• Obesity. The heavier the person, the more stress joints must bear. OA of the knee has been clearly linked to excess body weight.2

Risk Factors
How is it that some individuals experience multiple aches and pains and others never do? Specific risk factors for OA development have been identified and include the following:

• Age. OA typically develops after the age of 45. Like many other tissues, cartilage and other joint structures tend to degrade and become weaker over time. However, research has shown that OA is not inevitable as we age, even though the odds of developing it increase.

• Joint injury. Whether from a car accident or through a sports activity, injury increases the likelihood of OA development in affected joints.

• Repetitive joint stress. Anyone who overuses and repeatedly stresses a joint or joints can experience cartilage breakdown.

• Gender. Women are three times more likely than men to develop OA. The specific reason is unclear; it may be due to smaller joint structures or linked to estrogen.

• Genetics. There appears to be a genetic component to OA.

• Weight. Excess weight increases the risk of OA development.

Lifestyle as a Treatment Approach
Following a confirmed diagnosis of OA, you want a treatment plan that will alleviate symptoms and keep joint degradation to a minimum. What’s the next step?

Treatment approaches usually consist of a combination of options, including medication, both prescription and over-the-counter remedies; joint protection techniques and devices; and self-help skills. (For more information on these options, see the listed resources.)

Treatment also includes lifestyle approaches such as exercise, weight control, and diet.

Exercise
For many years, the belief was that if you have arthritis, you should not exercise because it will further damage the joints. Now, research has demonstrated that a lack of regular vigorous physical activity nearly doubles the risk for functional decline and eventual disability.3 In fact, researchers have found that expected two-year rates of functional decline in older people with arthritis could have been reduced by up to 32% with regular physical activity.

What type of activity is recommended? The best program depends on which joints are affected by OA and the severity of involvement. An exercise program can be designed for every individual. Patients should always consult their physician before beginning a program to determine what type of exercise is appropriate. Additionally, a physical therapist can help by conducting an assessment of specific exercise and joint protection needs.

Overall, an exercise program should offer a balance of three types of activity: flexibility (stretching, range-of-motion), strengthening (resistance), and cardiovascular (aerobic) exercises and can include many others, such as walking, yoga, and playing golf. It’s a matter of finding the best fit for personal needs, abilities, and interests.

Weight Loss
Being overweight by only 10 pounds increases the force on the knee by 30 to 60 pounds with each step. Without a doubt, being overweight increases the load placed on joints such as the knee, which increases stress and could possibly hasten the breakdown of cartilage. However, there is an unidentified connection between being overweight and OA because being overweight is also associated with higher rates of hand OA in some studies.4 This suggests the involvement of a circulating, systemic factor as well.

Overall, the numbers are compelling: Overweight women have nearly four times the risk of knee OA; for overweight men, the risk is five times greater.5 Population-based studies have consistently shown a link between overweight or obesity status and development of knee OA.5

Clearly, being overweight is a risk factor for developing OA. If obesity increases the risk of OA development, does weight loss help reverse the effects?

Research has demonstrated that in persons who are obese, losing as little as 15 pounds is associated with a nearly 50% improvement in knee OA symptoms.6 In The Framingham Osteoarthritis Study, researchers found that among women with a baseline body mass index greater than 25, weight loss was associated with a significantly lower risk of knee OA.

Furthermore, investigators have concluded that individuals who lose enough weight to move from the obese to the overweight category decrease their risk of knee OA by nearly 22%.7
It is interesting to note that the Arthritis, Diet, and Activity Promotion Trial found that the combination of modest weight loss plus moderate exercise provided better overall improvements in measures of mobility and pain than either the diet- or exercise-only groups.6

Diet
The idea that diet is related to arthritis is not new. For hundreds of years, physicians have “prescribed” various food-related treatments—such as cod liver oil, severe calorie restriction, and coffee enemas—for treatment of arthritis. While much is still under debate, research has shown that diet plays a valuable role in OA treatment plans.

Vitamin C
Nearly 20 years ago, The Framingham Osteoarthritis Study came forward through the now famous Framingham Heart Study.7 What the researchers observed was that OA progression was reduced by more than one half in people who consumed an average of at least 152 milligrams of vitamin C per day.

Researchers theorize that vitamin C helps reduce pain through two pathways. First is its role in the formation of collagen and proteoglycans. Second is its role as an antioxidant. Free radicals—highly reactive and unstable compounds produced by the body—can destroy cartilage and disrupt its structure. As damage occurs, inflammation is produced.

Inflammation is part of an immune response in cartilage; vitamin C is thought to be beneficial by neutralizing free radicals before they have an opportunity to destroy cartilage.

Research has continued to explore the therapeutic role vitamin C may play in OA. Overall, the findings to date have been mixed. While some studies have shown beneficial effects, others have not.8 The current advice is that vitamin C intake not be supplemented above the recommended dietary allowance.

Vitamin D
Additional findings from The Framingham Osteoarthritis Study showed that vitamin D also affects OA. Individuals with knee OA who consumed less than 350 international units (IU) of vitamin D per day had a threefold to fourfold greater risk for disease progression than those who consumed 400 IU or more per day.7

Bone is not structurally normal in OA; there is evidence of increased turnover and decreased bone mineral content and stiffness. Vitamin D is crucial for bone strength and structure. It may also play a direct role in cartilage formation itself through the chondrocytes. Even though there is a compelling biologic rationale for supplementation with vitamin D, as with vitamin C, there are conflicting results for its role in OA progression.9 Further study is underway.

Omega-3 Fatty Acids
Different types of oils contain different types of fatty acids. The fatty acids make their way into the membranes of every cell in the human body, including joint cells. Indeed, the fatty acid makeup of the cell membranes is a direct reflection of the fatty acids consumed. This is an important fact with regard to inflammation. Fatty acids are precursors of compounds called prostaglandins, some of which suppress inflammation and some of which support it. Research has provided considerable evidence that consumption of omega-3 fatty acids leads to the creation of anti-inflammatory prostaglandins.10

— Mary Kaye Sawyer-Morse, PhD, RD, LD, is a professional speaker, an author, and a wellness expert. She is owner and education director of The Center for Success, a Texas-based company that provides keynotes, in-service training, and seminars to diverse industries.

References
1. Howell DS, Altman RD, Buckwalter JA, et al. Osteoarthritis: Diagnosis and Medical/Surgical Management, 2nd ed., Philadelphia: W.B. Saunders Company Harcourt Brace Jovanovich, Increase; 1992:761-762.

2. Oliveria SA, Felson DT, Reed JI, et al. Incidence of symptomatic hand, hip, and knee osteoarthritis among patients in a health maintenance organization. Arthritis Rheum. 1995;38(8):1134-1141.

3. Shih M, Hootman JM, Kruger J, et al. Physical activity in men and women with arthritis National Health Interview Survey, 2002. Am J Prev Med. 2006;30(5):385-393.

4. Felson DT. Weight and osteoarthritis. Am J Clin Nutr. 1996;63(3 Suppl):430S-432S.

5. Creamer P, Hochberg MC. Osteoarthritis. Lancet. 1997;350(9076):503-508.

6. Messier SP, Loeser RF, Miller GD, et al. Exercise and dietary weight loss in overweight and obese older adults with knee osteoarthritis: The Arthritis, Diet, and Activity Promotion Trial. Arthritis Rheum. 2004;50(5):1501-1510.

7. Felson DT, Anderson JJ, Naimark A, et al. Obesity and knee osteoarthritis. The Framingham Study. Ann Intern Med. 1988;109(1):18-24.

8. McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum. 1996;39(4):648-656.

9. Demarco PJ, Constantinescu F. Does vitamin D supplementation contribute to the modulation of osteoarthritis by bisphosphonates? Arthritis Rheum. 2005;52(5):1622-1623.

10. Connor WE. Importance of omega-3 fatty acids in health and disease. Am J Clin Nutr.
2000;71(suppl):171S-175S.