Gout, a common form of arthritis, occurs when monosodium urate (MSU) crystals build up within joints following chronic high uric levels in the blood (hyperuricemia).1 It affects between 1 and 2 per cent of adults in developed countries, and is the most common inflammatory arthritis in men. Population studies suggest this painful condition is on the rise, probably due to the twin rise in metabolic syndrome (MetS), with which it’s intimately connected.
Gout and hyperuricemia are also associated with hypertension, type 2 diabetes, and renal and cardiovascular diseases.1 In fact gout appears to specifically be a risk for cardiovascular related illnesses and death, as well as death for any reason.2 This is likely linked to the high uric acid levels in the blood which drive inflammation.3
Alcohol, meat and more can raise gout risks
A 2011 review of the risk factors for gout identified 53 relevant studies.4 Drinking alcohol, especially beer and spirits, increased the risk for gout. A diet high in meat, seafood, sugar-sweetened drinks, and high fructose foods (in keeping with gout’s link to MetS, where more than 60 per cent of people with gout also have this disorder5) were all associated with the painful condition as well. On the other hand, dairy, folate and coffee were each associated with a lower incidence of gout.
Uric acid is normally formed in the body as a by-product of purine metabolism. However, we now understand that a diet high in fructose also leads to higher production of uric acid.6 The metabolism of fructose is different to glucose: it’s faster and lacks any negative feedback control. So when we down a sugary drink, a massive flux of fructose arrives in the liver sending the cells into metabolic hyper drive. The first step is the addition of a phosphate entity to the fructose to form fructose-1-phosphate. Because there’s no negative feedback control, the liver is obliged to do this for every fructose molecule it encounters. Adenosine triphosphate (ATP) is used to provide this phosphate group, with the resultant production of adenosine diphosphate (ADP).
Too much fructose leads to too much uric acid
Normally, the ADP would be converted back to ATP by the liver cells, but because all the available phosphate is being used up dealing with the high flux of fructose, they cannot do this. As a result ATP is depleted, and too much ADP is created. (This contrasts with glucose, which has a tightly controlled metabolism via negative feedback, preventing excessive glucose phosphorylation and ATP depletion). The excess ADP is metabolized over several steps to form xanthine, which is then converted to uric acid. So, in other words, dumping a load of fructose on the liver causes a rise in uric acid production that eventually results in higher levels in the blood.
Ditch the fructose – load up on dairy and cherries instead
If you suffer from gout you should severely limit the amount of fructose you eat. Cane sugar, honey and corn syrup should all be avoided, especially in drinks. In addition, dried fruit and fruit juices should be eliminated. You can eat whole fruit but stick to those fruits that are low in fructose, namely stone fruit, berries, tart or sour cherries (in preference to normal cherries), banana, pineapple and all the citrus fruits. If you need to add sugar to something it should be glucose or xylitol (but in moderation). Recent research has shown that eating a moderate amount of purine-rich vegetables (asparagus, mushrooms, peas and so on) or protein isn’t associated with an increased risk of gout.7 However, research has also confirmed the advice to avoid, or reduce red meat, offal, seafood and alcohol in your diet. 7,8 Low-fat dairy products can be increased, as these appear to be protective,9 and the inclusion of cherries in the diet is now supported by reasonable evidence (see below). Losing weight, getting daily exercise and maintaining a low glycemic index diet are also important.10
People have been using cherries to reduce their risk of a gout attack for a long time. But the first attempt to provide objective proof of this relationship was a US study published in 2003. Plasma urate, antioxidant and inflammatory markers were measured in 10 healthy women who ate sweet cherries.11 The women, aged 22 to 40 years, had two servings (280g) of cherries after an overnight fast. Blood and urine samples were taken before they ate the cherries and at times thereafter. Plasma urate was decreased five hours after cherry intake, being 183 ± 15 micromol/L, compared with a predose baseline of 214 ± 13 micromol/L (p < 0.05). Urinary urate was increased, indicating better excretion. Plasma C-reactive protein (CRP) and nitric oxide (NO) concentrations had decreased marginally at three hours postdose (p < 0.1), whereas plasma albumin and tumour necrosis factor-alpha were unchanged.
Tart cherry juice reduced uric acid by 25%
Much later in 2010, a combined UK/US research team investigated how well tart cherry juice could aid in recovery and reduce muscle damage, inflammation and oxidative stress.12 Twenty recreational marathon runners drank either cherry juice or a placebo for five days before, the day of and for 48 hours following a marathon run. Markers of muscle damage (creatine kinase, lactate dehydrogenase, muscle soreness and isometric strength), inflammation (interleukin-6 [IL-6], CRP and uric acid), total antioxidant status (TAS) and oxidative stress (thiobarbituric acid reactive species (TBARS) and protein carbonyls) were examined before and following the run. Isometric strength recovered significantly faster in the cherry juice group. No other damage measures were significantly different. Inflammation was reduced in the cherry juice group and TAS was about 10 per cent greater for all post-supplementation measures (p < 0.05). Protein carbonyls were not different; however, TBARS was lower in the cherry juice group than the placebo at 48 hours (p < 0.05). Specifically for the context of this article, uric acid was reduced by around 25 per cent post-race in the tart cherry group compared to the placebo group.
Cherries linked to 35% lower risk of gout attacks
Interesting as these impacts on serum uric acid might be, they didn’t link cherry consumption to fewer gout attacks. A new US/Australian study published in late 2012 does exactly that. A case-crossover design was used to examine the role of various factors, including cherry consumption, with recurrent gout attacks.13 People with gout were recruited and then followed up on online for one year. Participants were asked to provide the following information regarding gout attacks: the onset date of the attack, symptoms and signs, medications (including antigout medications), and exposure to potential risk factors (including daily intake of cherries and cherry extract) during the two-day period prior to the gout attack. The authors then assessed the same exposure information over four two-day control periods and estimated the risk of recurrent gout attacks related to cherry intake using conditional logistic regression. The study included 633 people with gout. Eating cherries over a two-day period was associated with a 35 per cent lower risk of gout attacks compared to no intake (multivariate odds ratio (OR) 0.65). Cherry extract intake showed a similar inverse association (multivariate OR 0.55).
Prevent future attacks with herbs
Herbs have also been traditionally used to help gout sufferers. In fact, gout is particularly suited to being treated with herbal remedies. There are a number which are believed to increase elimination of urate from the kidneys, notably celery (Apium graveolens), stinging nettles (Urtica species) and birch (Betula alba). These herbs do appear to ease the symptoms and even help to prevent gout attacks. Other herbs that are traditionally used include sarsaparilla (Smilax species) and dandelion leaf (Taraxacum officinale). A recent survey of 142 herbal practitioners in the UK found that celery, nettles and dandelion leaf were commonly chosen for their reputation for helping the excretion of uric acid, while birch and turmeric (Curcuma longa) were high among those chosen to reduce inflammation.14
Clinical trials are also emerging that suggest certain herbs can lower serum uric acid. The traditional Chinese medicine combination of liquorice (Glycyrrhiza species) and white peony (Paeonia lactiflora) is one such example.15 Study participants were male Buddhist vegetarians with asymptomatic hyperuricemia enrolled at Fu Yuan Buddhist College, Taipei, Taiwan. The control group was made up of normal, non-vegetarian healthy men. Both groups received a combination of the two herbs as a decoction three times a day for four weeks. While there was a small non-significant decrease in serum uric acid in the healthy control group, the average level in the hyperuricemic participants fell by 19.4 per cent (p < 0.01 compared to baseline). Changes in blood pressure were minimal; indicating the dose of liquorice used didn’t have a significant influence on the volunteer’s blood pressure.To your better health,
Nutrition & Healing
Vol. 8, Issue 10 – October 2014
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