The research, led by Dr. Georg Schett of the Department of Internal Medicine, University of Erlangen-Nuremberg, Germany, involved 927 adults aged 40 to 80 who were followed over a 20 year period. The researchers found that the presence of diabetes resulted in a 3.8-fold increase in the risk of requiring arthroplasty. Even after adjustment for potential confounders such as obesity and level of physical activity, the risk of arthroplasty remained higher in the diabetes group. In the fully adjusted model, diabetics were still at 2.1 times greater risk of requiring arthroplasty than non-diabetics.

The increased risk of arthroplasty applied to both men and women and across all ages and weight ranges. The researchers also noted that the diabetics who required arthroplasty had a longer duration of diabetes than those who did not require the surgery.

While it has long been known that diabetics are at a greater risk of suffering severe arthritis, it had been thought the risks were primarily due to lower levels of physical activity and higher rates of obesity among diabetes sufferers. This research suggests that other factors may be a play.

One possibile mechanism is that tnf-alpha, a cytokine which promotes the inflammatory response and plays a key role in the development of rheumatoid arthritis, also interferes with insulin signalling leading to the development of insulin resistance and diabetes. Support for this theory can be found in studies that have found lower rates of diabetes in arthritis sufferers treated with anti-TNF-alpha therapy. For example, a study published earlier this year in the journal Arthritis Care & Research found that among a group of 1,587 rheumatoid arthritis patients who were initially free of diabetes, the use of anti-TNF-alpha treatments reduced the subsequent risk of developing diabetes by 51%.

The graph to the right shows the prevalence of arthritis in both diabetics and the general population in the USA as calculated by a 2008 CDC report. The prevalence of arthritis is 52% in diabetic adults compared to just 26.9% in the general population.

The differences in prevalence are most striking for younger adults with diabetics aged under 45 more than 2.5 times more likely to have arthritis than the general population.

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Timothy Beukelman of the University of Alabama at Birmingham and colleagues looked at cancer rates in a group of 7812 children suffering from juvenile idiopathic arthritis (JIA) and compared them to two control groups who did not suffer from the disease. The children diagnosed with JIA were followed up for a total of 12,614 person-years, with 10 cases of cancer occurring over the course of the study. This represented a cancer incidence rate that was 4.4 times the rate seen in the control group.

Leukaemias and brain tumours are the two most common forms of cancer in children. The latest SEER data puts the yearly incidence rate at 4.5 per 100,000 and 3.2 per 100,000 for childhood leukaemia and brain cancer respectively. In this study, 3 cases of leukaemia and 3 brain malignancies occurred in children with JIA which corresponded to annual incidence rates in excess of 20 per 100,000.

The researchers also compared the rates of cancer in the JIA children by the treatment they had received. 44% of the JIA patients had received either methotrexate or leflunomide, 19% had received anti-TNF drugs, 5% other immunomodulatory agents, while 32% had not received any treatment. The methotrexate users had a slightly lower cancer rate than other JIA patients however it was was still 3.9 times greater than the control group. Amongst the group of anti-TNF users, no cases of cancer were diagnosed during 2,922 person-years of follow up .

The results of this study are reassuring in that it makes a strong link between treatment for JIA and an increased risk of childhood cancer unlikely, although given the relatively small numbers of cancer cases in the JIA group and the rarity of childhood cancer in general, larger studies are needed to confirm these findings.

Previous studies had suggested that both methotrexate and anti-TNF drugs could increase the risk of cancer in adults suffering from rheumatoid arthritis (RA). One study, published in the journal Arthritis Care and Research in June 2008, found that individuals with RA who were treated with methotrexate were at a 50% increased overall risk of developing cancer. Non-Hodgkin’s lymphoma, lung cancer, and melanoma were the forms of cancer most strongly linked to methotrexate use.

Other studies had linked anti-TNF drugs with an increased risk of a rare form of lymphoma known as Hepatosplenic T-Cell Lymphoma and an approximately 2-fold increase in the risk of non-melanoma skin cancers, however the absolute risk of developing either form of cancer is still very low, and in the case of non-melanoma skin cancer, the disease is rarely fatal or a cause of significant morbidity.

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A study, published in The American Journal of Medicine in 2003 found that in a group of 37 rheumatoid arthritis patients, low vitamin B6 status was associated with higher disability scores, more morning stiffness, and a greater degree of arthritis pain compared to those with higher levels of the vitamin.

Vitamin B6 is believed to reduce the severity of arthritis symptoms through a reduction in inflammation levels in the body. A 2010 study, published in the European Journal of Clinical Nutrtion, involved 35 rheumatoid arthritis who were randomized to receive either 5mg of folate a day (control group), or 5mg of folate and 100mg of vitamin B6 (intervention group) over a 12 week period.

At the conclusion of the study, the researchers found significant reductions in the levels of two inflammatory markers in the vitamin B6 group. Interleukin-6 levels were reduced by an average of 7.0% while TNF-alpha levels were reduced by 4.2% on average. No significant changes were observed in the control group.

The current RDA for vitamin B6 is 1.3mg for adults aged 19-50. For adults over 50, the RDA’s are 1.5mg to 1.7mg for women and men respectively although arthritis sufferers could benefit with intakes as high as 50mg per day. The tolerable upper intake (the highest level where side effects would not be expected for most people) for vitamin B6 is 100mg per day although it is extremely unlikely an individual would get close to this amount through dietary sources alone. Most vitamin B6 supplements contain between 50mg and 100mg although there are some on the market than contain as much as 500mg. If you choose to take more than 100mg of vitamin B6 a day, be aware of symptoms of toxicity such as nausea, poor coordination, a persistent fever, and numbness, particularly in the hands and legs.

Good dietary sources of vitamin B6 include (mg per serving in brackets): beef liver (1.3mg), tuna (1.18mg), pistachio nuts (1.0mg), bananas (0.68mg), spinach (0.44mg), garlic (0.35mg), red peppers (0.23mg), and sunflower seeds (0.2mg).

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The study focused on 13,639 women from the Nurses Health Study who were followed between 1976 and 2002. During that time 683 (5.0%) of the women developed rheumatoid arthritis. The researchers found that women with a birth weight greater than 10 pounds (4.54 kg) were 2.1 times more likely to develop rheumatoid arthritis later in life than women with a normal birth weight between 7 and 8.5 pounds (3.2 to 3.85 kg). The results persisted even after adjustment for potential confounders such as mothers socio-economic status, parental smoking, and maternal diabetes.

While the mechanism which links heavy babies to rheumatoid arthritis is unknown, researchers believe that hormone imbalances observed in rheumatoid arthritis sufferers may be “programmed” during early fetal development.

The study adds support to the idea that the probability of developing certain diseases may be influenced by processes that occur during pregnancy, a theory known as the “fetal origins of adult disease hypothesis”. A low birth-weight for example has been linked to an increased risk of heart disease, strokes, childhood asthma, and type-2 diabetes while a very high birth-weight has been linked to certain cancers such as leukemia, colo-rectal, ovarian, prostate, and breast cancer.

Another possible explanation for the link lies in the fact that very heavy babies are more likely to become obese later in life. The risk of developing rheumatoid arthritis is around 50% higher in obese individuals compared to the general population.

Interestingly, while the average weight of an American adult has steadily increased over the last 50 years, the average weight of infants at birth has actually decreased slightly. In 1995, the average infant weighed 3.35 kg compared to 3.32 kg in 2008. This is likely due to an increasing percentage of babies born to women aged over 45 (very young and very old mothers are more likely to give birth to underweight babies).

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The study, conducted by researchers at the Malmo University Hospital in Sweden, compared 136 individuals who had been diagnosed with rheumatoid arthritis to 544 women who were free of the illness.

The researchers found that when compared to not breast-feeding at all, breastfeeding for between one month and a year reduced rheumatoid arthritis risk by 26% while breast feeding for more than 13 months cut the risk by 54%.

The authors noted that the study was quite small and further research is required to establish the link between breastfeeding and rheumatoid arthritis.

The results of this study are actually in contrast with others which have found a slight increase in arthritis risk amongst breast-feeding mothers.

Breast-feeding raises the levels of certain hormones that may have both positive and negative effects on arthritis risk. The hormone prolactin for example is known to stimulate the immune system and may increase arthritis risk in the short term because rheumatoid arthritis is an autoimmune disease.

The percentage of mothers who breast-feed is currently increasing however most stop well before the baby reaches one year of age. Around 75% of mothers start out by breast-feeding with 40% still breast-feeding when the child is six months of age. Just 20% of mothers breast-feed for more than a year.

The researchers also looked at use of the oral contraceptive pill and the risk of arthritis but failed to find a significant link between the two.

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Researchers compared mice who were fed water containing 0.2% green tea polyphenols with mice who received pure water after the mice were injected with collagen in order to induce arthritis.

In three independent tests, the mice in the group fed the green tea extract were less likely to develop arthritis, tended to develop the disease later in life, and experienced less severe arthritis. In the first study 33% of mice developed arthritis in the green tea group compared to 100% in the pure water group. The average time to the onset of arthritis symptoms was 38 days for the green tea group and 32 days for the control group.

Results were similar in the other two studies with 50% of the mice developing arthritis in the green tea group in both the second and third studies while 100% and 83% of the mice in the control groups developing arthritis. The mean time to onset of arthritis in the green tea group was 36 and 45 days for studies two and three respectively compared to 32 days in both of the control groups.

Across the three studies combined, 44% of the mice fed the green tea extract developed arthritis while 94% of the mice who received pure water developed arthritis.

The severity of arthritis as measured by the arthritis index was also greater in the control groups than the green tea groups. Arthritis index scores were 1.00, 1.16 and 1.33 for the green tea groups and 4.16, 4.66 and 4.00 in the control groups.

Lead researcher Tariq M. Haqqi, who is the associate professor of medicine at Case Western Reserve University in Cleveland added that: “Extensive laboratory research and the epidemiologic findings of the last 15 years have revealed that polyphenolic compounds present in green tea may prevent the onset and subsequent progression of a variety of illnesses. Perhaps now arthritis can be added to the list.”

Polyphenol compounds including epicatechin, catechin, epigallocatechin (EGC), and epigallocatechin gallate (EGCG), are thought to be responsible for green teas positive effects on arthritis. A potential mechanism for the benefits of green tea may be through the ability of certain catechins to act as histidine decarboxylase inhibitors. Histidine decarboxylase is an enzyme involved in the conversion of histidine to histamine and some studies have linked histamine to the inflammatory process that occurs in rheumatoid arthritis. A 2007 study, published in the Journal of Agricultural and Food Chemistry, found that both EGC and EGCG were powerful inhibitors of histidine decarboxylase.

It is believed that green tea may also help prevent cardiovascular disease and some studies have shown consumption of green tea may reduce the incidence of some cancers such as prostate cancer.

Tea is the most popular beverage in the world excluding water. Black tea tends to be more popular than green tea accounting for almost 75% of global tea consumption. Black teas tend to have lower levels of antioxidants and phenolic compounds than green tea. Green tea has been very popular in Asia since 2,000 BC but has only recently started to gain popularity in the western world.

Those who have early stage rheumatoid arthritis, or who believe they may be at risk of the disease should consider switching from drinking coffee to tea as some studies have linked regular coffee consumption with an increased risk of arthritis.

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The largest study looking at the effect of vitamin D on rheumatoid arthritis was published in January 2004 in the journal Arthritis and Rheumatism. Researchers in that study analyzed 29,368 women who had participated in the Iowa Womens Health Study. The participants were aged between 55 and 69 and were initially free of rheumatoid arthritis. They were followed over an 11 year study period between 1986 and 1997.

During the study 152 cases of rheumatoid arthritis were identified. The researchers found that those who consumed more than 200 IU of vitamin D each day were 33% less likely to develop rheumatoid arthritis than those who consumed less than 200 IU of vitamin D. The associations were similar for vitamin D intake from both dietary sources and vitamin supplementation and the associations remained after the results were adjusted for other potential risk factors such as BMI and smoking.

The study did not however consider sunlight exposure, which is an important source of vitamin D, which may weaken the significance of the findings.

Vitamin D along with calcium are important for maintaining healthy joints and cartilage and preventing the loss of bone density. Vitamin D is also an immunosuppressant and because rheumatoid arthritis is an autoimmune disorder caused by an individual’s immune system attacks cells in the joints, vitamin D may help prevent this from occurring

The recommended daily intake of vitamin D is 200 IU/day for people up to the age of 50 and 400 IU/day for those over the age of 50 however vitamin D is thought to be safe in doses up to 10,000 IU/day. Although sunlight is the primary source of vitamin D for most people, in countries at very high and low latitudes, levels of UV-B from the sun are insufficient in winter to allow the body to synthesize vitamin D. In this situation getting vitamin D from foods becomes important. Significant dietary sources of vitamin D include mushrooms (200-1000 IU/serving), cod liver oil, salmon (360 IU/serving), tuna (200 IU/serving), eggs (20 IU/egg), and fortified beverages such as milk and orange juice.

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One of the largest studies on the impact of smoking on rheumatoid arthritis was a British case-control study published in the journal Annals of the Rheumatic Diseases in 2001. In that study, 239 people who had been diagnosed with rheumatoid arthritis were compared to 239 healthy control subjects who were matched by age, sex, and job status.

In the rheumatoid arthritis group, 100 (42%) were current smokers, 55 (23%) were ex smokers while the remaining 84 had never smoked, while in the control group, just 52 (22%) current smokers. The average age of both groups was 60.5 years.

The researchers found that those people who had never smoked were almost half as likely to develop rheumatoid arthritis compared to those who had ever smoked. The researchers also found a strong correlation between heavy smoking and rheumatoid arthritis, particularly in those without a family history of rheumatoid arthritis. Those who had smoked between 31 and 40 pack years had 5.72 times greater odds of developing rheumatoid arthritis while those who smoked between 41 and 50 pack years had 13.54 times greater odds of developing the disease. In contrast, less than 20 pack years of smoking did not appear to increase the risk of rheumatoid arthritis.

A pack year is defined as a year of smoking 20 cigarettes per day, the equivalent of 7,300 cigarettes. An individual who smoked 40 cigarettes a day for 30 years would therefore be considered to have smoked for 60 pack years.

It is believed that smoking may increase the levels in the blood of an antibody called rheumatoid factor (RF). RF antibodies are found in the majority of rheumatoid arthritis sufferers and the antibody is a strong indicator that a person will develop rheumatoid arthritis during their life. Just 5% of people without rheumatoid arthritis have RF while 70% of people with rheumatoid arthritis have the antibody.

While genetics plays a large role in whether a person will have the RF antibodies, some lifestyle factors are also thought to contribute to the development of RF. It is believed that smoking is one of these factors because RF is more commonly found, and found at higher levels in smokers compared to non smokers. An American study, published in the journal Annals of the Rheumatic Diseases in 1997 found that those who had smoked for more than 25 pack years were 3.1 times more likely to test positive for RF antibodies than non-smokers.

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One study, published in the journal Circulation in 2003, involved 114,342 women from the Nurses Health Study who were followed for 18 years. At the end of the study, 7,786 women (7%) reported to have developed symptoms of rheumatoid arthritis. The researchers found that both heart attacks and strokes were more common in women with rheumatoid arthritis compared to those without the disease.

After controlling for several variables including cholesterol, age, physical activity, BMI, and alcohol consumption, heart attacks were found to be twice as common in the rheumatoid arthritis group compared to the women without rheumatoid arthritis. Strokes were 1.5 times more common in the rheumatoid arthritis group however the association between strokes and rheumatoid arthritis was not statistically significant at the 95% confidence level.

A second study, published in 2006 by researchers in Boston, Massachusetts found similar results. That study included both men and women and found that rheumatoid arthritis sufferers were 1.6 times more likely to have one of three events: a stroke, a heart attack, or death due to cardiovascular disease.

The study also found that people who developed rheumatoid arthritis at a young age (before 40) had the greatest increase in cardiovascular risk. They were 3.3 times more likely to have one of the three events compared to a person of the same age without the illness.

While rheumatoid arthritis does not appear to be as significant a risk factor for cardiovascular disease as other known risk factors such as diabetes, hypertension, or obesity – rheumatoid arthritis sufferers do appear to be at a small, but significant increased risk of cardiovascular disease and therefore need to take extra care of their heart.

It is thought that certain genes, that are known to increase the risk of developing rheumatoid arthritis may also play a part in cardiovascular disease. It is also possible that heavy use of NSAID’s and other drugs used to treat rheumatoid arthritis may be the cause of the increased risk of heart problems.

According to Dr. Christopher Edwards, one of the authors of the Boston study, “Our findings are just another piece of evidence that demonstrates rheumatoid arthritis is a systemic disease and patients need systemic care. You can’t just look after their joints.”

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Researchers at the Gothenburg University in Sweden injected mice with collagen to initiate collagen induced arthritis (CIA) in the mice. The mice were injected at the beginning of the experiment and received an additional injection after three weeks. CIA development in mice is as established model of rheumatoid arthritis in humans.

25 of the mice drank water with 10% ethanol added while the remaining 27 mice received water only. 30 days into the study (9 days after the booster injections), 23 of the 27 control mice (85%) had developed collagen induced arthritis while just 5 of the 25 (20%) mice that drank ethanol developed arthritis.

After five weeks, all of the control mice had developed arthritis while more than 60% of the ethanol drinking mice remained free of arthritis. Furthermore, arthritis was less severe in the ethanol fed mice with less inflammation of joints and destruction of bone and cartilage observed.

Researchers believe that moderate alcohol consumption may increase testosterone levels circulating in the body. In the mice study, ethanol consumption led to a significant increase in testosterone levels compared to the control mice.

Treatment of arthritis with testosterone is known to reduce the severity of arthritis. Testosterone restricts the releasing of certain proteins known as cytokines that cause inflammation in the body. This is reinforced by the observation that males, especially younger males are less likely to develop rheumatoid arthritis at a given age than females.

Studies on the effects of alcohol on testosterone in humans have been mixed however with some studies finding heavy alcohol consumption actually inhibits testosterone secretion leading to a reduction in testosterone levels in the body.

The researchers also found that acetaldehyde or ethanal, which is produced when the body metabolizes alcohol, produces a similar protective effect against arthritis.

While mild alcohol consumption may benefit arthritis sufferers in addition to protecting against cardiovascular disease, heavy alcohol intake is known to increase heart disease risk, cause brain and liver damage, and supress the immune system, raising the risks of developing infections such as pneumonia and tuberculosis.

According to Professor Andrej Tarkowski, who led the research, it is difficult to translate the ethanol dose received by the mice into an amount that would create a similar effect in humans:”We can’t translate these results to find out the therapeutic dose in humans. The mice were given a dose of 10% of alcohol in their water, but we don’t know if it would be the same for humans. It would probably be lower.”

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97 patients took part in the nine month study which involved individuals being randomly assigned to a group receiving either a 10g cod liver oil capsule each day or an air filled placebo capsule. The participants were asked to gradually reduce or stop their NSAID intake.

At the conclusion of the study, 39% of the cod liver oil group were able to reduce their intake of NSAID’s by at least 30% while only 10% of the placebo group were able to reduce their NSAID intake by the same amount. Overall the cod liver oil group were able to reduce NSAID intake by an average of 40% while the placebo group achieved only a 16% reduction in NSAID usage.

Patients in the cod liver oil group also reported a significant reduction in pain as measured by the Visual Analogue Scale (VAS) compared to those in the placebo group.

While NSAID’s are relatively safe, their long term use can cause gastrointestinal problems including stomach ulcers, vomiting, and diarrhea. They may also increase the risk of cardiovascular events such as strokes and heart attacks, particularly in the elderly. There is also some evidence that long term, high dose use of non-aspirin NSAID’s increases the risk of kidney cancer. For these reasons, doctors advise against long term, high dose usage of NSAID’s when possible. The most common NSAID’s used by arthritis sufferers include aspirin, ibuprofen. voltaren, naproxen, and celebrex.

According to Alisa Bosworth, who is the United Kingdom National Rheumatoid Arthritis Society chief executive “People with rheumatoid arthritis still rely heavily on NSAID’s, even though the safety of these drugs is under scrutiny.”

Researchers believe the anti-inflammatory properties of the omega 3 essential fatty acids, DHA and EPA, which are found in high levels in cod liver oil are behind the reductions in pain. A 10g serving of cod liver oil typically contains 2.2g of these essential fatty acids although some high potency formulations may provide more. Although 10g is quite a high daily dose, fish oil capsules have an excellent safety profile and side effects are seldom observed in doses as high as 25g a day.

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The study, lead by researchers at the Karolisnka Institute in Stockholm, Sweden, followed 66 volunteers who had been diagnosed with rheumatoid arthritis. 38 of the volunteers followed a vegan, gluten free diet consisting of foods such as nuts, seeds, fruit, and vegetables. The diet consisted of around 10% protein, 60% carbohydrate, and 30% fats. The remaining 28 volunteers followed a healthy, non-vegan diet with the same proportions of carbohydrates, fats and protein. The volunteers remained on the diets for a year.

Those who switched to the vegan diet showed an improvement in the number of swollen joints they had, from an average of 5.3 joints to 4.3 joints. Those on the vegan diet also had reduced amounts of C-reactive protein (CRP) circulating in the blood, CRP is a measure of the amount of inflammation in the body. High CRP levels are often found in rheumatoid arthritis sufferers and are a predictor for future cardiovascular problems such as heart disease and strokes.

Those on the vegan diet also had higher levels of natural antibodies known as antiPC. AntiPC antibodies are thought to help protect against damaging compounds in the body that are thought to cause cardiovascular disease and arthritis.

The vegans also experienced reductions in body mass index and LDL cholesterol levels. BMI levels at 12 months were 22.7 compared to 24.1 at the beginning of the study while LDL cholesterol dropped from 3.2 mmol/L to 2.4 mmol/L. HDL cholesterol levels and triglyceride levels remained similar throughout the study.

The authors of the study, which is published in the journal Arthritis & Therapy, concede that due to the relatively small sample size, larger studies need to be conducted to confirm the benefits of vegan diets for those suffering rheumatoid arthritis.

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One such study was conducted by researchers at the University of Manchester and published in the American Journal of Clinical Nutrition in 2005, and involved following 25,000 participants from the EPIC study between 1993 and 2001. During the study, 88 people developed inflammatory polyarthritis, which was defined as arthritis in 2 or more joint groups.

On average, those who developed arthritis had a 20 percent lower daily intake of the carotenoid zeaxanthin and a 40 percent lower daily intake of beta-cryptoxanthin. Furthermore, those individuals in the top-third of zeaxanthin intake had a 52 percent reduced risk of arthritis compared to those in the bottom-third of zeaxanthin intake. Those in the top-third for beta-cryptoxanthin intake were at a 48 percent reduced risk of developing arthritis.

The study failed however to find an association between high intakes of two other carotenoids, lutein and lycopene, and reduced arthritis risk.

The researchers believe that carotenoids may help prevent arthritis by reducing inflammatory processes involved in the disease. Studies have found that individuals with high carotenoid consumption have lower levels of C-reactive protein, a measure of systemic inflammation. C-reactive protein levels are often elevated in rheumatoid arthritis sufferers.

The researchers did however note that while the overall number of people in the study was large, the number of inflammatory polyarthritis cases identified was relatively small, making it difficult to accurately determine the link between specific carotenoids and arthritis risk without further trials. The authors write: “there is perhaps sufficient evidence to suggest a trial to test whether an increase in the consumption of foods that are high in dietary carotenoids and other antioxidant nutrients during early inflammatory joint disease decreases the risk of persistent disease and possibly joint damage.”

The amount of beta-cryptoxanthin required to put an individual in the highest third of beta-cryptoxanthin intake in this study is the equivalent of just a glass of orange juice a day. Foods high in beta-cryptoxanthin include red peppers, pumpkin, tangerines, peaches, oranges, pineapples, papayas, lemons, other yellow and orange fruits, and herbs such as paprika. Studies have also shown that beta-cryptoxanthin can improve lung function and reduce the risk of lung cancer.

Foods high in zeaxanthin include corn, egg yolk, oranges, honeydew melons, orange peppers, and mangoes. Zeaxanthin also plays an essential role in eye health and may reduce the affects of macular degeneration.

This study backs up the findings of previous studies that have found diets rich in fresh fruits and vegetables may reduce arthritis risk. For example, this study found frequent consumption of cooked vegetables could reduce the odds of developing rheumatoid arthritis by as much as 61%.

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The majority of arthritis cases occur through wear and tear of joints, particularly the hip and knee. It is well known however that a small number of arthritis cases are the result of joint fractures. It had also been suspected that sprains or strains of certain joints such as the ankle could lead to arthritis.

The authors of the study, based at the University of Basel in northern Switzerland, studied 268 patients who had presented with arthritis of the ankle. A massive 221 (82.5 percent) of these individuals had experienced a fracture of the ankle. A further 47 (17.5 percent) of the individuals have experienced repeated ankle sprains and/or chronic ankle stability.

Interestingly, the delay between the onset of ankle problems and arthritis was quite long. Those with ankle fractures developed arthritis on average 21 years after the fracture. In the group with ankle sprains, arthritis developed an average of 22.5 years later.

One of the researchers, Dr. Victor Valderrabano, who is based at the Orthopedic Department at the University of Basel suggests that chronic instability of the ankle joint may increase the forces acting on it leading to increased wear and tear and consequently an increase in the risk of inflammation and arthritis development.

Ankle sprains and strains are the most common injuries experienced in sports and recreational activities. They are particularly common in running and jumping sports, accounting for over a quarter of all injuries.

Ankle care and rehabilitation following injuries is often inadequate with around a third of ankle injuries progressing to chronic ankle instability. Around three-quarters of people with chronic ankle instability will go on to develop arthritis of the ankle.

The researchers stressed the need for adequate rehabilitation of ankle injuries to prevent complications later in life. “The person should strengthen muscles to become more immune to injury. Follow-up with a doctor to determine if the ankle is still unstable is crucial, too,” concluded the research team.

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Some studies have also linked weight with osteoarthritis in other areas such as the hands which suggests there may be other factors associated with weight gain that increase osteoarthritis risk besides the extra load on weight bearing joints.

It is estimated that the force exerted on the knee joints while walking is between 2 to 7 times a persons body weight. This means a person just 20 pounds heavier than their ideal weight could be exerting more than 100 pounds of additional force on each knee joint.

Data from the first National Health and Nutrition Examination Survey (HANES I) has suggested that obese women are almost four times more likely to develop osteoarthritis in the knee compared to women of a healthy weight and that obese men are as much as five times more likely to develop osteoarthritis in the knee.

Another study called “Age, bodyweight, smoking habits and the risk of severe osteoarthritis in the hip and knee in men” which was published in the European Journal of Epidemology involved over 320,000 male construction workers. The study found a linear correlation between BMI and the incidence of osteoarthritis in both the hip and knee. This correlation was present even at relatively low BMI levels. An increase in BMI of 5 doubled the risk of developing osteoarthritis in the knee.

Finally a report, published in the Journal of Rheumatology involving the study of twin pairs, found that obesity was a risk factor in the development of both arthritis in the hands and in the joints of the knee. Overall the study found that the risk of developing osteoarthritis increased by between 9 and 13 percent per kg increase in body weight.

The good news is that losing even a moderate amount of weight can reduce your chances of developing arthritis significantly. Furthermore, those who have already developed arthritis can reduce both the pain caused by their arthritis and the progression of the disease by managing their weight.

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The study which was funded by the Arthritis Research Campaign and led by Dr. Tracey M. Farragher at the University of Manchester involved over 1,000 individuals with arthritis. At the conclusion of the study 242 of the patients had died with cardiovascular disease responsible for just under a third of the deaths.

The researchers found that individuals with a particular combination of a gene called HLA-DRB1, which is associated with an increased risk of developing rheumatoid arthritis, were three times more likely to develop cardiovascular disease than those without the gene combination. Furthermore their appeared to be interactions between the gene combination and smoking that increased the risk of cardiovascular disease even further. Individuals with the high risk gene combination who also had anti-CCP antibodies (antibodies directed against the bodies own proteins that are found in most, but not all RA sufferers), and who currently smoked were a massive 7.81 times more likely to die from cardiovascular disease.

According to Professor Alan Silman, who was involved in the research “We have known for some time that smoking is a major risk factor for developing rheumatoid arthritis, but this study confirms that rheumatoid arthritis patients with this particular genetic variant who continue to smoke are putting themselves in considerable danger of life-threatening cardiovascular disease.”

The inflammation associated with rheumatoid arthritis is thought to be associated with atherosclerosis (hardening of the arteries) which increases the likelihood of an individual suffering a heart attack or stroke. It is also possible that decreased exercise seen in individuals suffering from arthritis may also be responsible for increasing cardiovascular risk.

The research is reported in issue two of the February 2008 edition of “Arthritis & Rheumatism”, a peer reviewed journal of the American College of Rheumatology.

Previous studies have found a 2 to 3-fold increase in the risk of cardiovascular disease, even after adjustment for known cardiovascular risk factors. A 2003 study, involving 114,342 from the Nurses Health Study (NHS), and published in the journal Circulation, found that women who had been diagnosed with rheumatoid arthritis had 2.07 and 1.47 times the risk of suffering a heart attack or stroke respectively than women free of rheumatoid arthritis.

While the women suffering from arthritis had marginally decreased physical activity, increased rates of hypertension, and were less likely to have never smoked, adjustment for these and other cardiovascular risk factors made little difference to the results. Cardiovascular risk was also linked to the duration of rheumatoid arthritis with women suffering from the disease for at least 10 years 3.1 times more likely to suffer a myocardial infarction.

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Probably the largest clinical study of glucosamine’s effectiveness was funded by the National Institutes of Health (NIH), which is an agency of the US Department of Health and Human Services, and involved a 6 month trial where 1,583 osteoarthritis patients received one of five treatments. The treatments were glucosamine supplementation, chondroitin supplementation, a combination of both, a NSAID used for treating arthritis called celecoxib, or a placebo.

The researchers found that neither glucosamine nor chondroitin reduced arthritis pain compared to the placebo, however a subgroup of patients who had moderate to severe pain did experience a statistically significant benefit from taking both supplements. In this group, 79% of participants experienced at least a 20% reduction in pain compared to 54% for the placebo.

A separate study called “Glucosamine and chondroitin for treatment of osteoarthritis: A systematic quality assessment and meta-analysis” which was published in the Journal of the American Medical Association in 2000 and involved analyzing data from a large number of clinical trials concluded that “Trials of glucosamine and chondroitin preparations for OA symptoms demonstrate moderate to large effects, but quality issues and likely publication bias suggest that these effects are exaggerated. Nevertheless, some degree of efficacy appears probable for these preparations.”

A third study published in the Lancet, a British medical journal, found that in a trial involving 212 individuals with osteoarthritis, symptoms improved by 20 to 25 percent in the glucosamine group compared to a slight worsening of symptoms in the control group. Furthermore x-ray examinations of patients showed that the glucosamine group had reduced narrowing of the knee-join space, an indicator of osteoarthritis progression, when compared to the control group.

Benefits to osteoarthritis sufferers from glucosamine are thought to come through one of two mechanisms. First, through glucosamine’s anti-inflammatory action that can help reduce the pain associated with arthritis, and secondly, by stimulating the production of both proteoglycans and collagen, which are both essential elements of healthy cartilage.

Despite conflicting claims on the effectiveness of glucosamine, it has an excellent safety profile and with very few side-effects, even with long term use at high doses, it is probably worth a try for osteoarthritis sufferers.

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