Gout is the most common inflammatory joint disease in men, characterised by the formation of monosodium urate (MSU) crystals in the synovial joints and in other tissues. Urate is the final metabolite of dietary and endogenous purine metabolism. Although historically the condition was linked to men's excessive rich food and alcohol intake, food actually only contains little urate, which is mainly produced in the liver, and to a lesser extent the small intestine. A third of the urate is excreted via the gastrointestinal tract, and two thirds via the kidneys, although 90 percent of urate filtered by the kidneys is reabsorbed. There are both non-modifiable risk factors and modifiable risk factors for gout. Non-modifiable risk factors include age and gender.
Among industrialised nations, where the prevalence of gout is exceptionally high, it is reported that 25 percent of patients diagnosed with gout experience their first attack before age 30. This is despite the fact that gout is more commonly observed in older populations (over the age of 65 years). Gout primarily occurs in men, yet, with increasing age the ratio between men and women lessens. This being so, the ratio of 4 men to every 1 female, affected by gout, under the age 65, shifts to 3:1.
There is evidence to suggest that modifiable risk factors including alcohol consumption, elevated triglycerides, obesity, fruit intake and lack of physical activity have a role to play in increasing an individuals risk of developing gout or experiencing a flare. In a recent study, completed over 7 and a half years, documented that the risk of gout increased with higher alcohol intake, increased meat consumption, elevated body mass index, and a decline in fruit intake. Furthermore, the findings clearly indicated that being more physically active, maintaining ideal body weight and consuming diets enriched in fruit and limited in meat and alcohol could lower the risk of gout in men. However, one must clarify an increase in fruit consumption by stating that a study undertaken over 12 years demonstrated that the consumption of fructose rich fruits such as apples and oranges was strongly associated with an increased risk of gout.
However, what if you experience gout, yet apply the above strategies with little or no success. Then perhaps there are other factors influencing your susceptibility to gout. We know that an excessive build up of uric acid crystals in the blood is responsible for gout. However, there is new evidence to suggest that some individuals present with particular gene loci that may increase their susceptibility in storing high levels of uric acid in the blood. For example, the genetic variations in the gene SLC2A9, have been strongly associated with reduced urinary urate clearance and increased serum uric acid levels in various parts of the world including Croatia, Germany, Italy and United Kingdom.
There is also evidence to suggest that particular immune markers, known as cytokines are detected in higher levels in patients diagnosed with gout. High levels of the cytokines IL-1 Beta; IL-6, TNF-alpha, and chemokines such as IL-8 have been detected in the synovial fluid of patients with gout. Among new therapies, biological anti-cytokine agents have been explored with pleasant result. Nonetheless, they prove costly.
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