Gout is the most common inflammatory arthritis reported in the western world. It is a metabolic condition that is associated with elevated uric acid levels. In addition, it is associated with both obesity and hypertension (Rho, et al., 2016). In addition, hyperuricaemia is very common in people with metabolic syndrome (Villegas, et al., 2012).

About one third of total plasma uric acid comes from dietary sources of purines such as meat products, animal organs, seafood and mushrooms. Purine-rich sources significantly increase plasma uric acid as mentioned above. It is typically reported that eating foods very rich in purines can increase plasma uric acid by 1.0-2.0mg / dL within 24 hours, while taking a calorie-poor but purine-free food to achieve the same reduction in levels of blood will need to pass from 7 to 10 days. More specifically, foods containing more adenine have a greater effect on plasma UA levels than if the dietary source contained more guanine, and similar effects result from eating foods that contain more RNA than DNA, respectively. Also sources of hypoxanthine, AMP (adenosine monophosphate), GMP (guanosine monophosphate), IMP (inosine monophosphate) and adenine cause greater changes in UA levels than xanthine and guanine. It is therefore understood that under the same pathological conditions different effects can be caused by taking different types of purine from food. In addition, increased intake of purine-rich foods for long periods of time can lead to insulin resistance and finally intensification of hyperuricaemia through the reduced uric acid excretion induced by insulin resistance, thus having a vicious cycle (Ekpenyuk &, 2015).

However, summing up the consumption of plant sources rich in purines, it has not been associated with the risk of hyperuricaemia and gout, mainly due to their low content of purines compared to that of animal sources (Choi, et al., 2004) (Villegas, et al., 2012) (Ekpenyong & Nyebuk, 2015). In particular, the consumption of peas, lentils and beans is considered safe, but not the consumption of soy and dried mushrooms (Ekpenyong & amp; Nyebuk, 2015).

In general, alcohol has been shown to increase the risk of hyperuricaemia. More specifically, consuming more than 15 grams per day increases the risk by 93% compared to people who do not drink alcohol. Alcohol, and beer in particular, has been associated with a 2.5-fold increased risk of gout and heavy liqueurs by 1.6-fold (Torralba, et al., 2012). Regarding wine, consumption of about 240 ml of wine per day is not associated with an increased risk of hyperuricaemia and gout. This fact is probably due to the antioxidant properties of polyphenols contained in wine (Torralba, et al., 2012)

Finally, in several studies the effect of milk proteins compared to the effect of proteins from soy dairy intake has been studied. The results showed that in the groups of participants with dairy consumption the uric acid levels decreased while in the groups consuming soy dairy the levels increased. This decrease in the milk protein intake groups and the increase in soy protein intake is explained by the fact that dairy products do not have the increased purine load in soy products (Ekpenyong & Nyebuk, 2015).

Healthy eating choices with high consumption of carbohydrates, dairy products and fiber but also limited consumption of red meat high in fat, beer and liqueurs are likely to reduce plasma uric acid levels (Zykova, et al., 2015). Encouraging the adoption of prudent eating habits is an indisputable fact that can both prevent and reduce elevated plasma uric acid levels (Ekpenyong & Nyebuk, 2015).

In addition, it would be good to mention that in Edessa we have the best “medicine” for increased uric acid. This is none other than cherries. Studies have shown that consuming cherries dramatically reduces the increased uric acid in the blood. So a good solution would be to consume it in winter, in jam (with little or no sugar) at breakfast or in some yogurt.