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Purines, Gout, and Huel

What is gout?

Gout is regarded as the most common form of arthritis, affecting approx. 5% of the western population at some stage of their adult life[1]. Gout is characterized by causing sharp pain, redness and swelling, that is often accompanied by intense heat around the affected joint. The most common affected areas are the joints within the foot, especially the big toe (metatarsophalangeal joint), followed by the knee, elbow, wrist and finger joints[2]. Gout can flare up quickly and if untreated can last for prolonged periods of time and can be debilitating. However, if the attack is treated quickly, symptoms can be minimized[3].

Acute gout attacks are traditionally treated with pharmaceutical drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and colchicine which reduce the painful symptoms and the swelling[4]. However, the most effective and proven methods in gout treatment and prevention are changes in dietary habits and increasing physical activity, which can significantly reduce gout onset and flare-ups[5]. The major causes of gout are excessive consumption of purine-rich foods, high blood pressure and obesity[6]. Lifestyle changes have shown to have the highest positive effect on the long-term management of gout, along with a calorie-controlled diet that is abundant in phytonutrients, antioxidants and vitamin C[4-6].

What are purines?

Purines are naturally-occurring compounds found in the body, a lot of foods and some drinks[7]. Purines include the nucleobases adenine and guanine that are essential for the formation of RNA and DNA[8]. Other purines are the nucleotides; adenosine and guanosine, hypoxanthine and xanthine which are essential for the production of enzymes such as coenzyme A, adenosine triphosphate (ATP) for energy production, cell transcription, cyclic AMP and NADH for cell signaling and antioxidant reactions and the synthesis and oxidation of fatty acids[8].

Another common dietary purine is caffeine which is chemically related to adenine and guanine. However, research has indicated that those who regularly drink coffee are at no greater risk of developing gout[9]. Research even suggests that moderate coffee consumption is associated with a reduced gout risk, particularly with regular ingestion of fully-caffeinated coffee due to the antioxidant content and caffeine’s effect on circulation[10].

A moderate purine intake is key to the maintenance of normal uric acid levels for those prone to gout. Frequent and high intakes of purine-rich foods enhance serum uric acid levels which is involved in the process of gout[11].

What is uric acid?

The cause of gout stems from having too much uric acid circulating in the bloodstream.

Uric acid is as an important antioxidant that helps to prevent damage caused by free-radicals, and a continuous supply of uric acid is important for protecting blood vessels[12]. Uric acid is a waste product that is created from the breakdown of dietary purines. If levels of uric acid are too high for prolonged periods of time, crystals can form within the joint tissues causing them to swell and become painful[12].

The susceptibility to having elevated blood uric acid levels can develop acutely from inflammation brought on by a common virus or infection[13], chronically from kidney disease[14] or can be inherited[15], all of which lead the body’s inability to efficiently remove excess acids levels.

Increasing evidence points to gout flare-ups being heavily influenced by lifestyle and dietary habits[4-6]. Gout is also more common in people who are overweight and have type 2 diabetes, even when uric acid levels are within the normal range, as excess weight adds additional strain to joints and insulin resistance lowers the tolerance of uric acid[16].

How diet can impact gout

Diet has a significant role in both causing and reducing the likelihood of suffering further painful attacks of gout. Someone who already suffers from gout or has multiple risk factors, eating a diet that is lowered in purines can result in a reduction of gout attacks. The American College of Rheumatology recommends limiting purine-rich foods and increasing vitamin C intake to protect against elevating uric acid levels[17, 18].

General dietary guidelines to prevent and manage gout are in-line with those of a general healthy eating diet, such as the DASH diet which is aimed at reducing high blood pressure and creating a heart-healthy eating style[19]. The DASH diet is a plan that is rich in fruit, vegetables, and whole grains includes fat-free or low-fat dairy products and encourages the consumption of fish, poultry, beans and nuts[20].

One of the main risk factors for the onset of gout is being overweight, and studies suggest that just by reducing excess body fat and taking the strain off joints, even without lowering the intake of high purine foods, will reduce circulating uric acid levels and therefore reducing gout flare-ups[21].

Consuming a diet rich in a variety of fruits, vegetables, and whole grains has been shown to reduce gout attacks, largely linked to the vitamin and antioxidant content. Carbohydrate-rich foods that are lower in the glycaemic index (GI) have less inflammatory-causing properties[17, 21]. The intake of foods such as processed white bread, cakes, confectionery, beverages containing sugar and products with high-fructose corn syrup are all associated with increased risk and prevalence of gout[22].

By maintaining optimal hydration, the clearance of circulating uric acid is aided through excretion via the kidneys[23]. Limiting alcohol consumption is also important to reduce gout attacks, as the metabolism of alcohol increases uric acid production. In addition, large intakes of alcohol can contribute to dehydration, high blood sugar and a build-up of by-products that can cause DNA damage[24, 25].

Reducing the intake of overly-processed animal products, animal fats and excessive intake of dairy products have all been shown to have a positive reaction to gout flare-ups and risk, even though dairy products have low purine content[26]. This is also seen by limiting the intake of animal proteins, particularly organ meats[26]. However, the fatty acids found in salmon, flax, olive oil, and nuts have anti-inflammatory benefits and therefore a balanced intake is essential; however, affecting levels differ from person to person[27].

Whilst some vegetable, for instance, asparagus, spinach, peas, cauliflower or mushrooms, are high in purines, these vegetables do not increase the risk of gout or recurring gout attack due to their content of phytonutrients[28]. Indeed, some people find that foods such as citrus fruits, tomatoes, and nuts can trigger gout, even though they are not high in purines and this can make management tricky[29, 30].

Consuming dark berries have been shown to lower purine conversion into uric acid and further reduce inflammation[31]. This is due to them containing flavonoids and anthocyanins, both of which are antioxidants that enhance the collagen-content of tendons and cartilages surrounding affected joints[11].

Studies have shown that diets high in vitamin C and that are low in acid-forming foods (such as fruits, vegetables, herbs, and spices) are less likely to develop gout[32].

Vitamin C and gout

Vitamin C protects against gout by lowering serum uric acid, and this is thought to be due to greater removal of uric acid through the kidneys[32]. A broad range of research has been focused on vitamin C’s protective properties. Whilst some research did not produce statistically significant results, the research does see gout attacks, flare-ups and incidence reduce when vitamin C is increased[19, 30, 32]. One particular study over 20 years followed 47,000 participants and observed gout was significantly reduced, managed and limited when vitamin C intake was 500-1000mg per day, 5.5-11 times higher than the official recommended daily intake of 90mg[33-36]. Studies have shown that higher amounts of vitamin C in the bloodstream can significantly help to increase the amount of uric acid that is expelled through urine[37]. Because vitamin C is an antioxidant, it may also help to reduce inflammation[35, 38].

Gout and Huel

Huel contains moderate levels of purines from the oats and flaxseed. Laboratory tests on Huel Vanilla and Coffee (based on EU v2.3 formulation) have shown total purine levels of 0.15% and 0.13% respectively. The purine level of Huel is similar to that of spinach, soya and beef (see Table 1). However, Huel has a very high vitamin C content (61mg per 100g, or 300mg per 2000 calories) which helps to protect the body from gout attacks by aiding the reduction of circulating uric acid. Huel also has a high omega-3 fatty acid content which aids the reduction of inflammation. Furthermore, as obesity is increasingly becoming the recognised exasperating factor for gout, a calorie-controlled, nutrient-rich diet is advantageous to reduce symptoms, flare-ups, and occurrence. Huel has a clear advantage here (view the nutritional profiles of Huel powders here).

For those who are particularly prone to recurrent gout attacks due to poor uric acid clearance, it would, however, be prudent to gradually introduce Huel into the diet to see how it’s tolerated. Indeed, those who are notably susceptible to the negative effects of purines on their gout should limit their intake of Huel to a maximum of one to two servings per day.

Balancing the literature and research, looking at the levels of purines vs. the vitamin C, phytonutrient, antioxidant and omega-3 content as well as the GI (Huel Powder has a low GI of 17) (based on EU v2.3 formulation)[40]) of Huel powders, it is credible to conclude that a regular intake of Huel will not increase the risk of developing or exacerbating the symptoms of gout.

Table 1: Percentage of purines in commonly consumed foods[17, 18, 22, 28, 29, 37]

Grains Total Purine Content (%)
Barley 0.04
Buckwheat 0.07
Wheat flour 0.01
Rice 0.03
Soy-based produce
Tofu 0.05
Freeze-dried tofu 0.3
Soybean 0.11
Soy milk 0.02
Nuts, legumes, and beans
Almond 0.03
Adzuki 0.07
Peanuts 0.04
Vegetables and fruits
Asparagus 0.05
Avocado 0.01
Banana 0.003
Broccoli 0.07
Cauliflower 0.05
Cabbage 0.003
Cucumber 0.009
Garlic 0.02
Potato 0.006
Spinach 0.17
Strawberry 0.002
Sweet potato 0.02
Dairy and eggs
Egg (chicken) 0
Cheese 0.005
Semi-skimmed milk 0
Yogurt (2% fat) 0.005
Meat
Beef 0.13
Beef liver 0.21
Chicken 0.14
Chicken liver 0.3
Lamb 0.09
Pork 0.11

 

References

  1. Zhu Y, et al. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011; 63(10):3136-41.
  2. Saseen JJ, et al. Comparison of patient characteristics and gout-related health-care resource utilization and costs in patients with frequent versus infrequent gouty arthritis attacks. Rheumatology (Oxford). 2012; 51(11):2004-12.
  3. Fraile JM, et al. Metabolic syndrome characteristics in gout patients. Nucleosides Nucleotides Nucleic Acids. 2010; 29(4-6):325-9.
  4. Keenan RT, et al. New and Pipeline Drugs for Gout. Curr Rheumatol Rep. 2016; 18(6):32.
  5. Manara M, et al. Lifestyle and dietary habits of patients with gout followed in rheumatology settings. Reumatismo. 2015; 67(4):138-48.
  6. Juraschek S, et al. Should the DASH Diet be Recommended for Gout Patients? JCOM. 2017; 24(1).
  7. Lockyer S, et al. Diet and gout-what is the role of purines? Nutrition Bulletin. 2016; 41(2):155-66.
  8. Correa C, et al. Quality of Diet and Body Mass Index are Factors Involved in DNA Damage in Human Lymphocytes. The FASEB Journal. 2015; 29(1).
  9. Samanidou V. Determination of polyphenols and major purine alkaloids in coffee:
  10. An overview. Coffee in Health and Disease Prevention. 2015:971-81.
  11. Larsson SC, et al. Coffee consumption and gout: a Mendelian randomisation study. Ann Rheum Dis. 2018.
  12. Sidor A, et al. Advanced research on the antioxidant and health benefit of elderberry (Sambucus nigra) in food–a review. Journal of Functional Foods. 2015; 18:941-58.
  13. Choi HK, et al. Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2005; 52(1):283-9.
  14. Martinon F, et al. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature. 2006; 440(7081):237-41.
  15. Fuldeore MJ, et al. Chronic kidney disease in gout in a managed care setting. BMC Nephrol. 2011; 12:36.
  16. Major TJ, et al. An update on the genetics of hyperuricaemia and gout. Nat Rev Rheumatol. 2018; 14(6):341-53.
  17. Wijnands JM, et al. Individuals With Type 2 Diabetes Mellitus Are at an Increased Risk of Gout But This Is Not Due to Diabetes: A Population-Based Cohort Study. Medicine (Baltimore). 2015; 94(32):e1358.
  18. Khanna D, et al. 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. Arthritis Care Res (Hoboken). 2012; 64(10):1431-46.
  19. Choi HK, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004; 350(11):1093-103.
  20. Juraschek SP, et al. Effects of the Dietary Approaches to Stop Hypertension (DASH) Diet and Sodium Intake on Serum Uric Acid. Arthritis Rheumatol. 2016; 68(12):3002-9.
  21. Challa HJ, et al. DASH Diet (Dietary Approaches to Stop Hypertension). StatPearls Publishing: Treasure Island (FL); 2018.
  22. Nielsen SM, et al. Weight loss for overweight and obese individuals with gout: a systematic review of longitudinal studies. Ann Rheum Dis. 2017; 76(11):1870-82.
  23. Kuo CF, et al. Global epidemiology of gout: prevalence, incidence and risk factors. Nat Rev Rheumatol. 2015; 11(11):649-62.
  24. Saigal R, et al. Pathogenesis and Clinical Management of Gouty Arthritis. J Assoc Physicians India. 2015; 63(12):56-63.
  25. Tu HP, et al. Alcohol-related diseases and alcohol dependence syndrome is associated with increased gout risk: A nationwide population-based cohort study. Joint Bone Spine. 2017; 84(2):189-96.
  26. Langevin F, et al. Fancd2 counteracts the toxic effects of naturally produced aldehydes in mice. Nature. 2011; 475:53.
  27. Beyl RN, Jr., et al. Update on Importance of Diet in Gout. Am J Med. 2016; 129(11):1153-8.
  28. Abhishek A, et al. Low omega-3 fatty acid levels associate with frequent gout attacks: a case-control study. Ann Rheum Dis. 2016; 75(4):784-5.
  29. Shi Y, et al. Quercetin lowers plasma uric acid in pre-hyperuricaemic males: a randomised, double-blinded, placebo-controlled, cross-over trial. Br J Nutr. 2016; 115(5):800-6.
  30. Flynn TJ, et al. Positive association of tomato consumption with serum urate: support for tomato consumption as an anecdotal trigger of gout flares. BMC Musculoskelet Disord. 2015; 16:196.
  31. Flynn T. Experiencing Gout in New Zealand: The Genetic and Dietary Influences of a Complex Disease (Doctoral Dissertation, University of Otago). 2016.
  32. David A, et al. Overviews of Biological Importance of Quercetin: A Bioactive Flavonoid. Pharmacognosy Review. 2016; 10(20):84.
  33. Towiwat P, et al. The association of vitamin C, alcohol, coffee, tea, milk and yogurt with uric acid and gout. Int J Rheum Dis. 2015; 18(5):495-501.
  34. Choi HK, et al. Vitamin C intake and the risk of gout in men: a prospective study. Arch Intern Med. 2009; 169(5):502-7.
  35. Maiuolo J, et al. Regulation of uric acid metabolism and excretion. Int J Cardiol. 2016; 213:8-14.
  36. Mann J, et al. Essentials of Human Nutrition. 5 ed: Oxford University Press; 2017.
  37. National Institutes of Health. Labeling Daily Values [Available from: https://www.dsld.nlm.nih.gov/dsld/dailyvalue.jsp].
  38. Rai SK, et al. The Dietary Approaches to Stop Hypertension (DASH) diet, Western diet, and risk of gout in men: prospective cohort study. BMJ. 2017; 357:j1794.
  39. Ellulu MS, et al. Effect of vitamin C on inflammation and metabolic markers in hypertensive and/or diabetic obese adults: a randomized controlled trial. Drug Des Devel Ther. 2015; 9:3405-12.
  40. Lightowler H, et al. Glycaemic Index Value for Huel Vanilla Powder v1.1. Oxford Brookes Centre for Nutrition and Health, Oxford Brookes University; 2019.

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