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A common thought is that dietary restrictions are recommended for people susceptible to gout.

These restrictions often focus on fructose, purines and alcohol: if a food or beverage is 'high' in these, they should be avoided, but that theory seems to not really translate into empirical evidence when looking at actual levels of substances to avoid in food and beverages and the effect of actual food on the observable incidences.

Different sources may recommend different things, just following their 'school of thought'? But in the following text all these discrepancies are combined into one:

Several facets of the diet are important to the reduction of the risks of a gouty episode: meat and seafood intake, alcohol use, and obesity. Although many physicians still advise patients to reduce their dietary intake of purines, purine-restricted diets only reduce mean serum urate levels by 0.6 mM/l, and such diets are relatively unpalatable.

For the moment, the best data related to diet comes from a recent study of 47,150 men over a 12-year period that shows meat and seafood increase the risk of gout. In contrast, dairy products, especially low-fat dairy products, are able to decrease the risk of gout in men. In addition to food, alcohol is another significant risk factor for gout. The relationship between gout and alcohol is more complex. Acute alcohol intoxication in individuals documents a higher plasma urate concentration when urate levels are measured after individuals have become sober. Such urate alterations may also occur as a result of not eating and the presence of ketosis. The latter state and its circulating ketones and lactate block urate excretion causing hyperuricemia. In normal individuals, elevated plasma levels of ethanol (> 200 mg/dl) cause a reduction in urinary urate levels [869, 870]. When moonshine whiskey was produced from lead-soldered stills, saturnine gout or lead-induced gout was a common occurrence in the southern part of the United States.

Finally, beer contains a purine (guanosine) that can be metabolized to uric acid. Recent studies of 14,809 individuals in the Third National Health and Nutrition Examination Survey (NHANES) examined the role of beer, wine, and hard liquor in relation to uric acid. In this study, beer and hard liquor intake were positively correlated with hyperuricemia. It has been proposed that a glass of wine as a replacement for beer or hard liquor might reduce the incidence of gout. Both alcohol intake and obesity can cause an increase in urate production and a decrease in its elimination by the kidney.

Although medications are usually the means by which recurrent gouty episodes are controlled, there are certain dietary restrictions that may be useful as well. It has been shown that meat and seafood intake are associated with an increased risk of gout. Meat including beef, lamb, and pork as well as bologna, sausage, salami, bacon, hot dogs, chicken, turkey, hamburger, chicken liver, and beef liver are the most well-characterized offenders as inducers of gouty episodes. Seafood associated with an increase risk of gout include tuna, dark fish, shrimp, lobster, clams, and scallops. There are also some purine-rich vegetables like peas, lentils, spinach, mushrooms, oatmeal, and cauliflower, but they do not appear to increase the risk of gout.

Alcohol ingestion in excess and its association with gout has been known since antiquity. Beer has a special capacity to raise the serum uric acid levels and put patients at risk for gouty episodes since it contains guanosine, a purine that is easily converted enzymatically to uric acid. Finally, many patients will tell their physician that particular foods or alcoholic beverages will trigger an attack of gout. In these cases, physicians should heed the patient’s information and ask the patient to restrict their intake of the offending agent.

How to properly explain the associations between diet and gout that is at the same time theory guided, simple and accurate?

It seems that 'purine-rich' is too simple, as purine-rich vegetables don't seem to count?

It seems that 'alcohol' isn't a factor at all, as since antiquity beer is known to be bad, but wine with a much higher alcohol content is noted as not being bad?

The practical guideline is just that:

In general, the three foods/beverages that place patients at risk for gout are red meat, beer, and fructose, a sugar commonly found in sugar- sweetened soft drinks. Finally, patients with gout should decrease their use of hard liquor and beer with a substitution of wine if necessary.

Quotes from David S. Newcombe: "Gout. Basic Science and Clinical Practice", Springer: London, Heidelberg, 2013. (9 Management of Hyperuricemia and Gout, 291–385, DOI.)

Specifically for alcohol, which is sometimes even thought to be preventative if taken as wine in low doses:

In conclusion, our results suggest that the effect of individual alcoholic beverages on serum uric acid levels varies substantially: beer confers a larger increase than liquor, whereas moderate wine drinking does not increase serum uric acid levels.
Hyon K. Choi & Gary Curhan: "Beer, liquor, and wine consumption and serum uric acid level: The Third National Health and Nutrition Examination Survey", Athritis Care and Research, Volume 51, Issue 6, 15 December 2004, Pages 1023-1029. DOI

How does one explain 'avoid purines in food' if purine-rich plant food isn't counting?
How does one explain 'avoid alcohol' if alcoholic wine seems fine?

Is the above interpreted correctly? Is the theory wrong, incomplete or in need of modification?

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How does one explain 'avoid purines in food' if purine-rich plant food isn't counting?

Sustained increase in blood uric acid levels (hyperuricemia) is a risk factor for acute gouty arthritis (Current Pharmaceutical Design).

Purines can increase serum uric acid levels. Intake of hypoxanthine, the main purine in organ meats, red meat and seafood, strongly increases uric acid and increases the risk of gout, while guanine, the main purine in plant foods does not increase uric acid; this is why purine-rich plant foods are not associated with increased risk of gout (JN, J-Stage, Science Alert, NEJM).

Studies in which the intake of high-purine plants was not associated with increased risk of gout: NEJM, CO-Rheumatology

Vegetarians are at lowest risk of gout, followed by fish eaters, meat eaters and vegans, who are at the highest risk, supposedly due to lack of preventative effect of proteins from milk (Plos One).

How does one explain 'avoid alcohol' if alcoholic wine seems fine?

Ethanol increases serum uric acid levels by stimulation of the production of uric acid from purines (Arthritis Care and Research, Clinica Chimica Acta).

Beer is high in purines (225–1,145 μmol/L), especially in guanosine (Beer in Health and Disease Prevention). Guanosine is the most readily absorbed dietary purine, which can explain why beer increases serum uric acid levels (British Journal of Rheumatology) and the risk of gout attacks (CO-Rheumatology).

Wine is low in purines (28-108 μmol/L) (Biomedical Chromatography). According to some studies, moderate wine intake does not increase uric acid levels (Arthritis Care and Research). However, according to one study, even moderate wine intake increases the risk of gout attacks in the individuals with gout (American Journal of Medicine), probably due to ethanol.

Spirits are low in purines (0.7–26 μmol/L) (Biomedical Chromatography); they increase uric acid levels less than beer (Arthritis Care and Research). Spirit consumption is associated with an increased risk of gout attacks (CO-Rheumatology). Congeners (substances other than ethanol) in spirits can have different effects on uric acid (Phytotherapy Research); in one study whisky stimulated uric acid excretion and thus lowered its serum levels (Alcoholism: Clinical and Experimental Research).

Which dietary factors are associated with decreased uric acid levels and risk of gout?

What can one do to prevent gout?

Diet low in purines alone may not be very effective in prevention of gout attacks. Lowering beer and meat intake may reduce the risk of gout attacks, but more likely if done in combination with reduction of body weight and blood pressure (if necessary); uric acid-lowering drugs can also help (Annals of Internal Medicine, 2017, Autoimmunity Reviews, 2018, Journal of Advanced Research, 2017).

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