by Jennifer Novakovich
Gout is the most common form of arthritis in men over the age of 40 and was reported, in 2008, to affect over 8.3 million people in the United States. It is likely one of the oldest diseases and has even been observed in dinosaur bones. But it was first recognized by the Egyptians in 2640 BC. The disease is characterized by reoccurring episodes of extremely painful joint inflammation, caused by monosodium urate crystal deposits. Do you or someone you know have gout? Or are you concerned about developing gout in the future? Read on for more information about this painful disease.
Gout has markedly increased over the past few decades in parallel to the rise in obesity. In fact, more than 60% of individuals with gout have or later develop metabolic syndrome. Elevated uric acid levels, a precursor for gout, are associated with many other chronic diseases including diabetes, heart disease, hypertension, renal dysfunction, and obesity. For every 1mg of blood urate that is increased, there is a 13% heightened risk for hypertension!
Like I said before, higher levels of blood uric acid is a precursor for gout. So what is uric acid? Uric acid is a waste product of purines (e.g. adenosine, adenine, guanine) in the body following metabolism; it is our main fat soluble antioxidant, responsible for as much as two-thirds of our total antioxidant capacity. While short term increases in blood uric acid provide protection against oxidative stress, long term increases are associated with not only gout, but most chronic diseases.
Again, increased blood uric acid content is thought to be an attempt for protection against oxidative stress. Risk factors for higher uric acid include a higher weight and body fat percentage with lower muscle mass as well as the consumption of meat (especially red meat), seafood, aspirin, diuretics, alcohol and sugary foods. Drinking alcohol, at intakes higher than 15g/day, results in a 93% higher risk of gout. Risks are significantly raised by drinking as little as 10-14.9g/day. Beer has been associated with 2.5 times higher risk while liquor is 1.6 times higher (risks don't seem to be elevated through red wine consumption). Every additional meat serving per day leads to a 21% higher risk while seafood leads to a 7% higher risk. Lastly, daily consumption of sugary soft drinks increases risks for gout by 85%.
Most people with elevated blood uric acid never end up with gout, but for those who do, it usually happens by around 40–60 years of age in men and 65 in women. Males are over twice as likely to develop gout than females. Heightened uric acid in the blood can eventually lead to the formation of monosodium urate crystals, which are deposited in tissue. Eventually those deposits can lead to first acute gout—with little to no symptoms between gout attacks—and then, when not adequately treated, chronic gout—with symptoms between attacks and the formation of painful deformities. Acute gout usually begins in one joint in a lower limb and an attack results in a red, warm, swollen, and extremely painful joint. Gout is often a debilitating disease that significantly reduces the quality of life for those affected.
The goal in gout treatment is to lower blood urate levels and to dissolve urate crystals. Traditionally, on a pharmacological basis, acute gout is often managed with nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or glucocorticosteroids, while chronic gout is managed with urate-lowering therapy such as allopurinol, febuxostat, probenecid and sulfinpyrazone. Unfortunately for many, medical treatment for gout is often insufficient, and as a result individuals affected have little to no relief from gout symptoms and the development of the disease to chronic gout. Lifestyle interventions are an important component for the management of gout but unfortunately due to many factors (i.e. many doctors have little to no background in nutrition), patients are often not exposed to these recommendations.
What lifestyle interventions help manage gout? Exercise, weight loss, and also higher vegetable, nut, legume, coffee, and vitamin C consumption is associated with lower blood uric acid. Risks for gout are seen to be 40% lower with 4–5 cups of coffee a day. 1500 mg/day of vitamin C, in a supplemental form, is associated with a 45% decreased risk for elevated blood uric acid. Growing research is accumulating in the role of cherries, with their high vitamin C content, in the management of gout. Eating two servings of cherries a day is seen to significantly reduce blood uric acid, inflammation, and the number of gout attacks. There has been positive results with tart cherry juice concentrate in several small studies for the management of gout, but currently more research is needed to strengthen the validity of this treatment option. Purine-rich vegetables, nuts, legumes, and vegetable protein, despite their purine content, are not associated with gout. Furthermore, people who eat more vegetable protein have a 27% lower risk for developing gout.
So how can you take this information and apply it to yourself? First things first, you'll have to reduce things that are seen to elevate blood uric acid. Try to reduce (or eliminate) meat (especially red meat), alcohol (beer and liquor, wine can stay!), and sugary foods. Reducing fish consumption may also be a good idea but the heart protective components of fish should be considered (especially since gout increases risks for heart disease). A DHA based omega-3 supplement should be strongly considered, especially if you are to remove fish. And now, what to add.... Exercise! If you've previously led a very sedentary lifestyle, start small. Find something you enjoy so that you'll stick to it. Enrolling in a fitness class or finding a workout buddy is also another way to keep motivated. Most colleges have lots of fun workout classes—my personal favorite is aquafit! Eat more vegetables, nuts, cherries, and legumes and keep on drinking your coffee. Vitamin C supplements may also be a good addition. If you have gout and have had little relief from medical treatment, a tart cherry juice concentrate may be something good to try.
And that marks the end of my article, hopefully you now have a better idea of how to prevent and manage gout!Brook R, Forsythe A, Smeeding J, Edwards N.(2010) Chronic gout: epidemiology, disease progression, treatment and disease burden.doi:10.1185/03007995.2010.533647.Burns C, Wortmann R. (2012) Latest evidence on gout management:what the clinician needs to know. doi:10.1177/2040622312462056.Choi H. (2010) A prescription for lifestyle change in patients with hyperuricemia and gout. doi:10.1097/BOR.0b013e328335ef38.Perez-Ruiz F, Herrero-beotes A. (2012) Evaluation and Treatment of Gout as a Chronic Disease. doi:10.1007/s12325-012-0059-z.Oliveira E, Burini R. (2012) High plasma uric acid concentration: causes and consequences. doi:10.1186/1758-5996-4-12.Suresh E, Das P. (2012) Recent advances in management of gout. doi:10.1093/qjmed/hcr242.Oliveira E, Moreto F, Silveira L, Burini R. (2013) Dietary, anthropometric, and biochemical determinants of uric acid in free-living adults. doi:10.1186/1475-2891-12-11.So A, Busso N.(2012) Update on gout 2012. doi:10.1016/j.jbspin.2012.09.005.Stamp L, Chapman P. (2012) Gout and its comorbidities: implications for therapy. doi:10.1093/rheumatology/kes211.Torralba K, Jesus E, Rachabattula S. (2012) The interplay between diet, urate transporters and the risk for gout and hyperuricemia: current and future directions. doi:10.1111/1756-185X.Ye P, Yang S, Zhang W, Lv Q, Cheng Q, Mei M, Luo T, Liu L, Chen S, Li Q.(2013) Efficacy and Tolerability of Febuxostat in Hyperuricemic Patients With or Without Gout. doi:10.1016/j.clinthera.2012.12.011.See this and other articles on Jennifer Novakovich’s website JennovaFoodBlog.com
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