Study Spotlight

Study Spotlight

For Your Heart’s Sake, Skip the NSAIDs and Go with Curcumin Instead


While the non-steroidal anti-inflammatory drugs (NSAIDs) have been known to cause a variety of side effects, including liver, stomach, and heart risk, they continue to be popular over-the-counter and prescription choices for pain relief. This is especially true for anyone with chronic conditions like osteoarthritis.

However, research from the University of British Columbia in Vancouver has found that the use of NSAIDs themselves are actually the cause of 41 percent of cardiovascular disease (CVD) in people with osteoarthritis. The risk of stroke was even higher at 64 percent. In the past, the association was always understood as being due to extra load of inflammation and circulatory issues in individuals with the disease. Now, it turns out that the very drugs that people turned to for relief were truly life-threatening.

But there are alternative, effective solutions. That means that if these diseases could be managed without the use of these drugs, but with curcumin instead, the CVD risk could be potentially cut in half.

Curcumin, especially clinical studied curcumin that is blended with turmeric essential oil for enhanced absorption and blood retention, has been shown to equal – or outperform – conventional drugs for osteoarthritis pain.

 

Abstract:

Atiquzzaman M, Karim ME, Kopec J, Wong H, Anis AH. Role of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in the Association between Osteoarthritis and Cardiovascular Diseases: A Longitudinal Study. Arthritis Rheumatol. 2019 Aug 6. doi: 10.1002/art.41027. [Epub ahead of print]

OBJECTIVE: To disentangle the role of NSAIDs in the increased risk of CVD among OA patients.

METHODS: This longitudinal study was based on linked health administrative data (HAD) from British Columbia, Canada. From a population-based cohort of 720,055 British Columbians, we matched on age and sex to assemble 7,743 OA patients and 23,229 non-OA controls. We used multivariable Cox proportional hazards models to estimate the risk of developing incident CVD (primary outcome) as well as ischemic heart disease (IHD), congestive heart failure (CHF) and stroke (secondary outcomes). To estimate the mediating effect of NSAIDs, defined as current use of NSAID using linked PharmaNet data, in the OA-CVD relationship, we implemented a marginal structural model.

RESULTS: People with OA had a higher risk of developing CVD compared to people without OA. After adjusting for SES, BMI, hypertension, diabetes, hyperlipidemia, COPD, and Romano comorbidity score, adjusted HR (95% CI) was 1.23 (1.17, 1.28). Adjusted HR (95% CI) was 1.42 (1.33, 1.51), 1.17 (1.10, 1.26), 1.14 (1.07, 1.22) for CHF, IHD and stroke, respectively. Approximately 41% of the total effect of OA on increased CVD risk was mediated through NSAID. Among the secondary outcomes, the proportion mediated through NSAID was 23%, 56% and 64% for CHF, IHD and stroke, respectively.

CONCLUSION: Findings of this first study to evaluate NSAID's mediating role in OA-CVD relationship suggest that NSAID use substantially contributes to the OA-CVD association. 

 

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