Christmas is time of celebrations and indulgence, however, one must try to maintain some balance. Two dietary components contributing to gout and featuring during Christmas celebrations are excess alcohol and fructose (also known as fruits sugar). Considering that sugar is fructose (Bray et al 2004), it is easy to overindulge on fructose intake, especially during Christmas.
However, in his review Rizkalla (2010) argues that moderate fructose consumption of 50g/day – 100g/day has no deleterious effect. So read those labels!
Gout – ‘The Disease of Kings’
Gout is a metabolic disease associated with elevated blood levels of serum uric acid, the end product of purine metabolism (Jamnik et al 2016).
Gout is sometimes referred to the ‘Disease of the Kings’, as for many years the condition was thought to be directly linked to an overindulgence of rich foods such as wine and red meat that only wealthy individuals were considered to be able to purchase (Zychowicz 2011).
Uric acid – the major culprit in gout
As explained by Perez-Ruiz et al (2015), uric acid is a metabolic by-product found in high levels in the blood / joints of gout sufferers. Uric acid is a normal waste product of protein / purine breakdown.
Purines are natural substances and nitrogenous bases found in all cells (adenine, guanine & hypoxanthine), best known as building blocks of DNA and RNA, as well as components of high energy compounds in the cell (AMP, ADP & ATP) (Appleton & Vanberg 2015:90). A small number of foods contain concentrated amounts of purines – e.g. organ meats like kidney, fish like mackerel, herring, sardines, mussels, and also yeast (Perez-Ruiz et al 2015). In addition, high fructose drinks, red meat, beer or liquor also appear to increase the risk of developing gout (Zychowicz 2011).
Aetiology of gout
As explained by Doherty (2009), gout normally results from the interaction of genetic, constitutional and environmental risk factors. A major determinant is the degree of elevation of uric acid above the saturation point, principally caused by inefficient renal urate excretion. When serum uric acid concentrations are lowered below the monosodium urate saturation point, the crystals dissolve and gout can be cured (Richette & Bardin 2010).
Who is at risk?
Gut is five times more common in men (Wiederkehr & Moe 2011) and is strongly age related (Doherty (2009). According to Arthritis Action (2015), the prevalence of gout is highest in males over 40 years. Although gout is more common in men, its prevalence in women is increasing, particularly in older women (Bhole et al 2010).
Obesity, diabetes, kidney failure and Metabolic Syndrome are also risk factors (Doherty 2009).
What are the tell-tale sign of gout?
Acute gout is characterized by a sudden, rapid onset, with intense pain, mostly affecting the big toe at initial attacks), the foot, ankle, midtarsal, knee, wrist, finger, and elbow (Grassi & De Angelis 2012). Severe throbbing in the big toe is usually felt late at night and the swollen site may be red, warm to the touch, tender, the skin may look shiny, purple (looking bruised) or flaky (NHS Choices 2015). Attacks of gout usually last approximately 3 – 10 days (NHS Choices 2015).
Conventional treatment for gout
According to Wilson & Saseen (2016), NSAID’s are used to treat acute gouty arthritis as they reduce the levels of pain and inflammation and help to shorten the gout attack. However, Xanthine oxidase inhibitor therapy is used as the first-line treatment option for the prevention of recurrent gout.
How to avoid gout
Avoid purine rich foods – as noted by Choi et al (2014), you should limit or avoid your consumption of purine-rich foods (shellfish, sardines & anchovies, red & organ meat, poultry, yeast & meat extracts) and avoid alcoholic drinks (especially beer) and beverages sweetened with high-fructose corn syrup.
Avoid excessive red meat – as reported by Nickolai & Kiss (2016), each additional intake of meat potion per day increases the risk of gout. As explained by Zykova et al (2015) gout is most common among people whose diet is rich in meat and low in fruits & vegetables. Animal protein is abundant in sulfur-containing amino acids, a main determinant of urine acidity, hence, individuals whose diet is rich in animal protein will excrete more acidic urine, leading to the difficulty in uric acid excretion (Kanbara et al 2010).
Avoid excessive alcohol – as explained by (Choi et al 2005), alcohol consumption increases serum uric acid levels by decreasing uric acid excretion while increasing its production. Alcohol metabolism also favours lactic acid As noted by Yamamoto et al (2006), increased lactic acid in the blood accelerates reabsorption of uric acid in the kidneys, and its accumulation in the tissues, where uric acid crystallises causing gout.
Avoid beer drinking – beer is higher than other alcohols in purine content and can therefore increase the serum uric acid concentrations (Stibůrková et al 2014). The Third National Health and Nutrition Examination Survey by Choi et al (2005) showed that beer, despite having a lower alcohol content, increased the risk of gout per serving by compared to by spirits. The authors attributed this to the large purine content of beer.
Avoid fructose-rich foods and beverages – most soft drinks and fruit drinks, especially apple juice, canned fruits, dairy desserts, flavoured yogurts, most baked goods, many cereals, and jellies contain high fructose (Bray 2013).
A 12-year prospective cohort study by Choi & Curhan (2008), involving 46,393 men with no history of gout demonstrated that men who consumed > 2 sugar-sweetened beverages per day had an greater risk of the development of gout compared with infrequent consumers.
Why is fructose such a culprit?
Fructose is metabolized primarily in the liver. Unlike glucose, fructose uptake by the liver is unregulated by hepatic energy status, as the key regulatory enzyme phosphofructokinase-1 (PFK1), the ‘gatekeeper’ of glycolysis, is bypassed (Stanhope 2016).
As explained by Fox et al (1987), the first step in the metabolism of fructose is its phosphorylation to ADP, which serves as a substrate for the catabolic pathway to uric acid formation, as adenine nucleotides are degraded to purine metabolites (adenosine, inosine, hypoxanthine & xanthine) and uric acid.
In addition, approximately a quarter of ingested fructose could be converted into lactic acid within a few of hours (Sun & Empie 2012), which accelerates reabsorption of uric acid in the kidneys, contributing to gout.
Nutritional strategies to manage gout
Since gout patients present with other comorbidities such as obesity, diabetes mellitus, dyslipidemia and hypertension, following the Mediterranean diet (MD), has been shown particularly beneficial for gout sufferers (Nickolai & Kiss 2016).
MD is characterized by the following and abundant use of olive oil, high consumption of plant foods (fruits, vegetables, legumes, cereals, nuts, and seeds), frequent but moderate intake of wine (especially red wine) with meals, moderate consumption of fish, seafood, fermented dairy products (yogurt and cheese), poultry and eggs (Ros et al 2014)
Increase fruit & vegetable intake – a cross-sectional study by Zykova et al (2015) demonstrated that the alkalizing effect of fruit and vegetables might lower serum uric acid levels. Earlier studies by Kanbara et al (2010), demonstrated that uric acid is more transportable in alkaline urine, while uric acid excretion is suppressed in acidic medium. The authors concluded “our study provides a key to explain a long-standing view that gout is most common among people whose diet is rich in meat and low in vegetable and fruits”.
Enjoy moderate amount of wine – studies by Stibůrková et al (2014) confirmed earlier findings by Choi & Curhan (2004), which suggested that moderate wine drinking does not increase the serum uric acid concentration, as the antioxidant polyphenols in wine, may mitigate the effects of alcohol on uric acids concentrations.
Enjoy low-fat dairy products – dairy is associated with a lower risk of gout and blood levels of uric acid (Nickolai & Kiss 2016). The mechanism for such association is due to milk-forming proteins (lactalbumin and casein), which increase excretion of uric acid in urine (Ghadirian et al 1995).
Enjoy plant-derived proteins (e.g. nuts and legumes) – studies by Zhang et al (2012) support the notion that plant-derived foods should be the preferred sources of protein for gout patients, given that plant food items are excellent sources of protein, fibre, vitamins and minerals.
Enjoy cherries or cherry juice – an observational study found that cherry intake was associated with a lower risk of gout attacks compared with no intake (Zhang et al 2012). Anthocyanins, particularly in sour cherries, have been researched and proven highly beneficial to gout patients (Zhang et al 2012). Cherries are also high in vitamin C, which has also been shown to be useful nutrient for aiding gout. It is thought that vitamin C increases the excretion of uric acid in the urine (Stamp et al 2013).
Enjoy quercetin rich foods such as apples, onions, leeks, etc. Shi & Williamson (2016) demonstrated that a daily supplementation of 500 mg quercetin, containing the bioavailable amount of quercetin as present in approximately 100g red onions, for 4 weeks, significantly reduces elevated plasma uric acid concentrations in healthy males. They suggested that this could be due to quercetin, a flavonoid, inhibiting xanthine oxidoreductase, the final step in intracellular uric acid production.
Enjoy your coffee – coffee could be considered as a preventive measure for gout, as it can lower uric acid levels (Nickolai & Kiss 2016). However, a meta-analysis by Zhang et al (2016) concluded that currently there is insufficient evidences to validate the association between coffee consumption and a lower risk of hyperuricemia. Nevertheless, the authors acknowledged that there are several studies that have shown that coffee consumption may be associated with a lower risk of gout.
For example, 1,3,7-trimethyl-xanthine, a major component of coffee, was demonstrated to competitively inhibit xanthine oxidase in rats (Kela et al 1980). As commented by Choi et al (2010), this potential property of caffeine may exert a protective effect against gout that is similar to the effect of allopurinol.
Studies by Kiyohara et al (1999) suggested that 2 – 5 cups of coffee a day may reduce serum uric acid levels due to the diuretic action of coffee and increased renal excretion of uric acid. The authors also suggested that non-caffeine xanthines in coffee may also inhibit UA synthesis in a similar effect to allopurinol, which is a xanthine oxidoreductase (XOR)-inhibitor.
As explained by Stibůrková et al (2016), serum uric acid (UA) concentration depends on the balance between uric acid production and excretion. UA excretion occurs via the kidneys so adequate hydration is vital for healthy kidney function (Wesseling et al 2016).
The Institute of Medicine recommends that sedentary women and men over age of 19 should have a total water intake of 2.7 – 3.7 L / day from all fluids & foods (Kenefick et al 2012)
Avoiding dehydration is important as becoming dehydrated, especially after drinking alcohol, can trigger an attack (UK Gout Society 2015)
References available on request
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